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Query: UMLS:C0028754 (obesity)
124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have carried out a prospective survey of 25 cases of male hypogonadism attending one hospital, and a retrospective study of 73 men attending other endocrine clinics in Manchester. In total, 47 had pituitary disorders, 15 isolated gonadotrophin deficiency (including 4 with Kallmann's syndrome), 10 testicular atrophy of unknown cause, 12 testicular damage, 10 with Klinefelter's syndrome, and 4 had miscellaneous disorders. Our survey emphasises the importance of adequate history and examination. Most patients presented with reduced libido, with marital problems in 62% of married men. Less common problems were facial flushing, osteoporosis and gross obesity. Several patients with pituitary disorders were asymptomatic, even in the presence of visual field defects. Klinefelter's syndrome, and testicular atrophy, may present with infertility or gynaecomastia rather than symptoms of androgen deficiency. On examination, the presence of gynaecomastia or obesity were of no help in differential diagnosis, whereas visual field defects clearly indicated a pituitary cause. Measurement of height/span was of little help. The precise diagnosis was usually established with basal plasma LH, FSH, testosterone and prolactin, with karyotype and pituitary radiology, and without more elaborate dynamic hormone tests. Testosterone esters given by intramuscular injection as "Sustanon 250" was the most commonly used replacement therapy. Improved libido usually resulted. Side-effect occurred in 10%, usually as muscle cramps, pain at the injection sites, acne, or excessive sex drive. One tragic case illustrates the potential dangers of androgen replacement therapy in an unrecognised psychopath, and where doubt exists a psychiatric opinion should be sought before starting therapy.
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PMID:Clinical aspects of androgen deficiency in men. 689 Jul 81

Primary empty sella syndrome (ESS) is an anatomo-radiological picture characterized by the presence of an arachnoid herniation filled with liquor that compresses the pituitary against the sellar wall. ESS occurs particularly in obese, hypertensive, cephalalgic women. It is often asymptomatic but may be associated with ophthalmologic, neurologic and non-characterizing endocrine disorders. We report here 43 cases of primary ESS observed and assessed in our Departments of Internal Medicine from June 1983 to May 1993. The following endocrinological diagnostic procedures were carried out: hormonal (RIA) basal profile: FT3, FT4, TSH, PRL, ACTH, FSH, LH, 8.00 a.m. and p.m., blood cortisol, aldo, PRA, DHEA-S, FTe, E2, P, PTH, CT, and calcemia and phosphoremia; provocative tests: TRH, GnRH, etc.; inhibition tests: high dose dexamethasone. Clinical, neurologic (skull radiographs, sellar stratigraphy, computed tomography scan and magnetic resonance), and ophthalmologic (fundus, visual fields) assessments were also made. Our findings fit with the data in the literature concerning common symptoms of ESS, associated endocrinopathies and other illness. We found obesity (62.7%), oligo-amenorrhea (16.6%), galactorrhea (14.6%), hyperPRL (11.6%), hypopituitarism (9.3%), hypogonadism (4.6%), diabetes insipidus (2.3%), (micro-)polycystic ovary syndrome (19%), hyperACTH (2.3%). In 9.3% of the cases, endocrinopathy referred to pituitary adenomas. Moreover, we noted a high frequency of psychological disorders, to our knowledge not previously reported in the literature, including anxiety or dysthymic disorders with altered behavior (chiefly oral compulsion). We also make the hypothesis that obesity (occurring in 62.7% of our patients) and hypertension (62.7%) may be related to hypothalamic alterations.
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PMID:[43 cases of primary empty sella syndrome: a case series]. 761 55

Polycystic ovary syndrome (PCOS) is an association of oligomenorrhoea, anovulation, hyperandrogenism, obesity and enlarged polycystic ovaries. It provides a model of loss of cyclic ovarian function. It is classical to distinguish between type I and type II PCOS. In type I, the primary mechanism seems to be hypothalamic dysfunction, which causes an increase in the frequency and amplitude of LH pulses, with diminished FSH release. LH hypersecretion stimulates ovarian stroma hyperplasia while FSH insufficiency results in the failure of folliculare maturation and hence anovulation. Aromatization of androgens to oestrogens is responsible for permanent oestrogen overproduction, which favours LH hypersecretion. Type II PCOS is more frequent and may have multiple causes (local, endocrine, systemic, iatrogenic) that interfere with the gonadotropic axis and alter the FSH/LH ratio. The most efficient treatment of hirsutism is cyproterone acetate which alone has both antiandrogenic and antigonadotropic properties. Clomifene citrate remains the "first choice" treatment of infertility associated with anovulation.
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PMID:[Polycystic ovarian dystrophies. Diagnostic criteria and treatment]. 763 20

