[Adverse effect of 3,5,3 triiodothyroacetic acid in the treatment of obesity].
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Biomedical subjects
Publications and source records attributed to E Devoto.
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BACKGROUND: Male infertility is responsible for 35% of infertile couples. AIM: To investigate the causes of male infertility and the relative importance of endocrine factors. PATIENTS AND METHODS: Patients referred to an andrology clinic due to an abnormal spermiogram were studied. A testicular examination, spermiogram and determination of FSH, LH, testosterone and prolactin were done to all. Testicular biopsy was done to patients with severe oligospermia or azoospermia. Causes of infertility were defined and classified as pretesticular, testicular, posttesticular or unclassified. RESULTS: Two hundred fifty seven males were studied. In 3.5% of them, the cause of infertility was defined as pretesticular (that included hypothalamic and pituitary endocrine causes), in 66.9% it was classified as testicular, in 15.6% as posttesticular and in 14%, as unclassified. Thirty percent of infertility cases were idiopathic, 17.9% were associated to varicocele, 12.8% were associated to cryptorchidism, 8.9% to Klinefelter syndrome and 6.6% to exposure to toxic substances. In 50% of patients with cryptorchidism, this abnormality was found during the specialized andrological examination and referrals for surgical correction were made late. Two thirds of patients with Klinefelter syndrome were hypoandrogenic. CONCLUSIONS: Causes for male infertility should be investigated and diagnosed accurately. Primary hypoandrogenic testicular failures must be treated with hormone replacement therapy.
BACKGROUND: Spironolactone has an anti androgenic effect, inhibiting the binding of androgens to their receptor. This antagonistic effect is the basis for the use of spironolactone in the treatment of hirsutism. AIM: To study the effectiveness and safety of spironolactone in the treatment of hirsute women and of the association of spironolactone plus dexamethasone in the treatment of hirsutism with glucocorticoid sensitive hyperandrogenism. PATIENTS AND METHOD: Sixteen women (group 1) with peripheral hirsutism (defined as those with normal androgens levels, normal menstrual cycles and ovulation) and 24 women (group 2) with glucocorticoid sensitive hyperandrogenic hirsutism were studied. Group 1 was treated with spironolactone 50 mg hid and group 2 with same spironolactone dose plus dexamethasone 0.5 mg at 23 h during one month and 0.25 mg thereafter. Patients were followed during one year. RESULTS: After one year of treatment, a 54% reduction in Moncada hirsutism escore was observed in group 1 and 52% reduction in group 2. Observed secondary effects of spironolactone were increases in diuresis, fatigability, acne aggravation and seborrhea in two patients. Two additional patients had spotting. No secondary effect attributable to glucocorticoid use were observed. CONCLUSIONS: Spironolactone is effective and safe in the treatment of hirsutism. Androgenic supression did no increases its effectiveness, underscoring the peripheral anti androgenic activity os spironolactone.
BACKGROUND: Oligomenorrhea, defined as a menstrual cycle lasting 36 to 90 days, can be a normal condition in the first years after the menarche. When it persists or appears after a period of normal menstrual cycles, an underlying illness must be sought. AIM: To assess ovulation and causes of anovulatory cycles in women with oligomenorrhea, compared with causes of secondary amenorrhea. PATIENTS AND METHODS: One hundred one women of less the 35 years old, presenting with oligomenorrhea persisting 5 years after menarche or lasting more than two years after a period of normal menstrual cycles, were studied. Ovulation was studied measuring serial plasma progesterone during normal or induced (with intramuscular progesterone) menstrual cycles. RESULTS: Eighty nine percent of women had anovulatory oligomenorrhea. The main causes were polycystic ovarian disease in 51% and hypothalamic dysfunction in 31%. Thirty percent of women with secondary amenorrhea had polycystic ovarian disease and 14% had hyperprolactinemia. Women older than 20 years old or with more than 10 years of gynecological age had a higher frequency of polycystic ovarian disease and a lower prevalence of hypothalamic dysfunction. CONCLUSIONS: There is a high frequency of anovulatory oligomenorrheas. Therefore, this symptom deserves a thorough endocrinological assessment to uncover underlying diseases. Special attention must be paid to polycystic ovary syndrome, due to its importance in internal medicine as a risk factor for myocardial infarction, high blood pressure, and type 2 diabetes mellitus.
BACKGROUND: Obesity is considered a protective factor for osteoporosis improving bone mass and maintaining higher levels of estrogen during menopause. OBJECTIVE: To determine the association of obesity with bone mineral density (BMD), and its relationship with sex hormone levels. DESIGN: A case-control study in Caucasian obese and non obese postmenopausal women. SUBJECTS: 113 obese and 50 non-obese postmenopausal women. MEASUREMENTS: BMD (dual-photon X-ray absorptiometry) at cervical femur. Ward's triangle, proximal radius and lumbar spine. Plasma levels of glucose, insulin, total estrogen, follicle stimulating hormone (FSH), sex hormone binding globulin (SHBG), dehydroepiandrosterone sulfate (DHA-S) and testosterone. RESULTS: Mean BMD at femoral sites were significantly higher in obese women (femoral neck: 0.849 +/- 0.124 g/cm2 vs 0.753 +/- 0.095 g/cm2, P < 0.001; Ward's triangle: 0.634 +/- 0.134 g/cm2 vs. 0.553 +/- 0.100 g/cm2, P < 0.001). Mean BMD at lumbar spine was 0.906 +/- 0.138 g/cm2 in obese women and 0.849 +/- 0.137 g/cm2 in non obese, P < 0.017. A decreased risk of osteopenia in femoral neck (Age adjusted OR = 0.36, 95%CI 0.17-0.75) and in lumbar spine (Age adjusted OR = 0.43, 95%CI 0.20-0.91) in obese women was observed. Although total estrogen were similar in both groups, in obese women, SHBG was lower (68.6 +/- 26.84 nmol/l vs. 85.1 +/- 31.18 nmol/l, P < 0.001), and postglucose load insulin levels were higher, than in non obese (77.2 +/- 50.4 Ul/ml vs. 49.4 +/- 24.1 Ul/ml, P < 0.0005). CONCLUSION: The findings confirm a higher BMD in obese women and suggest that obesity exerts protection due to a decreased SHBG thus increasing free sex steroids. Besides, hyperinsulinemia may produce a decline in the production of IGFBG-1, leading to an increase of IGF-1, that may stimulate the proliferation of osteoblasts.
