Datasets:

AshtonIsNotHere

/

biosift-nli

like 2

Point-of-care platelet reactivity determination with VerifyNow-P2Y12 following administration of clopidogrel or prasugrel: data from a real-world, clinical care inpatient setting.

To describe VerifyNow-P2Y12 (VN-P2Y12, Accumetrics, San Diego, CA) results from patients treated with either clopidogrel or prasugrel who were seeking care in a hospital setting. VN-P2Y12 is a point-of-care device that measures platelet reactivity to adenosine diphosphate. Past assessments of thienopyridine therapy utilizing VN-P2Y12 have largely come from clinical trial settings. There are limited data from real-world settings. Electronic medical record data from Huntsville Hospital (Huntsville, AL) for those who underwent VN-P2Y12 testing for clopidogrel or prasugrel between January 1, 2009 and October 31, 2010 were analyzed. The VN-P2Y12 data included P2Y12 reaction units (PRUs) and device-reported percentage of inhibition. Descriptive analyses were conducted with t tests, and a logistic regression model was estimated to assess the association between patient characteristics and the likelihood of platelet nonresponse. In total, 2882 tests (2476 with clopidogrel and 406 with prasugrel) were analyzed. For clopidogrel and prasugrel, respectively, mean PRU standard deviation (SD) was 206 (90) and 107 (93; P < 0.0001) and mean % inhibition (SD) was 31% (26%) and 63% (31%; P < 0.0001). Treatment with clopidogrel alone (odds ratio [OR] = 5.25; P < 0.0001), being non-Caucasian (OR = 1.48; P = 0.0440), obese (OR = 1.49; P = 0.0010), anemic (OR = 3.29; P < 0.0001), diabetic (OR = 1.75; P < 0.0001), and having a history of myocardial infarction (OR = 1.57; P < 0.0001) were significant predictors of having PRU ≥ 235. This real-world data analysis shows results that are consistent with clinical trial results, namely that compared with clopidogrel, prasugrel is associated with significantly lower PRU and greater percentage of inhibition, regardless of age, race, gender, diabetes, obesity, or proton pump inhibitor use.

This study has a target drug

Point-of-care platelet reactivity determination with VerifyNow-P2Y12 following administration of clopidogrel or prasugrel: data from a real-world, clinical care inpatient setting.

To describe VerifyNow-P2Y12 (VN-P2Y12, Accumetrics, San Diego, CA) results from patients treated with either clopidogrel or prasugrel who were seeking care in a hospital setting. VN-P2Y12 is a point-of-care device that measures platelet reactivity to adenosine diphosphate. Past assessments of thienopyridine therapy utilizing VN-P2Y12 have largely come from clinical trial settings. There are limited data from real-world settings. Electronic medical record data from Huntsville Hospital (Huntsville, AL) for those who underwent VN-P2Y12 testing for clopidogrel or prasugrel between January 1, 2009 and October 31, 2010 were analyzed. The VN-P2Y12 data included P2Y12 reaction units (PRUs) and device-reported percentage of inhibition. Descriptive analyses were conducted with t tests, and a logistic regression model was estimated to assess the association between patient characteristics and the likelihood of platelet nonresponse. In total, 2882 tests (2476 with clopidogrel and 406 with prasugrel) were analyzed. For clopidogrel and prasugrel, respectively, mean PRU standard deviation (SD) was 206 (90) and 107 (93; P < 0.0001) and mean % inhibition (SD) was 31% (26%) and 63% (31%; P < 0.0001). Treatment with clopidogrel alone (odds ratio [OR] = 5.25; P < 0.0001), being non-Caucasian (OR = 1.48; P = 0.0440), obese (OR = 1.49; P = 0.0010), anemic (OR = 3.29; P < 0.0001), diabetic (OR = 1.75; P < 0.0001), and having a history of myocardial infarction (OR = 1.57; P < 0.0001) were significant predictors of having PRU ≥ 235. This real-world data analysis shows results that are consistent with clinical trial results, namely that compared with clopidogrel, prasugrel is associated with significantly lower PRU and greater percentage of inhibition, regardless of age, race, gender, diabetes, obesity, or proton pump inhibitor use.

