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The examination of 217 males suffering from diabetes mellitus revealed copulative dysfunction in 111 (51.1%) of them. The investigation of sex, gonadotropic hormones, testicular reserves, sexual constitution and sexual formula was carried out in 22-55-year-old males with sexual dysfunction and healthy controls. It was an erectile phase of the sexual cycle that suffered most frequently. Reduced libido was observed in 19% of the patients. All the diabetes examined showed constitutional predisposition to impaired potency. The patients had high serum concentrations of prolactin, lutropin and dihydroepiandrosterone in low testosterone and insignificantly elevated follitropin and estradiol. There was also low gonadal resistance to choriogonin stimulation. These findings and literature data lead to the conclusion that insulin insufficiency entailing hyperglycemia brings about a rise in prolactin and dihydroepiandrosterone levels which may reduce the sensitivity of the receptors and lutropin in the testes and inhibit testosterone secretion. This is confirmed by inactive gonadal response to stimulation of chorionic gonadotropin. Spermatogenic disorders observed in 25% of the patients were associated with sexual affections and local structural changes (hypotrophy) of the testes.

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A study was made of indices of the hypophyseogonadal system in men with diabetes mellitus, in men with autoimmune thyroiditis and hypothyroidism, and in men with Basedow's disease. Sexual dysfunction was detected in 51% of patients with diabetes mellitus and in 78.5% patients with hypothyroidism. A high level of serum prolactin in these patients resulted in a decrease in the sensitivity of testicles to LH, causing a decrease in testicular androgenic function. It was confirmed by a low blood level of T and a decreased response of the gonads to CG administration. Patients with hypothyroidism demonstrated a decrease in the blood level of LH and TSH causing testicular dysfunction. An increased level of LH and T was found in patients with Basedow's disease. The absence of an adequate rise of the blood concentration of T in response to CG administration in this group of patients can be attributed to the fact that in Basedow's disease the hypophyseogonadal system functions under great strain.

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Patients with primary chronic adrenal insufficiency (PCAI) in decompensation demonstrated a decrease in the total level of blood immunoglobulins, in particular IgG, with the normal level of B-lymphocytes. A decrease in IgG and an increase in IgA content was noted in the eucorticoid state; relative and absolute lymphocytosis determined by an increase in T- and B-lymphocytes was also noted. In overdosage of cortisone acetate the total number of immunoglobulins was normal, but IgA was raised and IgG lowered. The number of B-lymphocytes was significantly elevated. The number of T-lymphocytes was within normal but an increase in the level of T-suppressors was noted.

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A study was made of pituitary, thyroid, parathyroid, endocrine pancreatic, adrenocortical and immune system functions in 56 patients afflicted with visceral candidiasis. The clinical and laboratory data obtained point to the presence in some patients with visceral candidiasis of parathyroid, thyroid, pancreatic and adrenocortical dysfunctions, attesting to their importance in the disease pathogenesis. The role of immune disorders, particularly that of the T component of the immunity system is found to be of paramount importance as well in the pathogenesis of candidiasis. Correction of endocrine disorders coupled with antimycotic therapy brought about a more rapid and steadier therapeutic effect.

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Examination of 13 untreated patients with Itsenko--Cushing disease and syndrome showed an increase in total Ig as well as IgA, IgM and IgG, a decrease in the number of O-cells, and the absence of significant change in in the blood content of T-lymphocytes. A decrease in the amount of B-lymphocytes was noted in this group of patients with GTT of diabetic type or mild diabetes mellitus. Repeated examination of 7 of these patients 1-1.5 mos. after the resection of one adrenal gland showed that the content of O-cells had returned to normal, tension of the system of humoral immunity was on a decrease and combined with a decrease in the excretion of 17-OCS fractions though they were still above normal. Hyperlymphocytosis with a high level of T- and B-lymphocytes and the normal content of O-cells was noted in 11 patients after bilateral adrenalectomy for Itsenko--Cushing disease receiving maintenance doses of cortisone.

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A total of 46 boys aged 11 to 13 with the abnormal puberty syndrome were examined. The authors assessed various methods of correction of delayed puberty by the time course of anthropometric and genitometric indices and blood testosterone, LH and FSH levels 1 year after the initiation of treatment, at the age of 14 to 16 and 17 to 19. The ejaculate composition of 12 adolescents over 17 was examined. In 3/4 of the adolescents the indices of physical development and pubescence, blood testosterone and gonadotropic hormone levels achieved physiological values by the age of 14-16, but in 1/4 of the patients delayed puberty with lowered FSH and testosterone levels and raised LH in the blood was noted. The normalization of puberty was noted at the age of 17 to 19 with normal spermatogenesis. The necessity and methods of therapeutic correction of delayed puberty in boys and adolescents with the abnormal puberty syndrome were discussed.

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A noticeable masculinizing effect with a high level of testosterone (T) in the blood up to its level in healthy males was obtained during treatment of 10 patients with primary (hypergonadotropic) hypogonadism using sustanon-250 at a dose of 1 ml i. m. once in 3-4 weeks. However no decrease in the initially elevated levels of the follicle-stimulating and luteinizing hormones was observed. The treatment of 21 patients with hypogonadotropic hypogonadism by small doses of chorionic gonadotropin (CG) (up to 1500 Units i. m. 3 times a weeks) turned out ineffective. The use of high doses of CG (3000-4000 units i. m. 3 times a week) or CG combined with menopause gonadotropin in most patients of this group produced a short-term clinical effect with an elevated T level in the blood. Hypogonadotropic hypogonadism combined with an acute decrease in the response of the testes to CG treatment even at large doses was found in 4 patients under 6 years with cryptorchidism who had undergone surgery for descent of the testes into the scrotum.

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To differentiate tuberculous and autoimmune affections of the adrenal cortex the Mantoux test was made in 15 patients with primary chronic adrenal insufficiency (PCAI), indirect hemagglutination with tuberculin antigen was performed and antibody titre to corticosteroma homogenate antigens was determined, in addition to the clinical pattern examination, by means of passive hemagglutination (the Boyden test). Antibodies to antigens from corticosteroma cells in the high titre (1 : 10240) were found in 5 of 6 patients without tuberculous affection of adrenals and in 4 of 9 subjects with adrenal tuberculosis. The study of the level of antibodies to corticosteroma homogenate antigens in the blood serum of patients suffering from PCAI cannot serve as a reliable criterion for differentiating the tuberculous affection and adrenal cortex destructive atrophy, often induced by autoimmune process.

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Experiments were conducted on 21 female rabbits. Prolonged excessive feeding with food rich in readily assimilated carbohydrates (bisquits) started at immature age caused hypertrophy and hyperplasia of the insular apparatus of the pancreas, particularly in ovariectomy. The average blood sugar level on fasting stomach displayed a significant reduction in ovariectomized female rabbits. Some female rabbits displayed signs of "exhaustion" of beta-cells of the islets of the pancreas, with the development of latent diabetes mellitus in one of them. Prolonged excessive feeding with food rich in readily assimilated carbohydrates led to the intensification of atherogenesis, most pronounced in the animals with signs of "exhaustion" of beta-cells of the islets of the pancreas.

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