Objectives: Testosterone formulations that have more steady-state pharmacokinetics, such as subcutaneously implanted testosterone pellets, may cause less erythrocytosis than i.m. injections of shorter acting androgen esters. We, therefore, sought to define the prevalence, predictors, and proximate basis (role of erythropoietin) for polycythemia (hematocrit O0.50) in hypogonadal men receiving testosterone implants long term. Design: A cross-sectional study was conducted in an academic andrology center with a longitudinal subgroup analysis. Patients: A total of 158 hypogonadal men aged 14-84 years (mean age 46.7 years) treated on average for 8 years (range 0-21 years). Measurements: Trough blood testosterone and hematocrit. Serial serum erythropoietin concentrations were measured in 16 volunteers. Results: Positive univariate associations between polycythemia (hematocrit O0.50) and log(testosterone) (odds ratio (OR) 24.7, 95% confidence interval (CI): 4.3, 141.2, P!0.01) and age (OR 1.1, 95% CI: 1.0, 1.1, PZ0.03) and a borderline relationship with current smoking (OR 4.2, 95% CI: 0.9, 20.0, PZ0.08) were unveiled. A sensitivity analysis using alternate definitions of polycythemia was performed to capture all potential covariants. Multivariate regression analysis incorporating all potential covariants disclosed the independent OR of developing polycythemia (after adjusting for smoking and age) for log(testosterone) to be 15.0 (95% CI: 2.5, 90.8). Duration of testosterone therapy did not alter the risk of polycythemia. A direct relationship between testosterone and erythropoietin was observed (PZ0.05). Conclusions: Higher trough serum testosterone concentrations but not duration of treatment predict the development of polycythemia in men receiving long-acting depot testosterone treatment.
SummaryBackground: Obese women with gestational diabetes mellitus (GDM) represent a high-risk group in pregnancy, although the effects of increasing degrees of obesity and weight gain in pregnancy in this group is poorly defined. LGA (OR 3.8, 95% CI: 1.3 -11.3; OR 5.0, 95% CI: 2.0 -12.1, respectively) compared with Group A. Group C also had a lower risk of SGA (OR 0.4, 95% CI: 0.2 -1.0) and a higher risk of postpartum dysglycaemia (OR 6.8, 95% CI: 1.7 -26.9) compared with Group A. Conclusion: Greater degrees of obesity are associated with higher risk of abnormal metabolic outcomes after pregnancy. Excessive weight gain in pregnancy in obese women increases adverse obstetric and glycaemic outcomes. Our findings suggest that targets for weight gain in pregnancy for obese women should be reduced from current recommendations.
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