Sleep apnea syndrome in endocrine diseases.
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It is increasingly recognized that sleep-disordered breathing (SDB) - from snoring to apnea-hypopnea syndrome (SAHS) - can affect patients with various endocrine diseases (ED). Different mechanisms are implied in SDB, promoting either central or, more frequently, obstructive apnea in different ED. In the past, acromegaly and hypothyroidism were first associated with both central and obstructive SAHS. Today, great attention is placed on the complex cause-effect relationship between diabetes mellitus and obstructive SAHS (and vice versa). Symptoms and signs of SAHS may complicate the clinical course of these diseases and should be promptly suspected to detect and possibly treat the accompanying SDB. (+info)
A plant food-based diet modifies the serum beta-sitosterol concentration in hyperandrogenic postmenopausal women.
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Plant sterols or phytosterols are common components of plant foods, especially plant oils, seeds and nuts, cereals and legumes. The most common phytosterols are campesterol, beta-sitosterol and stigmasterol. Phytosterols have anticarcinogenic properties. Previous studies have suggested that populations with low breast cancer incidence often consume diets high in phytosterols. The present study evaluated whether consumption of a plant food-based diet, low in animal fat, may increase serum phytosterol levels in postmenopausal women. One hundred and four women volunteers were randomized to dietary intervention or control groups. The dietary intervention included intensive dietary counseling to replace animal products with plant-based foods. Subjects in the dietary intervention group participated twice a week for 18 wk in workshops about the preparation and consumption of a plant food-based diet. The absolute change in serum total phytosterol concentration was greater in the dietary intervention group than in the control group. The percent change tended to differ between groups (P = 0.06). However, only for beta-sitosterol did the absolute and percent changes within a group differ significantly between groups (P = 0.0017). The decrease in serum total cholesterol in the dietary intervention group (-14%) was greater than that in the control group (-4%; P = 0.0005). The results of this study show that circulating levels of phytosterols can be affected by dietary modification. These findings indicate that phytosterols, in particular beta-sitosterol, can be used as biomarkers of exposure in observational studies or as compliance indicators in dietary intervention studies of cancer prevention. (+info)
Revised 2003 consensus on diagnostic criteria and long-term health risks related to polycystic ovary syndrome (PCOS).
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Since the 1990 NIH-sponsored conference on polycystic ovary syndrome (PCOS), it has become appreciated that the syndrome encompasses a broader spectrum of signs and symptoms of ovarian dysfunction than those defined by the original diagnostic criteria. The 2003 Rotterdam consensus workshop concluded that PCOS is a syndrome of ovarian dysfunction along with the cardinal features hyperandrogenism and polycystic ovary (PCO) morphology. PCOS remains a syndrome and, as such, no single diagnostic criterion (such as hyperandrogenism or PCO) is sufficient for clinical diagnosis. Its clinical manifestations may include: menstrual irregularities, signs of androgen excess, and obesity. Insulin resistance and elevated serum LH levels are also common features in PCOS. PCOS is associated with an increased risk of type 2 diabetes and cardiovascular events. (+info)
The follicular excess in polycystic ovaries, due to intra-ovarian hyperandrogenism, may be the main culprit for the follicular arrest.
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This review exposes the follicular abnormalities responsible for anovulation in polycystic ovary syndrome (PCOS). The putative pathophysiological explanations involve the principal intra- and extra-ovarian regulators which intervene during normal folliculogenesis to control the initial recruitment and growth and then the cyclic recruitment. We propose the hypothesis that the follicular problem in PCOS is 2-fold, but with the two abnormalities being linked. First, the intra-ovarian hyperandrogenism may promote early follicular growth, leading to a 2-5 mm follicle excess. Second, the ensuing excessive number of selectable follicles would inhibit the selection process, presumably through follicle-follicle interaction involving granulosa cell (GC) products such as the anti-Mullerian hormone (AMH). These factors would induce a reversible refractoriness to the FSH-induced differentiation of GC. This explanation challenges but does not exclude other hypotheses about the follicular arrest, such as the premature LH action on the GC of selectable follicles. Hyperinsulinism or insulin resistance would act as a second hit, worsening the follicular arrest either through amplification of the intra-ovarian hyperandrogenism or through dysregulation of the GC. The loss of cyclic rhythm would prevent the inter-cycle elevation of FSH, thus perpetuating the impairment of the ovulation process. (+info)
Clinical profiles, occurrence, and management of adolescent patients with HAIR-AN syndrome.
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The syndrome of hyperandrogenism, insulin resistance, and acanthosis nigricans (HAIR-AN) is a subphenotype of the polycystic ovary syndrome. It is one of the most common causes of menstrual problems, hyperandrogenic symptoms, and insulin resistance among young women. Review of clinical data in an outpatient adolescent clinic showed that of the 1,002 young women (ages 10-21 years) attending the clinic over a 2-year period, 50 (5%) were diagnosed with HAIR-AN syndrome. Mean age of the patients was 15.5, initial mean weight at diagnosis was 94.5 kg, and the mean BMI was 33.33 kg/m2. Patients were treated with a weight-stabilization and -reduction program, oral contraceptive pills, and in most cases metformin. Of the patients, 80% were compliant with the follow-up and treatment regimen, 60% maintained or reduced their weight, 95% had regular menstrual cycles, and in most patients, the acne and/or hirsutism were the same or better than at the start of treatment. We conclude that HAIR-AN syndrome is a common disease in young women and multifaceted, aggressive treatment appears to be effective in reducing the severity of symptoms and preventing further consequences. (+info)
Glucose and insulin components of the metabolic syndrome are associated with hyperandrogenism in postmenopausal women: the atherosclerosis risk in communities study.