In polycystic ovarian disease there is a strong association between hyperinsulinemia and hyperandrogenism but not with obesity alone. The magnitude of peripheral insulin resistance is similar to that seen in non-insulin-dependent diabetes mellitus. Mild hyperinsulinemia in PCOD patients is not impair the carbohydrate metabolism. The elimination of the cause of hyperandrogenism by bilateral oophorectomy, long-acting Gn-RH agonist or antiandrogen cyproterone acetate did not improve the associated insulin resistance. In opposition to insulin resistance in the tissues responsible for metabolism of carbohydrate, the ovary remains sensitive to the effects of pancreatic hormone. Presumably this mechanism involved the interaction with IGF-I receptors to stimulate thecal and stromal androgen production. Insulin may sensitize the stroma to the stimulatory effect of LH. In the mechanism of follicular arrest take part increased level of binding proteins for IGF-I, mainly IGFBP 2, -4 and 5 inhibit FSH and IGF-I action.
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PMID:[Insulin resistance in the pathogenesis of polycystic ovarian disease (PCOD)]. 772 20

The endocrinology of the perimenopause--the time between pre- and postmenopause--is characterized by changes in the metabolism of the steroid hormones caused by increasing insufficiency of the ovaries. Until the age of 48 the concentrations of the estrogens are relatively constant with a median level of 120 pg/ml serum for estradiol and of 75 pg/ml for estrone. Between the age of 49 and 54 the levels decrease to concentrations of 35 pg/ml for estrone and 10 pg/ml for estradiol. In the corresponding time, there is a tenfold rise of the level of FSH. The level remains constant until high age. The decrease of the estrogens causes the menopause in an age of 51 to 52. In the postmenopause the ovaries don't play a role for the concentrations of the estrogens. The concentrations are determined by the conversion of the androgens secreted by the adrenal cortex. The serum concentrations of androstenedione are five times higher than those of testosterone. The function of the adrenal cortex remains until high age; there is no 'adrenopause' comparable to the 'menopause'. The suppression of the adrenal cortex by treatment with corticoids (e.g. for asthma) causes a dramatic decrease of the androgens and consecutively for the estrogens. The lack of estrogens play an important role in the induction of osteoporosis and other disturbances of the late postmenopause, e.g. coronary heart disease. Obese women show in the pre- and the perimenopause more often dysfunctional bleedings caused by anovulation or corpus luteum insufficiency.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Endocrinological changes in pre- and postmenopause]. 783 30

To evaluate whether the PRL, TSH and gonadotropin secretion is altered in conditions with elevated body mass index, 7 patients with central Cushing's disease before and after transsphenoidal surgery, 7 untreated patients with Cushing's syndrome caused by adrenal adenoma, 17 simplex obese (obese) women and 9 non-obese controls (all females, aged 18-45 years) were tested with TRH (200 micrograms i.v. bolus) and GnRH (100 micrograms i.v. bolus) and the hormone responses were measured. There were no differences in the basal pituitary hormone secretion among the groups. In obese subjects the PRL response was reduced as compared to untreated patients with corticotrop pituitary adenoma. No significant differences of TSH release could be observed among the groups, whereas serum total T4 levels were higher in obesity than in patients with hypercorticism either caused by pituitary or adrenal Cushing's syndrome. No differences were found in the LH response, but the stimulated FSH release was lower in obesity, in patients with central Cushing's disease after transsphenoidal surgery and in patients with primary Cushing's syndrome as compared to the normal controls.
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PMID:[Anterior pituitary responsiveness in central Cushing disease and in Cushing syndrome caused by adrenal cortex tumors, as well as in simple obesity]. 786 32

A 27-year old woman was admitted to our hospital because of oligomenorrhea, hirsutism and obesity. Her menstrual period has been irregular since she was 14 years old. Her weight increased rapidly after the age of 15 and she became obese. Hirsutism was noticed at the age of 16. The diagnosis of polycystic ovary syndrome was made on her illness through the endocrinological examinations: (1) The response of LH to LH-RH administration was much higher than that of FSH. (2) The concentration of plasma testosterone was increased. (3) Plasma level of E2 was decreased while that of E1 was increased. (4) CT scan showed bilateral ovarian cyctic masses. In addition, hyperinsulinemia was observed during the 75g glucose tolerance test and the presence of insulin resistance was suggested. As she was overweight (BMI; 33.6 kg/m2), weight loss was expected to improve her hormonal abnormalities. She went on a very low calorie diet of 420 kcal/day (Optifast, Sandoz, USA). When she lost around 9kg of weight, her menstruation period started that has not been observed for the previous 5 months. Plasma levels of LH, FSH and testosterone were lowered following the weight loss. The responses of LH to LH-RH and IRI to glucose were decreased as well. She left the hospital after the second menstruation occurred at the proper period. From these results, the importance of weight loss was suggested in overweight patients with polycystic ovary syndrome. The benefit of very low calorie diet was also noticed since it brought a rapid weight loss as well as rapid improvements of hormonal abnormalities.
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PMID:[Hormonal abnormalities were improved by weight loss using very low calorie diet in a patient with polycystic ovary syndrome]. 795 30

