Paredes PJC, Mora PJ, Balladares ML, Sierra RA

Language: Spanish
References: 11
Page: 164-169
PDF size: 196.07 Kb.

ABSTRACT

Background: The 21-hydroxylase deficiency is characterized by deficiency of cortisol, androgens and progestin hypersecretion; this may influence the synthesis and secretion of other hypothalamic hormones.
Objectives: 1) To identify and quantify concentrations of PRL and TSH in women with 21-hydroxylase deficiency and controls. 2) To investigate the characteristics of pituitary dopaminergic tone in women with 21-hydroxylase deficiency.
Patients and methods: An observational, transversal, analytical case-control study was done in which five patients with 21-hydroxylase deficiency were included as well as five healthy women. Blood samples were obtained every 20 minutes during for hours, after which a single oral dose of 10 mg of metoclopramide was administered, and sampling continued for two hours, in each of the samples were quantified: PRL, TSH, 17-OHP4, cortisol, FSH, dehydroepiandrosterone sulfate (DHEA-S) and free testosterone. After administration of metoclopramide PRL and TSH were measured.
Results: In patients with 21-hydroxylase deficiency, cortisol concentrations were higher than in the control group (6 ‹vs 4 µg/dL, p ‹ 0.05), TSH was lower in cases (1.7 vs 0.9 µUl/mL, p ‹ 0.05) and PRL concentrations were higher in the control group with no statistical significance. It was established an inverse correlation with cortisol and PRL and TSH (r-r-0.62 and 0.07) in patients with 21-hydroxylase deficiency.
Conclusions: The PRL and TSH secretion in basal conditions and after stimulation with metoclopramide in patients with 21-hydroxylase deficiency with respect to controls were lower even statistically significantly in the case of TSH.

REFERENCES

1. Cabrera MS, Vogiatzi MG, New MI. Long term outcome in adult males with classic congenital adrenal hyperplasia. J Clin Endocrinol Metab 2001;86:3070-3078.

2. Pinto G, Tardy V, Trivin C, Thalassinos C, et al. Follow-up of 68 children with congenital adrenal hyperplasia due to 21-hydroxylase deficiency: relevance of genotype for management. J Clin Endocrinol Metab 2003;88:2624-2633.

3. White PC, Speiser PW. Congenital adrenal hyperplasia 21-hydroxylase deficiency. Endocr Rev 2000;21:245-291.

4. Speiser PW, White PC. Congenital adrenal hyperplasia. N Engl J Med 2003;349:776-788.

5. Merke DP, Bornstein SR, Avila NA, Chrousos GP. Future directions in the study and management of congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Ann Intern Med 2002;136:320-334.

6. New MI. Extensive clinical experience: nonclassical 21-hydroxylase deficiency. J Clin Endocrinol Metab 2006;91(11):4205-4214.

7. Rotterdam ESHRE/ASRM-Sponsored PCOS Consensus Workshop Group. Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome. Fertil Steril 2004;81(1):19-25.

8. Lever EG, McKerron CG. Auto-immune Addison’s disease associated with hyperprolactinaemia. Clin Endocrinol (Oxf) 1984;21(4):451-457.

9. Hangaard J, Andersen M, Grodum E, Koldkjaer O, Hagen C. The effects of endogenous opioids and cortisol on thyrotropin and prolactin secretion in patients with Addison’s disease. J Clin Endocrinol Metab 1999;84(5):1595-1601.

10. Adriaanse R, Brabant G, Endert E, Wiersinga WM. Pulsatile thyrotropin secretion in patients with Cushing’s syndrome. Metabolism 1994;43(6):782-786.

11. Vanvugt DA, Webb MY, Reid RL. Naloxone antagonism of corticotropin-releasing hormone stimulation of prolactin secretion in rhesus monkeys. J Clin Endocrinol Metab 1989;68(6):1060-1066.