This study does not have a target drug

Point-of-care platelet reactivity determination with VerifyNow-P2Y12 following administration of clopidogrel or prasugrel: data from a real-world, clinical care inpatient setting.

To describe VerifyNow-P2Y12 (VN-P2Y12, Accumetrics, San Diego, CA) results from patients treated with either clopidogrel or prasugrel who were seeking care in a hospital setting. VN-P2Y12 is a point-of-care device that measures platelet reactivity to adenosine diphosphate. Past assessments of thienopyridine therapy utilizing VN-P2Y12 have largely come from clinical trial settings. There are limited data from real-world settings. Electronic medical record data from Huntsville Hospital (Huntsville, AL) for those who underwent VN-P2Y12 testing for clopidogrel or prasugrel between January 1, 2009 and October 31, 2010 were analyzed. The VN-P2Y12 data included P2Y12 reaction units (PRUs) and device-reported percentage of inhibition. Descriptive analyses were conducted with t tests, and a logistic regression model was estimated to assess the association between patient characteristics and the likelihood of platelet nonresponse. In total, 2882 tests (2476 with clopidogrel and 406 with prasugrel) were analyzed. For clopidogrel and prasugrel, respectively, mean PRU standard deviation (SD) was 206 (90) and 107 (93; P < 0.0001) and mean % inhibition (SD) was 31% (26%) and 63% (31%; P < 0.0001). Treatment with clopidogrel alone (odds ratio [OR] = 5.25; P < 0.0001), being non-Caucasian (OR = 1.48; P = 0.0440), obese (OR = 1.49; P = 0.0010), anemic (OR = 3.29; P < 0.0001), diabetic (OR = 1.75; P < 0.0001), and having a history of myocardial infarction (OR = 1.57; P < 0.0001) were significant predictors of having PRU ≥ 235. This real-world data analysis shows results that are consistent with clinical trial results, namely that compared with clopidogrel, prasugrel is associated with significantly lower PRU and greater percentage of inhibition, regardless of age, race, gender, diabetes, obesity, or proton pump inhibitor use.

This study has a target disease

Point-of-care platelet reactivity determination with VerifyNow-P2Y12 following administration of clopidogrel or prasugrel: data from a real-world, clinical care inpatient setting.

To describe VerifyNow-P2Y12 (VN-P2Y12, Accumetrics, San Diego, CA) results from patients treated with either clopidogrel or prasugrel who were seeking care in a hospital setting. VN-P2Y12 is a point-of-care device that measures platelet reactivity to adenosine diphosphate. Past assessments of thienopyridine therapy utilizing VN-P2Y12 have largely come from clinical trial settings. There are limited data from real-world settings. Electronic medical record data from Huntsville Hospital (Huntsville, AL) for those who underwent VN-P2Y12 testing for clopidogrel or prasugrel between January 1, 2009 and October 31, 2010 were analyzed. The VN-P2Y12 data included P2Y12 reaction units (PRUs) and device-reported percentage of inhibition. Descriptive analyses were conducted with t tests, and a logistic regression model was estimated to assess the association between patient characteristics and the likelihood of platelet nonresponse. In total, 2882 tests (2476 with clopidogrel and 406 with prasugrel) were analyzed. For clopidogrel and prasugrel, respectively, mean PRU standard deviation (SD) was 206 (90) and 107 (93; P < 0.0001) and mean % inhibition (SD) was 31% (26%) and 63% (31%; P < 0.0001). Treatment with clopidogrel alone (odds ratio [OR] = 5.25; P < 0.0001), being non-Caucasian (OR = 1.48; P = 0.0440), obese (OR = 1.49; P = 0.0010), anemic (OR = 3.29; P < 0.0001), diabetic (OR = 1.75; P < 0.0001), and having a history of myocardial infarction (OR = 1.57; P < 0.0001) were significant predictors of having PRU ≥ 235. This real-world data analysis shows results that are consistent with clinical trial results, namely that compared with clopidogrel, prasugrel is associated with significantly lower PRU and greater percentage of inhibition, regardless of age, race, gender, diabetes, obesity, or proton pump inhibitor use.

