Gonadal Function in Men with Cushing Syndrome 

Authors

  • Farida Chentli Department of Endocrinology and Metabolic Diseases, Bab El Oued Hospital, Algiers, Algeria
  • Said Azzoug
  • Djamila Meskine Department of Endocrinology and Metabolic Diseases, Bologhine Hospital, Algiers, Algeria
  • Fetta-Amel Yaker Department of Endocrinology and Metabolic Diseases, Bab El Oued Hospital, Algiers, Algeria
  • Fadila Chabour
  • Hayet Boudina

DOI:

https://doi.org/10.12970/2310-9971.2013.01.01.2

Keywords:

 Hypercortisolism, erectile dysfunction, hypogonadism.

Abstract

 Cushing syndrome (CS) is scarcely observed in males. Because of this rarity, the real prevalence of gonadal dysfunction in men with hypercortisolism is unknown. Our aim was to analyze gonadal abnormalities in 37 males with CS (median age=28.9±11years) comparatively to age matched healthy men (n=10). For the homogeneity of the study men over 50, children, patients taking medications and those with pituitary deficits were systematically excluded. For the remaining group, we took into account medical history, clinical examination, and hormonal assessment, by radio immunoassay, for testosterone (T), prolactin (PRL), follicle stimulating hormone (FSH), and luteinizing stimulating hormone (LH). Results: 21% consulted for impotency and/or gynecomastia. When questioned, 65.7% complained about decreased libido and erectile dysfunction. Except for 3, body hair growth and repartition, and testicular volume were normal. Gynecomastia was observed in 18.9%.Testosterone was equal to 2.79±1.62ng/ml vs 6.69±3.87ng/ml (p<0.0005). Low testosterone (<3ng/ml) was observed in 67.5%. PRL =9.8 ± 4.2ng/ml vs 4.9 ± 2.6ng/ml (p<0.01). FSH = 3.87 ± 1.9mu/ml vs 3.75 ± 2.25mU/ml (p<0.30). LH = 2.7 ± 2.2mU/ml vs 3.66 ± 0.86 (p<0.30). We have not found any correlation between cortisol and T, PRL or LH, but there was a positive and significant one with FSH (r=0.57, p<0.005). Conclusion: CS causes a franc hypogonadism in 65%. According to FSH and LH results glucocorticoids excess acts probably at hypothalamic pituitary level, but an increase in testosterone degradation and/or inhibition of testis receptors cannot be ruled out. So men with hypogonadism and/or gynecomastia should be systematically checked for CS. 