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In 1990-1992, the authors investigated the association of total and free testosterone with the metabolic syndrome in postmenopausal US women not taking hormone replacement therapy (n=362) in a prevalent case-control study of carotid atherosclerosis. Free testosterone was estimated by using the free androgen index (FAI) (total testosterone/sex hormone-binding globulin ratio). The metabolic syndrome was defined as the presence of three or more of the following criteria: waist circumference > or =35 inches (88.9 cm), triglycerides > or =150 mg/dl, high density lipoprotein cholesterol <40 mg/dl, blood pressure >130/80 mmHg, fasting insulin > or =100 pmol/liter, or impaired glucose homeostasis (fasting glucose > or =110 mg/dl or diagnosed diabetes mellitus). FAI, but not total testosterone, was strongly associated with the metabolic syndrome. Compared with women in the lowest FAI quartile, those in the highest quartile had a fivefold greater odds of having the metabolic syndrome (odds ratio=5.38, 95% confidence interval: 2.70, 10.7) after adjustment for age, race, and carotid atherosclerosis status. In multivariate analyses, the three-component metabolic syndrome combinations that contained both hyperinsulinemia and hyperglycemia were most strongly associated with increased FAI (absolute increase=0.41-0.54 compared with that for women who did not have these combinations; all p's < 0.001). Higher FAI was associated with the hyperinsulinemia and hyperglycemia components of the metabolic syndrome. The role of androgens in glucose homeostasis in postmenopausal women requires further study. (+info)
Islets secretory capacity determines glucose homoeostasis in the face of insulin resistance.
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BACKGROUND: Debate surrounds the relative importance of impaired beta-cell secretory function versus insulin resistance in type 2 diabetes. We therefore defined insulin secretion and sensitivity in patients with impaired glucose homoeostasis of varying aetiology and duration. METHODS: 126 consecutive patients undergoing an oral glucose tolerance test (OGTT) between 1999 and 2003 were included. Whole-body insulin sensitivity index (ISI) and insulinogenic index derived from the OGTT were determined in 32 healthy controls, 65 type 2 diabetic patients, 15 patients with acromegaly, 10 patients with insulinoma, and 4 patients with HAIRAN syndrome. RESULTS: Median ISI (quartiles Q25-Q75) of healthy controls and of patients with insulinoma were similar (3.5 [2.8-5.6] and 3.2 [1.7-4.2] respectively) but significantly decreased in patients with acromegaly, type 2 diabetes, and HAIRAN syndrome (2.8 [1.8-3.3], 1.9 [1.4-3], and 0.8 [0.6-1.3] respectively). Despite the decrease in ISI, patients with HAIRAN syndrome and acromegaly maintained normal glucose tolerance by adapting insulin secretion as reflected in the insulinogenic index (106.5 [90.4-127.5] and 49 [24.4-89] in HAIRAN and acromegaly respectively, versus 46.9 [27.3-66.7] in controls). In contrast, type 2 diabetic patients failed to adapt and displayed severely hampered insulin secretion (insulinogenic index of 7.6 [3.8-14.7]). Furthermore, the level of the insulinogenic index correlated significantly with duration of diabetes and HbA1c, which was not the case for the ISI. Insulinoma patients had a decreased insulinogenic index (38.7 [32-83.8]), leading to impaired glucose tolerance despite normal ISI. CONCLUSIONS: The data are compatible with the notion that beta-cell function rather than insulin sensitivity determines the evolution of hyperglycaemia. (+info)
Recurrent severe hyperandrogenism during pregnancy: a case report.
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This report describes the case of a 28 year old woman with virilisation occurring in two successive pregnancies. Recurrent maternal virilisation is rare (seven previous reports) and this case is unique in its severity. Differential diagnoses include ovarian disease and fetal aromatase deficiency. New techniques to exclude a fetal cause were used in this case. This patient presented during the third trimester of her first pregnancy with rapid onset of hirsuitism, increased musculature, and deepening voice. A blood hormone profile revealed significant hyperandrogenism (testosterone, 72.4 nmol/litre; normal range, 0.5-3.0). She delivered a normal boy and maternal androgen concentrations returned rapidly to normal (testosterone, 0.8 nmol/litre). She presented two years later, during her second pregnancy, with similar symptoms and biochemistry (testosterone, 47.5 nmol/litre). Again, she delivered a healthy normal boy and androgens returned immediately to normal (serum testosterone, 2.0 nmol/litre). Ultrasonography revealed no evidence of ovarian (or adrenal) masses in either pregnancy. Umbilical cord venous blood sampling and placental assays revealed no evidence of fetal aromatase deficiency. Recurrent hyperandrogenism during pregnancy is rare. Ovarian luteoma rarely recurs and hyperreactio luteinalis does not lead to such pronounced androgen concentrations. Therefore, this patient has a unique ovarian condition that could be harmful to offspring and mother. (+info)