This study does not have a target disease

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study has a cohort study or clinical trial

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study does not have any cohorts or clinical trial

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study has a control, double-blind, or comparison patient group

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study does not have any comparison patient group

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study has human subjects

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study does not have human subjects

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study contains population size or sample size information

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study does not contain population size information

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study does not have any quantitative outcomes

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study has a target drug

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study does not have a target drug

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study has a target disease

Management of Severe Bleeding in Patients Treated with Direct Oral Anticoagulants: An Observational Registry Analysis.

The use of prothrombin complex concentrates and the role of plasma concentration of anticoagulants in the management of bleeding in patients treated with direct oral anticoagulants are still debated. Our aim was to describe management strategies and outcomes of severe bleeding events in patients treated with direct oral anticoagulants. We performed a prospective cohort study of 732 patients treated with dabigatran, rivaroxaban, or apixaban hospitalized for severe bleeding, included prospectively in the registry from June 2013 to November 2015. Bleeding was gastrointestinal or intracranial in 37% (212 of 732) and 24% (141 of 732) of the cases, respectively. Creatinine clearance was lower than 60 ml/min in 61% (449 of 732) of the cases. The plasma concentration of direct oral anticoagulants was determined in 62% (452 of 732) of the cases and was lower than 50 ng/ml or higher than 400 ng/ml in 9.2% (41 of 452) and in 6.6% (30 of 452) of the cases, respectively. Activated or nonactivated prothrombin complex concentrates were administered in 38% of the cases (281 of 732). Mortality by day 30 was 14% (95% CI, 11 to 16). Management of severe bleeding in patients treated with direct oral anticoagulants appears to be complex. The use of prothrombin complex concentrates differs depending on bleeding sites and direct oral anticoagulant plasma concentrations. Mortality differs according to bleeding sites and was similar to previous estimates.

This study does not have a target disease

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study has a cohort study or clinical trial

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study does not have any cohorts or clinical trial

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study has a control, double-blind, or comparison patient group

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study does not have any comparison patient group

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study has human subjects

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study does not have human subjects

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study contains population size or sample size information

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study does not contain population size information

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study does not have any quantitative outcomes

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study has a target drug

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study does not have a target drug

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study has a target disease

Assessment of echocardiographic left ventricular mass before and after acute volume depletion.

Left ventricular mass calculations are often performed to assess the need or effectiveness of antihypertensive drug therapy. However, there are multiple potential errors that may affect the accuracy of these calculations, which can possibly include acute changes in preload. Therefore, to assess the hypothesis that acute volume depletion might alter calculated left ventricular mass, 15 normotensive healthy male volunteers underwent standard M-mode echocardiographic evaluations (at the level of the chordae tendineae guided by two-dimensional echocardiography) before and 2 h after 40 mg of intravenous furosemide. One patient was eliminated due to hypotension prior to the final echocardiogram. The echocardiograms were blinded to patient identity and the time sequence and read separately by two investigators. Four to five cycles were read per echocardiogram by each investigator. All values measured were the mean of the two investigators. Echocardiographic measurements were derived by both the American Society of Echocardiography and Penn conventions. An average urine volume of 1728 mL was collected, and the mean weight change 2 h after furosemide administration was 1.78 kg (P = .001). Penn left ventricular diastolic diameter (1.8 mm, P = .015) and left ventricular mass index (10 g/m2, P = .04) were significantly decreased; however, there was no significant change in septal, posterior, or relative wall thicknesses. As it is unreasonable to believe that acute remodeling of the left ventricle resulted in a decline in left ventricular mass in 2 hours, it is concluded that acute volume changes resulted in a decrease in left ventricular mass measurement due to the influence of diastolic diameter on the calculation of cardiac mass.

This study does not have a target disease

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study has a cohort study or clinical trial

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study does not have any cohorts or clinical trial

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study has a control, double-blind, or comparison patient group

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study does not have any comparison patient group

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study has human subjects

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study does not have human subjects

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study contains population size or sample size information

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study does not contain population size information

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study does not have any quantitative outcomes

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study has a target drug

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study does not have a target drug

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study has a target disease

Facial pain following sinonasal surgery or facial trauma.

