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

Five patients were found to have hyperthecosis ovarii as evidenced by the presence of large lipid containing thecal cells in the ovarian stroma. The clinical picture was similar in all of them, featuring mild virilization, obesity and oligomenorrhea, with refractoriness to clomid therapy. Plasma FSH levels were low normal, while LH levels were slightly elevated. Urinary 17-ketosteroids levels were elevated, and plasma testosterone concentrations were upper normal. The response to dexamethasone suppression and HCG stimulation is discussed. The effect of wedge resection on the clinical and endocrinologic pictures is evaluated.
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PMID:Hyperthecosis syndrome. Clinical, endocrinologic and histologic findings. 41 61

Hyperandrogenism in adolescent girls can be a troubling problem because of the difficulty in establishing a diagnosis and in prescribing appropriate therapy. Androgen excess in adolescent patients encompasses a spectrum of clinical presentations, including acne, hirsutism, oligomenorrhea, amenorrhea, virilism, and ovarian cysts. Androgen excess is a clinical and chemical feature of idiopathic hirsutism, late-onset forms of congenital adrenal hyperplasia, and polycystic ovarian disease; in some cases, functional hyperandrogenism is discussed. We recommend screening for hyperandrogenism by measuring blood levels of testosterone, dehydroepiandrosterone sulfate, and delta 4-androstenedione, while others propose a first dexamethasone suppression test for evaluation of free testosterone, dehydroepiandrosterone sulfate, and cortisol. Treatment will be chosen according to particular symptoms such as acne, hirsutism, obesity, or oligomenorrhea.
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PMID:Management of hyperandrogenism in adolescent girls. 184 Jan 43

The most common signs of androgen excess in women are acne, alopecia, and hirsutism. Less common manifestations include android obesity, virilization, and acanthosis nigricans. These changes appear to be the result of excessive androgen production or increased target organ sensitivity. To evaluate excessive androgen production, an androgen screening protocol is recommended that includes measurement of dehydroepiandrosterone sulfate, testosterone, androstenedione, prolactin, follicular stimulating hormone, and luteinizing hormone. When androgen excess is confirmed, dexamethasone suppression is recommended to determine the source of the androgen(s). Once excessive androgen production is confirmed, more specific therapies can be administered.
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PMID:Diagnostic approach to androgen disorders in women: acne, hirsutism, and alopecia. 214 37

Hirsutism as a sign of hyperandrogenism is a common endocrinological disorder in women. Its spectrum varies from mild forms with dominating psychic component to severe forms associated with virilization. The severity should be assessed by semiobjective scoring systems, the use of which also allows the systematic follow-up of the results of treatment. An increase in serum androgen levels or an increased turnover of androgens can be detected in most patients. Enhanced peripheral conversion of androgens to locally acting androgen also leads to hirsutism. The thorough investigation of the endocrinological milieu is required to rule out androgen producing neoplasms. In most patient, however, disturbances are functional, among which polycystic ovary syndrome is the commonest. It is a disorder exhibiting a complexity of changes in endocrinological interactions. Besides inappropriate gonadotropin secretion insulin and insulin like growth factor are also involved. The opioidergic system also seems to be affected. Polycystic ovary syndrome is also associated with obesity and infertility, both of which require attention.
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PMID:Hirsutism: definitions and etiology. 219 64

It is important to diagnose hyperandrogenism in women. By disturbing ovulation, it is actually one of the most frequent causes of infertility. In this particular case, its diagnosis has specific implications: sometimes specific treatment is indicated, or the risk of fetal virilization should be prevented. There is always the possibility of a diagnosis of polycystic ovary, prompting precautionary measures to be taken that are likely to limit the risks linked to the multifollicular development that is so frequent with this disorder. In addition, hyperandrogenism exposes the patient to various gynecological and general complications: cancer of the endometrium, progressive increase in menstrual disturbances and infertility, obesity, metabolic disturbances and probably increase in cardiovascular risks. Certain types of hyperandrogenism give rise to diseases that expose the patient to specific risks: virilizing tumors, Cushing's syndrome, neonatal risks linked to congenital hyperplasia of the adrenal glands. Hyperandrogenism should be borne in mind not only when the clinical picture is that of virilization, but also when there is any disturbance in eugonadal ovulation, whether or not this is manifested as menstrual disturbances or as infertility, and especially whether or not it is accompanied by hirsutism.
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PMID:[When and why should hyperandrogenism be searched for in women?]. 267 67

The aim of this article is to present evidence of hyperostosis frontalis interna in a 40-year-old female recovered from a Meroitic cemetery (ca. 300 A.D.) in Sudanese Nubia. A review of the literature concerning the Morgagni-Stewart-Morel (MSM) syndrome suggests that the changes in the skull fragment are consistent with this diagnosis. This case is the earliest example of the condition so far reported, and therefore, in archaeological time and space, this is a disease not only of modern civilization, but also of antiquity. Current endocrinological reports suggest that the hyperostosis is the hallmark of a generalized disorder of bone metabolism, with increased androgens, prolactin, and somatotropins. Hyperostosis frontalis interna is the central feature of a syndrome first described over 200 years ago by the early pathologist Giovanni Batistta Morgagni, professor of anatomy at Padua (1719). He found thickening of the internal tables of the frontal bones in association with virilism and obesity. Stewart (1928) and Morel (1929) independently added several neuropsychiatric problems to this complex and questioned the possibility of an endocrine basis for the syndrome.
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PMID:Hyperostosis frontalis interna: a Nubian case. 304 35