Excessive ethanol ingestion induces hypoandrogenism in male subjects. To confirm its presence and to study its relationship with the degree of liver damage and alcohol abstinence, plasma sex hormones were measured in alcoholic patients without liver failure, after two different abstinence periods. Patients were 30 male chronic alcoholics admitted to the Alcoholism Ward for treatment of their addiction. On admission, we measured: testosterone (T), estradiol (E), follicle stimulating hormone (FSH), luteinizing hormone (LH) and sex-hormone binding globulin (SHBG). A liver biopsy was also performed. These measurements were repeated at discharge and were also done in 15 normal volunteers. On admission (mean abstinence 1.9 +/- 1.7 days) total T was similar to controls, FSH was lower (p < 0.02) and high levels of SHBG were found (3.5 fold increase, as compared to controls). Histologically, 9 patients had normal liver; 14 had moderate alterations and 7 showed marked alterations. Hormonal values were not different in these 3 groups. At discharge, 11.1 +/- 4.7 days after admission, T, E and FSH did not show significant changes but LH decreased (8.2 +/- 5.2 mIU/ml vs 12.9 +/- 4.1, p < 0.001); SHBG also decreased (65.4 +/- 21.6 nmol/l vs 117.2 +/- 33.3, p < 0.001) to values that still were twice those of controls. It is concluded that alcoholic patients without clinical signs of liver failure have normal plasma testosterone levels, irrespective of their histologic liver alterations and high plasma SHBG levels that decreased significantly after a short abstinence. The concomitant LH decrease suggests that hypoandrogenism is likely in these patients. Fast changes in SHBG levels rise the possibility that this protein is candidate marker of alcoholism.
Adrenal androgen hypersecretion either produced by genetic defects or reticular disfunction, is reduced by exogenous glucocorticoid administration and, as with any suppression therapy, it should relapse when the therapy is discontinued. However, prolonged remissions of adrenal androgen hypersecretion after discontinuing glucocorticoids have been described. We report 15 patients with adrenal hyperandrogenism and elevated levels of dehydroepiandrosterone sulfate that received treatment with dexamethasone. After one month of treatment with dexamethasone 0.5 mg/day, dehydroepiandrosterone sulfate levels returned to normal and remained so during a mean of 19 months receiving dexamethasone 0.25 mg/day. One year after discontinuing therapy, hormone levels continued within normal range in all patients. It is concluded that a long remission period of adrenal hyperandrogenism was achieves after discontinuing glucocorticoid therapy.
The approach to adrenal hyperandrogenism, due to genetical or non-genetical enzymatic alterations, has changed dramatically during the last 50 years. To allow a better understanding of the subject, we focused it from a historical perspective, defining four stages analyzed in detail. Now there is consent on the existence of a functional adrenal hyperandrogenism, which has an important role in acne, hirsutism and menstrual disturbances.
Antiandrogens are substances that block androgen receptors. The antiandrogenic action of some of these medications, as H2 blockers and some diuretics, was discovered as a collateral effect. They are used for the treatment of acne, hirsutism and seborrhea in women; they are also used in precocious puberty and sexual hyperexcitability states. The clinical usefulness of these drugs is unquestionable, but their prescription requires a through knowledge of their endocrinological effects.
Two cases of HAIR-AN syndrome (hyperandrogenism, insulin resistance and acanthosis nigricans) are presented. The first case corresponds to a female with a systemic lupus erythematosus and acanthosis nigricans in which an insulin resistance was documented; the patient was in amenorrhea with severe hypoestrogenism, although she did not have clinical signs of hyperandrogenism and serum androgen levels were normal. This case corresponds to a HAIR-AN syndrome associated to autoimmune diseases or type A of Kahn. The second case is a young female with clinical signs of hyperandrogenism associated to high testosterone levels; she had acanthosis nigricans and fasting and postprandial hyperinsulinemia. Probably, this case corresponds to a type A or C HAIR-AN syndrome in which there is a decrease in the number of insulin receptors or a post receptor defect in insulin action.
One hundred and eighty-two patients who complained of amenorrhea were tested with progesterone and oestrogen. The results are correlated with the diagnosis of the causes. The etiology is related with hypothalamic, hypophysiary, ovarian and/or uterine origins and dysfunction.
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A 50 year-old male with diffuse hyperthyroid goiter treated with I131 who develops a papillary carcinoma is presented. After thyroid resection, substitution therapy with thyroid hormone (levothyroxine) was started, and a selective malabsorption for this hormone was verified.
The autoimmune polyglandular syndrome is characterized by the association of 2 or more endocrine disorders of autoimmune origin which may coexist with autoimmune disorders in other organs. Roughly 25% of patients with an autoimmune endocrinopathy show evidence of autoimmune disease elsewhere. We report 21 patients with autoimmune polyglandular syndrome classified according to Neufeld.
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