The case notes of 22 patients who reported facial pain after sinonasal surgery or trauma out of a cohort of 973 patients seen in a rhinology clinic were reviewed retrospectively. This group included 10 patients who had undergone endoscopic sinus surgery and four who had suffered facial fractures. None of the patients reported any facial pain before surgery or trauma. In only one case was there any evidence, clinically, endoscopically, or radiologically, of any paranasal sinus disease and when this resolved with nasal medical treatment the pain remained. The treatment of these patients' facial pain centred on the use of neurological medical treatment. One third of the patients responded to low-dose amitriptyline, a further third showed some response to other pharmacological agents including carbamazepine, and the remaining third showed no response. These cases illustrate the characteristics and management of facial pain after sinonasal surgery and highlight the importance of medical neurological treatment in the absence of any objective evidence of sinus disease.

This study does not have a target disease

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study has a cohort study or clinical trial

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study does not have any cohorts or clinical trial

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study has a control, double-blind, or comparison patient group

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study does not have any comparison patient group

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study has human subjects

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study does not have human subjects

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study contains population size or sample size information

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study does not contain population size information

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study does not have any quantitative outcomes

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study has a target drug

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study does not have a target drug

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study has a target disease

Anti-inflammatory interventions in end-stage kidney disease: a randomized, double-blinded, controlled and crossover clinical trial on the use of pravastatin in continuous ambulatory peritoneal dialysis.

Inflammation is highly prevalent in patients on dialysis. Statins have anti-inflammatory actions but their use has been scarcely studied in continuous ambulatory peritoneal dialysis (CAPD). We undertook this study to compare the effect of pravastatin vs. placebo on the serum concentrations of C-reactive protein (CRP) in patients on CAPD. In a double-blind, controlled and crossover clinical trial, 76 CAPD patients were randomized to either pravastatin or placebo for 2 months. After this first period of treatment, patients had a 1-month wash-out period and, finally, they were crossed-over to receive the other drug (or placebo) for 2 more months. Measurement of clinical and biochemical variables and CRP was performed at the beginning and at the end of each treatment period. Median CRP was only significantly decreased in the pravastatin group in both periods of treatment: first period (baseline vs. final, mg/L): pravastatin 7.4 (2-21) vs. 2.6 (1-6), p <0.05; placebo 3.9 (2-10) vs. 6.8 (3-12), pNS; second period: pravastatin 4.3 (2-15) vs. 1.9 (1-7), p <0.05; placebo 4.9 (2-17) vs. 6.8 (2-19), p <0.05. Results were significantly different (p <0.05) between groups only at the end of each treatment period. Additionally, total and LDL-cholesterol significantly decreased in the pravastatin group. Pravastatin significantly reduced serum levels of CRP and total and LDL-cholesterol compared to placebo. This treatment may be of great help to decrease the inflammatory status and probably the cardiovascular disease of CAPD patients.

This study does not have a target disease

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study has a cohort study or clinical trial

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study does not have any cohorts or clinical trial

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study has a control, double-blind, or comparison patient group

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study does not have any comparison patient group

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study has human subjects

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study does not have human subjects

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study contains population size or sample size information

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study does not contain population size information

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study does not have any quantitative outcomes

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study has a target drug

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study does not have a target drug

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study has a target disease

Can type 2 diabetes mellitus be considered preventable?

The primary prevention of type 2 diabetes mellitus (T2DM) is of great importance. There is now substantial evidence that T2DM can be prevented or delayed by lifestyle modification. A statistically significant reduction of relative risk of newly diagnosed T2DM was observed in large clinical trials with metformin, acarbose or orlistat in subjects with impaired glucose tolerance as well as with troglitazone in women with previous gestational diabetes. A relative risk reduction of newly diagnosed diabetes was observed in prospective, double blind clinical studies evaluating the effect of different antihypertensive drugs (ACE-inhibitors, angiotensin repector blockers, calcium channel blockers) or that of lipid-lowering agents (pravastatin) on the cardiovascular morbidity and mortality in high risk patients. In studies with postmenopausal hormone replacement therapy a relative risk reduction of newly developed T2DM was also observed. Thus, T2DM should be considered as a preventable disease. Nevertheless, it is noteworthy that oral antidiabetic drugs with an indication of preventing T2DM are not registered in several countries at present, so that drug therapy should not be used as a routine for preventing diabetes. On the other hand, patients with pre-diabetes (impaired fasting glycaemia, impaired glucose tolerance) should be given counseling on weight loss as well as instruction for increasing physical activity in order to prevent T2DM.

