Bone Mineral Density in Adults With Congenital Adrenal Hyperplasia: A Systematic Review and Meta-Analysis.

Background: Decreased bone mineral density (BMD) is a concern in patients with congenital adrenal hyperplasia (CAH) due to lifelong glucocorticoid replacement. Studies till date have yielded conflicting results. We wanted to systematically evaluate the available evidence regarding BMD in adult patients with CAH. Methods: We searched Medline, Embase and Cochrane Central Register of Controlled Trials to identify eligible studies. Studies comparing BMD in CAH patients with age- and sex-matched controls were included. Age <16 years and absence of controls were exclusion criteria. Two authors independently reviewed abstracts, read full-text articles, extracted data, assessed risk of bias using Newcastle-Ottawa scale, and determined level of evidence using Grading of Recommendations Assessment, Development, and Evaluation methodology. Results: Nine case-control studies with a total sample of 598 (cases n = 254, controls n = 344) met eligibility criteria. Median age was 31 years (IQR 23.9-37) and 65.7% were female. Total body BMD (Mean Difference [MD]-0.06; 95%CI -0.07, -0.04), lumbar spine BMD (MD -0.05; 95%CI -0.07, -0.03) and femoral neck BMD (MD -0.07; 95%CI -0.10, -0.05) was lower in cases compared to controls. Lumbar spine T-scores (MD -0.86; 95%CI -1.16, -0.56) and Z-scores (MD -0.66; 95%CI -0.99, -0.32) and femoral neck T-scores (MD -0.75 95%CI -0.95, -0.56) and Z-scores (MD -0.27 95%CI -0.58, 0.04) were lower in cases. Conclusion: BMD in adult patients with CAH was lower compared to controls. Although insufficient data precludes a dose-response relationship between glucocorticoid dose and BMD, it would be prudent to avoid overtreatment with glucocorticoids.

Predictors of significant coronary artery disease in atrial fibrillation: Are cardiac troponins a useful measure.

BACKGROUND: Cardiac Troponin I (cTnI) is frequently measured in patients presenting with symptomatic atrial fibrillation (AF). The significance of elevated cTnI levels in this patient cohort is unclear. We investigated the value of cTnI elevation in this setting and whether it is predictive for significant coronary artery disease (sCAD). METHODS: We conducted a retrospective, single-center, case-control study of 231 patients who presented with symptomatic AF to The Prince Charles Hospital emergency department, Brisbane, Australia between 2006 and 2014. Patients who underwent serial cTnI testing and assessment for CAD were included. Clinical variables that are known to predict CAD and could potentially predict cTnI elevation were collected. Binary logistic regression was performed to identify predictors of sCAD and cTnI elevation. RESULTS: Cardiac Troponin I elevation above standard cut off was not predictive for sCAD after adjustment for other predictors (OR 1.62, 95% CI 0.79-3.32. p=0.19). However, the highest cTnI concentration value (cTnI peak) was predictive for sCAD (OR 2.02, 95% CI 1.02-3.97, p=0.04). Dyspnea on presentation (OR 4.52, 95% CI 1.87-10.91, p=0.001), known coronary artery disease (OR 3.44, 95% CI 1.42-8.32, p=0.006), and ST depression on the initial electrocardiogram (OR 2.57, 95% CI 1.11-5.97, p=0.028) predicted sCAD in our cohort, while heart rate on initial presentation was inversely correlated with sCAD (OR 0.99, 95% CI 0.971-1.00, p=0.034). CONCLUSION: Troponin elevation is common in patients presenting to hospital with acute symptomatic AF and it is not a reliable indicator for underlying sCAD in this patient cohort. However, cTnI peak was a predictor of significant coronary artery disease.