Adrenocortical tumors can be divided into two groups based on their histopathological characteristics, i.e., benign (adenoma) and malignant (carcinoma), and also classified as functioning (or hormonal) and non-functioning (or non-hormonal) tumors, depending on the presence or absence of recognizable clinical syndromes due to excessive steroids. The syndrome of functioning adrenocortical tumors includes Cushing's syndrome, primary aldosteronism and the adrenorge genital syndrome, of which a minority presents most of the specific clinical features: Cushing's syndrome; red face, typical moon face, truncal obesity, and purplisch red striae, primary aldosteronism; muscle weakness, noctural polyuria, hypertension and hypokalemia, adrenogenital syndrome; virilization or feminization, but many of them present complete clinical picture. The diagnosis of these syndromes needs to measure urinary 17-OHCS and 17-KS and plasma concentrations of cortisol, aldosterone, dehydroepiandrosterone (DHEA) and the other steroids. Dexamenthasone suppression test, various stimulation tests and the measurement of plasma ACTH are also useful for diagnosis. Usually, adrenocortical tumors can be detected preoperatively by physical examination or radiographic studies. Some are massive enough to be palpable through the abdominal wall. Some are large enough to cause displacement of the kidney, as seen intravenous urography. Most are visible by adrenal scintigraphy using 131I-iodocholesterol, computerized tomography, or adrenal arteriography. The standard treatment for adrenocortical tumors are surgical resection. Unresectable adrenocortical carcinomas may be treated with an adrenocorticolytic drug, o'p'-DDD. Metyrapone and aminoglutethimide can be also employed to inhibit the production of steroids.
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PMID:[Diagnosis and treatment of adrenocortical tumors]. 631

Blood production rates of testosterone, dihydrotestosterone (DHT), and 3 alpha-androstanediol (3 alpha-diol) were found to be approximately 2-fold elevated in morbidly obese, nonhirsute, normally menstruating women. Values were intermediate between those found in normal women and those in a group of nonobese normally menstruating women with idiopathic hirsutism. Elevated androgen production rates in obese women were associated with 2- to 3-fold increases in MCRs, presumably due to decreased levels of sex hormone-binding globulin. Thus, increased production rates were offset by increased MCRs, resulting in plasma testosterone, DHT, and 3 alpha-diol concentrations that were similar in the obese and normal women. By contrast, women with hirsutism had increased production rates associated with elevated plasma androgens as well as increased MCRs. Urinary excretion of testosterone glucuronide and 3 alpha-diol glucuronide (3 alpha-diol G) were elevated in both obese and hirsute women, paralleling the increased androgen production rates. Despite increased production rates and excretion of androgens, obese women exhibited no menstrual abnormalities, hirsutism, or other signs of virilism. To explore the apparent ineffectiveness of increased androgen production to produce virilizing symptoms, we measured plasma 3 alpha-diol G levels as a measure of peripheral androgen action. The mean +/- SE plasma 3 alpha-diol G was 53 +/- 8 ng/dl in obese women and 36 +/- 6 in normal women; by contrast, women with idiopathic hirsutism had levels of 440 +/- 99, a 12-fold elevation. Plasma testosterone glucuronide in obese and hirsute women were only 2- to 3-fold elevated, while plasma DHT glucuronide was not increased in obese women and was only 2-fold elevated in hirsute women. Thus, obesity is a state of increased androgen production and accelerated clearance. 3 alpha-diol G levels in obese women were only minimally elevated, in contrast to values in the hirsute women, perhaps reflecting the apparent androgen ineffectiveness.
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PMID:Elevated production and metabolic clearance rates of androgens in morbidly obese women. 648 Aug 13

Virilization in women is associated with increased production of testosterone as well as a variety of androgenic prehormones, including androstenedione, androstenediol, DHEA, DHEA-sulfate, dihydrotestosterone and androstanediol. Of these hormones, it is likely that testosterone is the androgen which initiates a series of androgen-receptor mediated events resulting in stimulation of 5 alpha reductase in the skin and hair follicles, producing dihydrotestosterone locally. The metabolism of testosterone to dihydrotestosterone within the hair follicle results in increased clearance of testosterone, however at the expense of hair follicle stimulation. Increased 5 alpha reductase of the skin and hair allows other prehormones to be metabolized to dihydrotestosterone and androstanediol, further stimulating the hair follicle (multiplier effect). In obese women, androgen production rates are elevated and SHBG levels are depressed, in many cases to the same magnitude as that observed in hirsute women. Increased androgen production rates in obesity, however, are associated with major increases in clearance rates of these androgens. Resultant androgen blood levels are even lower than observed in the non-obese population. It appears likely that adipose tissue is the site of the increased clearance rates and metabolism of prehormones to dihydrotestosterone and androstanediol. A delicate balance likely exists between production and clearance of these biologically active hormones. Minor aberrations in this balance may result in the increased incidence of hirsutism seen in the obese female population.
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PMID:A comparison of androgen production and clearance in hirsute and obese women. 688 88

Hyperostosis frontalis interna is the name generally applied to skull thickening more or less restricted to the squamous portion of the frontal bone and involving, in particular, its subdural or inner surface. The association of this calvarial thickening with virilism and obesity is a clinic-anatomic complex often know as the Morgagni's syndrome and is also referred to as the Stewart-Morel syndrome or metabolic craniopathy, when accompanied by mental disorders. Hyperostosis frontalis interna is being discussed here mainly in connection with the Stewart-Morel's syndrome of which it is the pivotal feature. Frontal headache is a common complaint and is severe in some cases. In addition various neuropsychiatric disturbances may be manifested.
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PMID:[The Stewart-Morel syndrome in the differential diagnosis of patients with frontal headache]. 821 44


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