Low testosterone levels have been identified in 43% of patients with lepromatous leprosy and 5% of those patients with borderline lepromatous leprosy. Low testosterone levels were originally reported in patients with lepromatous leprosy in 1968 by Martin et al. and have since been confirmed by a number of other studies. The testosterone response to human chorionic gonadotropin was attenuated in patients with lepromatous leprosy. This is in keeping with the 1952 report by Grabstald and Swann that the testes are invaded in 90% of males with lepromatous leprosy. Destruction of the Leydig cells occurs after destruction of the seminiferous tubules. Histopathologic examination of lepromatous testes showed inflammatory, degenerative, and fibroric changes. Although reduced testicular size has been observed in up to half of lepromatous leprosy patients, this is not a universal finding, particularly in early disease. Additionally, some patients develop Leydig cell hyperplasia.

In view of the testicular atrophy, it is not surprising that both urinary gonadotropins and serum luteinizing hormone and follicle-stimulating hormone levels have been reported to be elevated in lepromatous leprosy. The gonadotropin response to gonadotropin-releasing hormone is exaggerated in patients with lepromatous leprosy compared to those with tubercu-loid leprosy and normal controls.

Estradiol levels have been found to be either low or elevated, in patients with lepromatous leprosy. Prolactin levels are typically increased. In one study, 12 out of 16 patients with lepromatous leprosy had oligospermia or azoospermia.

The situation in the tuberculoid form of Hansen’s disease is less certain. Some authors have reported no effect of tuberculoid leprosy on gonadal function. Two studies, however, have suggested that testosterone levels were low, with normal or reduced luteinizing hormone and follicle-stimulating hormone levels suggestive of secondary hypogonadism. Prolacrin and estradiol levels were elevated. In addition, patients with the tuberculoid type of Hansen’s disease were found to have a reduction in sperm count and motility and an increase in abnormal forms of spermatozoa. Because these studies utilized healthy young men as controls, however, it is possible that the physiological hypogonadorropic hypogonadism associated with aging was a predominant factor that clouded their results. Alternatively, these findings could be explained by the presence of granulomatous disease of the meninges affecting the hypothalamic-pituitary stalk.

In conclusion, patients with Hansen’s disease of the lepromatous type have primary hypogonadism due to testicular invasion by the lepra bacilli. It is possible that patients with the tuberculoid form of leprosy develop a secondary hypogonadism secondary to granulomatous disease involving the hypothalamus or pituitary.

Myotonic Dystrophy

Myotonic Dystrophy is a genetic disorder caused by multiple CTG repeats lying upstream of a gene that encodes a novel protein kinase. This disease is characterized by muscle weakness, baldness, cataracts, and abnormal regulation of adrenocorricorrophic hormone and cytokine production. Metabolic disturbances, peripheral insulin insensitivity, and cognitive dysfunction are common features, including the failure of testicular and adrenal testosterone production. Testicular atrophy was first reported in 1909 in patients with myotonic dystrophy. Approximately 80% of patients with myotonia will develop hypogonadism, although this typically occurs later in life, where many patients could have completed their families earlier in life. On testicular biopsy, tubular fibrosis and abnormal spermatogenesis are the most common findings. luteinizing hormone and follicle-stimulating hormone levels are elevated, and the response to gonadotropin-releasing hormone is exaggerated. A poor testicular response to human chorionic gonadotropin has been reported in one patient. The hypogonadism in myotonic dystrophy is of the primary type. Although testosterone treatment increases muscle mass in patients with myotonic dystrophy, it does not increase muscle strength.


Patients with paraplegia have decreased skeletal muscle and a relative increase in adiposity. They also develop osteoporosis, particularly of the pelvis and lower limbs. Gynecomastia is not an uncommon finding in patients with paraplegia. Early studies suggest that evidence of testicular dysfunction could be found in up to half of men who become paraplegic following trauma.

Testicular biopsies are abnormal in approximately 40% of persons with paraplegia. In these patients, there is generalized hypoplasia of the germinal epithelium associated with spermatogeneric arrest. Leydig cells are usually normal, but nodular hyperplasia is seen in some subjects. Interestingly, the higher the level of the spinal cord lesion, the greater the degree of seminiferous tubule damage. Sperm counts have been reported to be greater than 20 million in just over 60% of subjects. Motility, however, was low, with 77% of patients exhibiting less than 20% motility, which may be related to elevated follicle-stimulating hormone levels. Perkash et al. have suggested that the minimization of urinary tract infections and the prevention of sperm stagnation in the lower storage areas by periodic rectal probe elecrrostimularion may improve spermatozoa motility.

Plasma testosterone levels tend to be below normal for the first two to three months following the acute trauma before rising into the normal range. This increase is thought to be due to an earlier posttraumaric increase in circulating epinephrine levels, which occurs very soon after the acute trauma has taken place. In quadriplegics, testosterone levels remain low for a longer period of time. Interestingly, some paraplegic patients demonstrate slightly higher long-term testosterone levels than in nonparaplegics, but another study has suggested that other patients might develop lower than normal levels. One study reported that the majority of free androgen indices (testosterone / sex hormone binding globulin) in persons with paraplegia were within the normal range. In another study with small numbers of patients, adequate testosterone response to human chorionic gonadotropin was found.

In contrast to the normal testosterone levels, elevated luteinizing hormone and follicle-stimulating hormone levels associated with an exaggerated gonadorropin response to gonadotropin-releasing hormone have been reported in many patients with paraplegia. This suggests that many of these patients have, in fact, compensated primary hypogonadism. In quadriplegics, however, luteinizing hormone levels appear to be low, particularly in the acute period following the traumatic injury, suggesting that these patients, who often also have low testosterone, have secondary hypogonadism. Plasma prolactin levels are elevated in a number of paraplegics.

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