Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With the aim of examining central opioid influences on the control of luteinizing hormone (LH) secretion, we evaluated the LH response to naloxone, an opioid receptor antagonist, in patients affected by normo-, hyper-, and hypogonadotropic amenorrhea, polycystic ovarian disease and hyperprolactinemia. The results indicate that opioid influences are altered in well-defined pathologic conditions (hyperprolactinemia, obesity), in addition to being modified by gonadal steroids.
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PMID:Impairment of opioid control of luteinizing hormone secretion in menstrual disorders. 388 35

The present study was designed for exploration of hormonal disturbances underlying common forms of amenorrhea. Polycystic ovary syndrome (PCO) patients and obese amenorrheic subjects had significantly elevated estrone (E1) levels, elevated luteinizing hormone/follicle-stimulating hormone ratios, and an exaggerated luteinizing hormone response to luteinizing hormone-releasing hormone. However, androstenedione (delta 4A), the precursor of E1, was elevated only in PCO. Thus, the E1/delta 4A ratio, which provides an indirect index of aromatase activity in extraglandular sites, was raised in obese subjects as a group but not in PCO subjects. These findings suggest that elevated E1 levels, which give rise to abnormal gonadotropin secretion, arise from increased available androgens in PCO but from an increased effect of aromatase (present in adipose tissue) in obese subjects. Measurement of androgens and the E1/delta 4A ratio provides insights into the relative contributions of hyperandrogenemia and enhanced aromatase activity to the genesis of amenorrhea in these groups. In patients with suppressed estradiol levels associated with hyperprolactinemia or weight loss, follicle-stimulating hormone levels were suppressed, while luteinizing hormone was not elevated. Prolactin excess explains these findings in hyperprolactinemia. Plasma E1 levels and the E1/delta 4A ratio were suppressed in patients with weight loss, possibly as a consequence of reduced adiposity. This finding suggests that hypothesis that a minimum level of E1, dependent upon adequate adiposity, is critical for the normal mature function of the hypothalamic-pituitary-ovarian axis. Abnormal E1/delta 4A ratios, high in obesity-associated amenorrhea and suppressed in weight loss-associated amenorrhea, may provide specific markers for these groups of patients.
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PMID:Altered androstenedione and estrone dynamics associated with abnormal hormonal profiles in amenorrheic subjects with weight loss or obesity. 388 79

18 patients with "primary empty sella" were reviewed for this study. In 3 of them the sellar enlargement was discovered occasionally by performing skull radiographs for other reasons. The galattorrhea-dismenorrhea or amenorrhea syndrome and obesity were the most common clinical features. Endocrinological tests were normal in ten patients and abnormal in eight. Slight elevation of serum PRL was the most common record. 12 patients had enlarging of the sella turcica; in 4, only the floor was asymmetric and in 2 the sella was quite normal. In 5 patients C.T. without intra-thecal contrast was sufficient to discover the E.S. In 13 patients we performed C.T. cysternography by injecting in the lumbar subarachnoid space 8-10 ml of Iopamidolo 200. This is an excellent and safe technique to perform C.T. cysternography.
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PMID:[Primary empty sella. Clinico-radiologic considerations in 18 cases]. 403 90

The right suprarenal mass was found in a 21-year-old housewife. Her major clinical features were amenorrhea, polydipsia and buffalo hump obesity. Endocrinological and roentgenological studies suggested the presence of Cushing's syndrome due to adrenocortical carcinoma in addition to ipsilateral renal stone. The huge adrenal tumor and renal calculus were successfully removed. The histological diagnosis was adrenocortical carcinoma. Seventeen days after the operation, cis-platinum was administered to prevent the recurrence of tumor development. No recurrence has been observed for approximately 2 years after the surgery. Long follow-up must be pursued to clarify the real efficacy of cis-platinum treatment.
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PMID:[Cis-platinum used for the prevention of the recurrence of adrenal cortical carcinoma: report of a case]. 405 Jun 25

Polycystic ovarian disease (PCOD) was first described as a single disease by Stein and Leventhal in 1935, but now has been separated into several distinct entities, comprising a symptom complex. The most frequent presenting symptoms associated with PCOD are obesity, hirsutism, amenorrhea or anovulation, dysfunctional uterine bleeding, irregular menses, and infertility. The common finding of hirsutism in PCOD patients is a reflection of the hyperandrogenism resulting from elevation of all the androgens, including testosterone, androstenediol, dehydroepiandrostrone sulfate (DHEA-S), and androstenedione. Some patients with all the clinical features of PCOD can be shown, through appropriate testing, to have an attenuated form of classic congenital adrenal hyperplasia (CAH). Serum follicle stimulating hormone (FSH) levels are usually low or in the normal range, and serum luteinizing hormone (LH) levels are usually elevated in patients with PCOD, resulting in an altered LH/FSH ratio. Treatment for PCOD must be based on the needs and desires of the individual patient, and on the pathophysiology of the patient's particular abnormalities. When pregnancy is desired, ovulation induction with clomiphene is indicated. Clomiphene is a weak estrogen that induces a transient rise in serum LH and FSH, followed by a gonadotropic pattern similar to normal cycles. A 72% ovulation rate and a 41.8% conception rate have been reported after treatment with clomiphene. In patients who do not respond to clomiphene, or clomiphene with added human chorionic gonadotropin (hCG), human menopausal gonadotropin (hMG) can be used to induce ovulation, but the patient should be closely monitored for multiple ovulation, multiple pregnancy, or hyperstimulation syndrome. For patients not interested in conception, regular menstrual cyclicity can be restored and hyperandrogenism reduced with oral contraceptives (OCs).
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PMID:Polycystic ovarian disease. 623 74

