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Gonadal Dysfunction in Systemic Diseases

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Gonadal Dysfunction in Systemic Diseases European Journal of Endocrinology (2005) 152 501–513 ISSN 0804-4643 REVIEW Gonadal dysfunction in systemic diseases Asterios Karagiannis and Faidon Harsoulis Second Propedeutic Department of Internal Medicine, Division of Endocrinology, Medical School, Aristotle University of Thessaloniki, Hippokration Hospital, Thessaloniki, Greece (Correspondence should be addressed to A Karagiannis, 44 Tsimiski str., Thessaloniki, 54623, Greece; Email: [email protected]) Abstract Gonadal function is significantly affected in many acute and chronic systemic diseases. As the func- tion of the testes and the ovaries is determined by the integrity of the hypothalamic–pituitary–gona- dal axis, it is obvious that a systemic disease may affect one or more levels of the axis in such a manner that the gonadal dysfunction may have various clinical and laboratory manifestations. In this brief review, the most common disturbances seen in the main systemic diseases will be discussed. European Journal of Endocrinology 152 501–513 Testicular function in systemic diseases The pulsatile secretion of LH has been studied in cases with elevated gonadotropin levels and it has In acute stresses, testicular function is harmed been ascertained that the amplitude of the pulsatile indirectly via gonadotropin suppression and directly wave was reduced while the frequency remained by the action of cytokines upon the testes. In chronic normal (6). In patients with chronic renal failure, stresses, testicular dysfunction is due to primary testi- apart from the indirect testicular effect, the elevated cular failure with reduced production of testosterone LH levels are due to insufficient renal excretion (7), and semen and elevated gonadotropin levels (1). It is while concurrently there is obvious reduction of the interesting that both types of testicular dysfunction amplitude and frequency of the pulsatile waves of appear to be reversible, since studies performed in LH (8). patients after kidney or liver transplantation have In most cases of primary or secondary hypogonad- shown full recovery of testicular function (2, 3). How- ism, Leydig cells present a functional disturbance, as ever, primary and secondary hypogonadism may alter- has been demonstrated by the human chorionic gon- nate or may be superimposed. For example, a adotropin (hCG) test. Even if the baseline testosterone suppression of previously high gonadotropin levels levels are within normal limits, the rise after a maxi- occurs during the terminal stages of cirrhosis with mally effective dose of hCG is usually less than the the onset of hepatic coma (4). normal doubling of pretreatment levels. Defective Acute illnesses are associated with gonadotropin sup- Leydig cell function may result from altered paracrine pression and secondary testicular failure. There is a signals by damaged seminiferous tubules (9). common underlying mechanism of reduced secretion An important factor affecting sex hormone levels and of gonadotropin-releasing hormone (GnRH) similar to more specifically the efficient relationship between the seasonal regression of reproductive function in ani- estrogen and androgen is the level of sex hormone- mals. Many toxic mechanisms are implicated, such as binding globulin (SHBG). Of the circulating testosterone fever, drugs, cytokines and stress hormones which act in adult men, approximately 45% is bound with high directly upon the testes or indirectly upon the hypo- affinity to SHBG, 50% is loosely bound to albumin thalamus and pituitary. The type of hypogonadism and less than 4% is free (not protein bound). SHBG is may vary in proportion to the process of the illness. a carbohydrate-rich b-globulin produced by hepato- Severe starvation leads to low luteinizing hormone cytes; it binds testosterone and other steroids with (LH)/follicle-stimulating hormone (FSH) levels, which high affinity and prolongs their metabolic clearance. may rise during refeeding, causing a transient excess Because of the role of SHBG as a plasma testosterone- of estrogen production and refeeding gynecomastia (5). binding protein, there is a positive correlation between The hypogonadism that accompanies most chronic its level and the level of testosterone in human adult systemic diseases is primary and is characterized by male plasma. It is well known that the production of reduced testosterone levels and elevated levels of gon- SHBG by the liver is suppressed by androgens and adotropins and inhibin B. It must be noticed that in stimulated by estrogens. An excess of estrogen increases many cases the derangement is located at both levels. serum SHBG levels, leading to reduced free testosterone q 2005 Society of the European Journal of Endocrinology