References


[1] Dekkers OM, Horváth-Puhó E, Jørgensen JO, Cannegieter SC, Ehrenstein V, Vandenbroucke JP, et al. Multisystem morbidity and mortality in Cushing's syndrome: a cohort study. J Clin Endocrinol Metab 2013; 98: 2277-84. http://dx.doi.org/10.1210/jc.2012-3582
[2] Lado-Abeal J, Rodriguez-Arnao J, Newell-Price JDC, Perry LA, Grossman AB, Besser GM, Trainer PJ. Menstrual abnormalities in women with Cushing’s Disease are correlated with hypercortisolemia rather than raised circulating androgen levels. J Clin Endocrinol Metab 1998; 83: 3083-88. http://dx.doi.org/10.1210/jc.83.9.3083
[3] Hardy MP, Sottas CM, Ge R, Mckittrick CR, Tamashiro KL, McEwen BS, et al. Trends of Reproductive Hormones in male rats during psychosocial stress: Role of glucocorticoids metabolism in behavioral dominance. Biol Reprod 2002; 67: 1750-55. http://dx.doi.org/10.1095/biolreprod.102.006312
[4] Kuhn JM, Gay D, Lemercier JP, Pugeat M, Legrand A, Wolf LM. Testicular function during prolonged corticotherapy. Press Med 1986; 15: 559-62.
[5] Bertagna X, Guignat L, Groussin L, Bertherat J. Cushing's disease. Best Pract Res Clin Endocrinol Metab 2009; 23: 607-23. http://dx.doi.org/10.1016/j.beem.2009.06.001
[6] Lahera Vargas M, da Costa CV. Prevalence, etiology and clinical findings of Cushing's syndrome. Endocrinol Nutr 2009; 56: 32-9. http://dx.doi.org/10.1016/S1575-0922(09)70191-3
[7] Arnaldi G, Mancini T, Tirabassi G, Trementino L, Boscaro M. Advances in the epidemiology, pathogenesis, and management of Cushing's syndrome complications. J Endocrinol Invest 2012; 35: 434-48.
[8] de Betue CT, Deutz NE. Changes in Arginine Metabolism during Sepsis and Critical Illness in Children. Nestle Nutr Inst Workshop Ser. 2013; 77: 17-28. http://dx.doi.org/10.1159/000351370
[9] van Waardenburg DA, de Betue CT, Luiking YC, Engel M, Deutz NE. Plasma arginine and citrulline concentrations in critically ill children: strong relation with inflammation. Am J Clin Nutr 2007; 86: 1438-44.
[10] van den Berghe G, Weekers F, Baxter RC, Wouters P, Iranmanesh A, Bouillon R, Veldhuis JD. Five-day pulsatile gonadotropin-releasing hormone administration unveils combined hypothalamic-pituitary-gonadal defects underlying profound hypoandrogenism in men with prolonged critical illness. J Clin Endocrinol Metab 2001; 86: 3217-26. http://dx.doi.org/10.1210/jc.86.7.3217
[11] Luton JP, Thieblot P, Valcke JC, Mahoudeau JA, Bricaire H. Reversible gonadotropin deficiency in male Cushing’s disease. J Clin Endocrinol Metab 1977; 45: 488-95. http://dx.doi.org/10.1210/jcem-45-3-488
[12] Contreras LN, Masini AM, Danna MM, Kral M, Bruno OD, Rossi MA, Andrada JA. Glucocorticoïds: their role on gonadal function and LH secretion. Minerva Endocrinol 1996; 21: 43- 6.
[13] Mc Kenna TJ, Lorder D, Lacroix A, Rabin D. Testicular activity in Cushing’s disease. Acta Endocrinol (Copenh) 1979; 91: 501-10.
[14] Smals AG, Kloppenborg PW, Benraad TJ. Plasma testosterone profiles in Cushing’s syndrome. J Clin Endocrinol Metab 1977; 45: 240-5. http://dx.doi.org/10.1210/jcem-45-2-240
[15] Bezvekhaia TP, Varga SV, Verkhogliadova LM. Interrelation of sex hormone-binding and the androgen-estrogen balance in patients with hypercorticism. Probl. Endokrinol (Mosk) 1986; 32: 48-51.
[16] Ferramosca B, Bertoni F, Serra D, Ravaglia G. The male gonad in an adreno-metabolic syndrome. Morpho-functional findings. Minerva Med 1982; 73: 3005-13.
[17] Vierhapper H, Nowotny P, Waldhausl W. Production rates of testosterone in patients with Cushing’s syndrome. Metabolism 2000; 49: 229-31. http://dx.doi.org/10.1016/S0026-0495(00)91429-X
[18] Meij BP, Mol JA, Bevers MM, Rijnberk A. Alterations in anterior pituitary function of dogs with pituitary-dependent hyper adrenocorticism. Endocrinol 1997; 154: 505-12. http://dx.doi.org/10.1677/joe.0.1540505
[19] Krieger DT, Samojlik E, Bardin CW. Cortisol and androgen secretion in a case of Nelson’s syndrome with paratesticular tumors: response to cyproheptadine therapy. J Clin Endocrinol Metab 1978; 47: 837-44. http://dx.doi.org/10.1210/jcem-47-4-837
[20] Dubey AK, Plant TM. A suppression of gonadotropin secretion by cortisol in castrated male rhesus monkeys (Macaca mulatta) mediated by the interruption of hypothalamic gonadotropin-releasing hormone release. Biol Reprod 1985; 33: 423-31. http://dx.doi.org/10.1095/biolreprod33.2.423
[21] Ahima RS, Harlan RE. Glucocorticoids receptors in LHRH neurons. Neuroendocrinology 1992; 56: 845-50. http://dx.doi.org/10.1159/000126315
[22] Boccuzzi G, Angeli A, Bisbocci D, Fonzo D, Giadano GP, Ceresa F. Effect of synthetic luteinizing hormone releasing hormone (LH-RH) on the release of gonadotropins in Cushing’s disease. J Clin Endocrinol Metab 1975; 40: 892- 95. http://dx.doi.org/10.1210/jcem-40-5-892
[23] Schaison G, Durand F, Mowszowicz I. Study of plasma androstenedione and testosterone levels in hypercorticism syndromes. Ann Endocrinol (Paris) 1979; 40: 51-2.
[24] Ge RS, Hardy DO, Catterall JF, Hardy MP. Developmental changes in glucocorticoid receptor and 11B-hydroxysteroid dehydrogenase oxidative and reductive activities in rat Leydig cells. Endocrinology 1997; 138: 5089-95. http://dx.doi.org/10.1210/en.138.12.5089

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2013-02-02

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