Salivary and plasma androstenedione and 17-hydroxyprogesterone levels in congenital adrenal hyperplasia.

Androstenedione (A-dione) and 17-hydroxyprogesterone (17-OHP) levels were measured in matched samples of saliva and of plasma collected from patients with congenital adrenal hyperplasia (CAH) due to 21-hydroxylase deficiency (eight patients) and 11-hydroxylase deficiency (one patient). Positive correlations were found between salivary and plasma values of either steroid with correlation coefficients of 0.968 for A-dione and 0.935 for 17-OHP. All five inadequately treated patients with 21-hydroxylase deficiency had greatly elevated plasma and salivary 17-OHP concentrations compared to values in age matched controls. In two of three well controlled patients plasma 17-OHP levels were less than 40 nmol/liter and salivary levels were less than 1.5 nmol/liter, the upper limits which have been formulated as a guideline for monitoring control in treated CAH patients. Patients in good control had A-dione levels in plasma (0.6-2.2 nmol/liter) and saliva (0.04-0.15 nmol/liter) which were both within the normal range for prepubertal children (0.14-2.40 nmol/liter and 0.02-0.25 nmol/liter respectively). Patients in poor control had A-dione levels in plasma of 5.2-25.4 nmol and in saliva of 0.50-2.21 nmol/liter. These values exceeded without exception the normal ranges for their respective ages. Salivary A-dione and 17-OHP determinations are a useful adjunct in the diagnosis and the monitoring of CAH patients since they can be obtained easily and nonstressfully.

Testosterone and delta 4-androstenedione in the saliva of patients with Klinefelter's syndrome.

This study compares salivary and total plasma levels of testosterone and androstenedione in healthy controls and chromatin positive patients with Klinefelter's syndrome. The mean plasma testosterone level in fifteen Klinefelter patients was significantly lower than in ten control subjects, but the mean androstenedione levels were similar. Saliva of the normal men and patients with Klinefelter's syndrome did not differ significantly in binding potency for testosterone or androstenedione. The mean salivary testosterone level in the Klinefelter patients was significantly lower than in the controls but again salivary androstenedione levels were similar. Although testosterone as well as androstenedione showed a fair correlation between the salivary and plasma concentrations, preliminary data suggested that salivary testosterone levels better characterize the clinical state of androgenicity than do plasma levels. When salivary testosterone and androstenedione were expressed as a percentage of total steroid levels in plasma, the ratios for both steroids were similar in Klinefelter patients and healthy controls and closely approximated to the reported percentages of free steroid levels in plasma. The absolute salivary testosterone concentrations also were almost identical to the reported free plasma hormone levels. Together the data provide indirect evidence that in Klinefelter patients testosterone and androstenedione binding in plasma and saliva does not differ from that in normal men, and measurement of salivary steroids, by reflecting their free hormone concentration in plasma, may be useful in evaluating endocrine function in both health and disease.