This study does not have a target disease

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study has a cohort study or clinical trial

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study does not have any cohorts or clinical trial

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study has a control, double-blind, or comparison patient group

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study does not have any comparison patient group

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study has human subjects

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study does not have human subjects

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study contains population size or sample size information

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study does not contain population size information

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study does not have any quantitative outcomes

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study has a target drug

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study does not have a target drug

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study has a target disease

Occurrence and Genomic Characterization of Clone ST1193 Clonotype 14-64 in Uncomplicated Urinary Tract Infections Caused by Escherichia coli in Spain.

We conducted a prospective, multicenter, specific pilot study on uncomplicated urinary tract infections (uUTI). One-hundred non-duplicated uropathogenic Escherichia coli (UPEC) from uUTI occurred in 2020 in women attending 15 primary care centers of a single health region of northern Spain were characterized using a clonal diagnosis approach. Among the high genetic diversity showed by 59 different phylogroup-clonotype combinations, 11 clones accounted for 46% of the isolates: B2-ST73 (CH24-30); B2-ST73 (CH24-103); B2-ST131 (CH40-30); B2-ST141 (CH52-5); B2-ST372 (CH103-9); B2-ST404 (CH14-27); B2-ST404 (CH14-807); B2-ST1193 (CH14-64); D-ST69 (CH35-27); D-ST349 (CH36-54), and F-ST59 (CH32-41). The screening of the UPEC status found that 69% of isolates carried ≥ 3 of <i>chuA, fyuA, vat</i>, and <i>yfcV</i> genes. Multidrug resistance to at least one antibiotic of ≥ 3 antimicrobial categories were exhibited by 30% of the isolates, with the highest rates of resistance against ampicillin/amoxicillin (48%), trimethoprim (35%), norfloxacin (28%), amoxicillin-clavulanic acid (26%), and trimethoprim-sulfamethoxazole (24%). None extended-spectrum beta-lactamase/carbapenemase producer was recovered. According to our results, fosfomycin and nitrofurantoin should be considered as empirical treatment of choice for uUTI by E. coli (resistance rates 4% and 2%, respectively). We uncover the high prevalence of the pandemic fluoroquinolone-resistant ST1193 clone (6%) in uUTI, which represents the first report in Spain in this pathology. The genomic analysis showed similar key traits than those ST1193 clones disseminated worldwide. Through the SNP comparison based on the core genome, the Spanish ST1193 clustered with isolates retrieved from the Enterobase, showing high genomic similarity than the global ST1193 described in the United States, Canada and Australia. <b>IMPORTANCE</b> Analyzing the clonal structure and antimicrobial resistance of E. coli isolates implicated in uncomplicated urinary tract infections, one of the most frequent visits managed in primary health care, is of interest for clinicians to detect changes in the dynamics of emerging uropathogenic clones associated with the spread of fluoroquinolone resistance. It can also provide consensus concerning optimal control and antibiotic prescribing.

This study does not have a target disease

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study has a cohort study or clinical trial

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study does not have any cohorts or clinical trial

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study has a control, double-blind, or comparison patient group

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study does not have any comparison patient group

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study has human subjects

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study does not have human subjects

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study contains population size or sample size information

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study does not contain population size information

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study has quantitative outcomes like numbers, P-value, OR, CI, HR, RR, or patient ratios

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study does not have any quantitative outcomes

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study has a target drug

Effects of trazodone hydrochloride and imipramine on polysomnography in healthy subjects.

Polysomnography was performed on eight healthy men with trazodone hydrochloride, imipramine and placebo. Trazodone hydrochloride increased slow wave sleep significantly. Imipramine prolonged rapid eye movement (REM) latency and decreased the percentage of REM sleep significantly. Trazodone decreased stages 1 and 2 sleep, while imipramine increased it. These findings suggest that the antidepressive effect of trazodone might be different from that of imipramine with the suppression of REM sleep.

This study does not have a target drug