The study was aimed at investigating the effect of monosodium glutamate administered during the perinatal period on the reproductive system of sexually mature male rats. Monosodium glutamate (at a dose of 4 mg/g of body weight) or hypertonic saline was administered subcutaneously to newborn rats at 2--nd, 4-th, 6-th, 8-th and 10-th day of life. At the age of four months the rats were killed and histological and morphometric examinations of testes, epididymis, seminal vesicles and ventral prostate were carried out. Blood serum levels of LH, FSH, testosterone and 17-beta-estradiol were determined by radioimmunoassay. The administration of monosodium glutamate caused inhibition of growth, obesity and decrease in weight of pituitary glands and testes. Blood serum levels of and FSH as well as the height of epithelial cells of accessory sexual glands remained unchanged, whereas testosterone level was lowered.
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PMID:[Effect of perinatal administration of monosodium glutamate (MSG) on the reproductive system of the male rat]. 805 18

Obesity, the most frequent nutritional problem throughout the rich nations, can have a vast and significant influence on different aspects of endocrinology, in particular on ovulation disfunction, on hyperandrogenemia, on hormone-sensitive carcinomas. Our study proposes to value the response to adrenal cortex to stimulation with adrenocorticotropin (ACTH) hormone in obese patients, with particular attention to the behavior of adrenocortical androgens and their precursor. We recruited 30 female patients so divided: 12 obese, nonhirsute, eumenorrheic patients (group A); 10 normal weight, hirsute patients in situation of secondary amenorrhea (group B); 8 normal weight, nonhirsute, eumenorrheic patients (group C). Cortisol, progesterone, 17 OH progesterone, dehydroepiandrosterone sulfate, androstenedione, testosterone were measured at 60, 120, 180, 240, 300 min during continual infusion i.v., for 5 h, of ACTH 1-17 at 100 mcg dose, in physiological sodium chloride solution. All the women with monthly menstruation were studied between the IV and VIII day of their cycle. In the patients with secondary amenorrhea the value of basic progesterone was used to completely exclude an eventual luteal phase and the relationship LH/FSH was so as to logically exclude a diagnosis of polycystic ovary. This exclusion was also confirmed from the report of the ultrasonography. The basic concentration of hormone dosage is not significantly different between the patients of the three groups, except for T. This hormone is different because it is found to be significantly (p < 0.01) increase in the hirsute patients, in respect of the patients in group A and group C. Also P and 17OHP have been found to be higher, if only in insignificant measure, in hirsute patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Probable role of obesity on the adrenal response to acute stimulation with adrenocorticotrophic hormone in eumenorrheic and hirsute, non-eumenorrheic women]. 823 17

In 82 females with hyperandrogenism and polycystic ovaries, the sensitivity and diagnostic accuracy of the free-androgen index (FAI) were compared with those of testosterone (T), free testosterone (fT), androstenedione (A), LH and the LH/FSH ratio. Normal ranges for each parameter were derived as 95th percentile in 53 healthy controls of similar age. T, fT, A, FAI, LH and LH/FSH were significantly (p < 0.001) higher in patients than controls. The sensitivity and diagnostic accuracy of the FAI (0.46 and 0.64) were lower than those of T (0.67 and 0.78) and A (0.56 and 0.73) and similar to those of fT and LH/FSH. The overall variance of the FAI was highest among all parameters. The FAI was significantly (p = 0.05) elevated in a subgroup with obesity (n = 34), whereas T and fT did not differ in obese and nonobese subjects with polycystic-ovary syndrome. We cannot recommend the routine measurement of the FAI in the rational laboratory evaluation of female hyperandrogenism for the following reasons. (1) The adequate normal range for the FAI (< 8.7) is substantially higher than previously thought in normal individuals, which has serious consequences for the accuracy of the test. (2) The values of the FAI showed the widest overlap with controls. (3) The significant positive correlation between FAI and fT allows the prediction of the FAI from the measurement of fT, rendering the determination of a second parameter for the free bioactive T unnecessary. (4) The FAI as well as sex-hormone-binding globulin are influenced by body weight, whereas T and fT are markers for hyperandrogenism independent of obesity.
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PMID:[Is determination of the "free androgen index" for hormone screening in polycystic ovaries of value?]. 829 11


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