DOI: 10.1530/eje.1.01886 Online version via www.eje-online.org Downloaded from Bioscientifica.com at 09/30/2021 12:40:28AM via free access 502 A Karagiannis and F Harsoulis EUROPEAN JOURNAL OF ENDOCRINOLOGY (2005) 152 and dihydrotestosterone (DHT), while the metabolic with cirrhosis present reduced spermatogenesis and clearance of estrogen is not affected. This has been peritubular fibrosis. called the estrogen amplification effect of SHBG and The normal function of the hypothalamic–pitu- may contribute to the clinical signs of feminization in itary–gonadal axis is affected in liver diseases. The pul- conditions such as cirrhosis, senescence and thyrotoxi- satile secretion of LH and the response to GnRH and cosis, in which serum SHBG levels are elevated (10). clomiphene are reduced. As has already been men- Consequently, every factor altering SHBG levels may tioned, in late stages of cirrhosis the patients present influence the hormone changes during the process of features of feminization, suggesting altered levels of a systemic disease. sex hormones. The clinical signs of hypogonadism are The hormonal control of SHBG in plasma is complex. more pronounced in alcoholic patients due to the Table 1 lists those factors that are known to decrease or direct effect of ethanol upon the testes. In cirrhotic increase plasma SHBG levels. Only insulin and thyrox- patients, the estrogen/androgen ratio is usually ine influence SHBG levels through effects on steady- increased. The levels of testosterone and dihydroepian- state mRNA levels (11). How other factors increase or drosterone are reduced, while the estradiol levels decrease circulating SHBG levels remains unknown. are normal or slightly elevated. These alterations are The peripheral metabolism of steroids is altered in dependent on the severity of the liver disease and many forms of hypogonadism, including cirrhosis, are more pronounced in patients with higher Child– chronic renal failure, thyrotoxicosis, old age, Klinefelter Pugh score (14, 15). Several other factors may contrib- syndrome and testicular atrophy after mumps orchitis. ute to these hormonal changes in cirrhosis, including In healthy men, the major quantity of estrogens comes hepatic overproduction of SHBG, changed SHBG iso- from the biological conversion of testosterone to estra- forms with different steroid-binding affinities, elevated diol and of androstendione to estrone by the enzyme prolactin levels, direct suppression of Leydig cell func- aromatase, which is found in fat, muscles, kidneys tion by estrogens, increased estrogen receptors in the and liver. In clinical practice, the features of feminiza- liver and cyclic variation in the severity of the liver ill- tion, such as gynecomastia, are not directly related to ness producing the hormonal changes of refeeding the plasma estrogen levels (12). The ratio of estrogen gynecomastia (16). It must be kept in mind that the to androgen and the wide range of responsiveness of gynecomastia and impotence of cirrhotics are augmen- male breast tissue to estrogen are considered more ted by the chronic use of spironolactone, a receptor important factors, as shown by the great variability in antagonist of aldosterone and testosterone, which the extent of gynecomastia in men given estrogens for reduces the testosterone levels and slightly increases metastatic prostatic cancer. Finally, in both men with the levels of estradiol. idiopathic seminiferous tubular failure and patients suf- Portocaval shunts in normal rats result in testicular fering from celiac disease with an acquired androgen atrophy manifested histologically by loss of germinal resistance or 5a-reductase deficiency, defects of andro- epithelium due to decreased mitosis and increased gen receptors have been reported as a different patho- apoptosis with loss of spermatogonia, loss of spermato- physiologic mechanism (13). zoa in the lumen of the seminiferous tubules and event- ual complete atrophy of the seminiferous tubule, which Disorders associated with testicular failure are then lined only by Sertoli cells (3). The primary event after portocaval shuntings increases estrogen- Liver disease Hepatic cirrhosis is associated with hypo- suppressing LH secretion which leads to decreased tes- gonadism and signs of feminization irrespective of the tosterone levels and hypogonadism. direct toxic effect of ethanol upon the testes. Testicular atrophy, low testosterone levels, decreased libido, infer- Alcoholism – alcoholic cirrhosis Most alcoholics, tility, reduced secondary sex hair and gynecomastia are particularly those with cirrhosis, present features of found in men with cirrhosis. Fifty percent of patients hypogonadism, such as feminization, impotence, reduced fertility and testicular atrophy. There is a large body of data providing evidence that ethanol Table 1 Factors that
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