Hyperprolactinemia is common and mainly encountered in premenopausal women. The most prevalent causes are drugs (estrogens, neuroleptics), hypothalamic and pituitary disorders (functional abnormalities, intrasellar adenomas, suprasellar lesions) and hypothyroidism. Although the typical picture is the amenorrhea-galactorrhea syndrome, hyperprolactinemia may be revealed by many other features, including obesity, hirsutism and sterility. When plain roentgenograms show a normal sella, neither dynamic tests nor polytommography can lead to unequivocal diagnosis of a tumor. Computerized tomography scanning is now the most reliable investigation in patients with hyperprolactinemia resulting from an obvious or suspected tumor.
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PMID:[Pathologic hyperprolactinemia. I. Positive diagnosis and etiology]. 629 80

After widespread publicity about major adverse reactions to oral contraceptive agents, combinations were tested that contained lower doses of sex steroids than had been used before. Among them, the combination of levonorgestrel, 150 micrograms, and ethinyl estradiol, 30 micrograms, was studied intensively. European studies exclusive of the British Isles were conducted on 3,733 patients through approximately 36,000 cycles. There were nine pregnancies, for a Pearl index of 0.3. Cycle regulation was excellent, with normalization of menstrual flow. Amenorrhea was reported in 2.3% or less of cycles. No serious side effects were reported. The decrease in estrogen dosage, usually accompanied by a decrease in the progestational component, has resulted in a decrease in reported thromboembolic disease. Factors still important are diabetes mellitus, hypertension, obesity and cigarette smoking.
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PMID:Clinical experience with a low-dose contraceptive agent. European studies. 640 3

10 examine the relationship between obesity and chronic anovulation, we compared basal serum LH, FSH, and PRL levels, determined at 20-min intervals, and basal C21 [progesterone, 17- hydroxyprogesterone , pregnenolone, 17-hydroxypregnenolone ( 17Pe ), and cortisol], C19 [testosterone (T), delta 4-androstenedione (A), and dehydroepiandrosterone] and C18 (estrone and estradiol) steroid hormone concentrations measured at 1- to 2-h intervals for a 24-h period in five normal weight cycling women (NC) and in two groups of weight-matched obese women. Five of the obese women were regularly cycling (OC), and six were amenorrheic (OA). Sex hormone-binding globulin (SHBG) and non-SHBG-bound T and estradiol concentrations were also measured in each woman. Compared to NC women, OC women had normal basal protein and steroid hormone concentrations, except for reduced 17Pe levels (P less than 0.05). Mean SHBG concentrations were reduced by approximately 30%, and non-SHBG-bound T was increased by 70%, although the differences were not significant. In addition, when six precursors of testosterone (pregnenolone, 17Pe , dehydroepiandrosterone, progesterone, 17-hydroxyprogesterone, and A) were considered together as a group and the data analyzed by the kappa 2 test, a reduction in basal levels of these precursors was found in OC women relative to those in NC women (P less than 0.005). In OA women, mean concentrations of SHBG were markedly reduced and those of total T, A, estrone, and non-SHBG-bound T were significantly increased compared to those in both NC and OC women. Mean 24-h concentrations of LH tended to be greatest and FSH lowest in this group, but were not significantly different from those in the other groups. The mean LH pulse frequency was significantly greater in OA than in OC women (P less than 0.05). Mean 24-h PRL and cortisol levels were also reduced in OA women relative to those in NC women. These data suggest the possibility of a compensatory decline in total T production in OC women in an attempt to maintain normal hormonal homeostasis; as a consequence, ovulation continues in a cyclic fashion. In OA women, such compensatory mechanisms are no longer operative. Instead, a central and/or peripheral defect, resulting in overproduction of androgen, may also exist and lead to anovulation in OA women. In conclusion, our data imply that obesity is not a primary factor causing chronic anovulation. However, obesity may aggravate an already existing subtle defect in some women and result in amenorrhea.
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PMID:Endocrine comparison of obese menstruating and amenorrheic women. 642 58

Bulimia is an eating disorder characterized by the ingestion of large amounts of food, usually followed by self-induced vomiting or laxative abuse. Although sometimes a symptom of obesity or anorexia nervosa, bulimia is often associated with borderline weight and nutritional status and thus may be difficult to detect. Since secrecy and shame accompany this syndrome, patients are reluctant to seek treatment. We present ten diagnostic clues for identifying bulimic patients: (1) preoccupation with weight, (2) gastrointestinal complaints, (3) dental and oropharyngeal changes, (4) salivary gland enlargement, (5) edema and bloating, (6) amenorrhea, (7) dermatologic complaints, (8) substance abuse, (9) laboratory changes, and (10) serious consequences. A case study illustrates the major features of the disorder and its treatment.
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PMID:Bulimia: diagnostic clues. 657 18

A 26-year-old woman had hyperphagia, obesity, aggressive behavior, visual hallucinations, reversal of wake-sleep patterns, hypothermia, hypothyroidism, and amenorrhea. She died of pancreatitis, probably secondary to hypothermia. Autopsy revealed a low-grade astrocytoma in the third ventricle and medial anterior and mid hypothalamus, primarily on the right. Although she exhibited thyroid and ovarian hypofunction, the patient had intact median eminence and pituitary function, suggesting end-organ failure, possibly of an autoimmune nature.
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PMID:Hypothalamic astrocytoma. Syndrome of hyperphagia, obesity, and disturbances of behavior and endocrine and autonomic function. 657 19


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