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

Polycystic ovary syndrome is a disorder of unknown cause characterized by anovulation, hyperandrogenism, and gonadotropin secretory abnormalities producing oligo-ovulation or anovulation. Hyperinsulinemia and insulin resistance are important features of this syndrome. Because other causes of androgen excess may produce similar clinical and biochemical findings, PCO remains a diagnosis of exclusion. Treatment is directed toward relieving symptoms of hyperandrogenemia in order to stimulate ovulation, correcting obesity, and inducing regular menses to reduce the risk of endometrial cancer.
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PMID:Polycystic ovary syndrome. 226 12

Investigation of patients presenting with hirsutism to a gynaecological endocrine clinic revealed a high incidence of anovulation, obesity and elevated androgen levels. The underlying abnormality was polycystic ovarian syndrome (PCOS) in the majority of patients. Low levels of sex hormone binding globulin were common; these increased with oestrogen treatment. Treatment with a combined oral contraceptive pill and low dose spironolactone was often effective in reducing symptoms.
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PMID:Hirsutism in a gynaecological context. 240 Mar 60

We studied a group of obese hyperandrogenic amenorrheic women to determine the effects of weight loss on anthropometry, hormonal status, menstrual cycles, ovulation, and fertility. Fourteen women had polycystic ovaries, two the hyperandrogenism-insulin resistance-acanthosis nigricans syndrome, one hirsutism of adrenal origin, and three idiopathic chronic anovulation. The duration of amenorrhea before the study ranged from 3-17 months [mean, 8.6 +/- 4.5 (+/- SD)]. All women ate a hypocaloric diet for a period of 8.0 +/- 2.4 months. Weight loss ranged from 4.8 to 15.2 kg (mean, 9.7 +/- 3.1 kg; 1.35 +/- 0.56 kg/month) and the waist to hip ratio, which was used as a measurement of body fat distribution, decreased from 0.86 +/- 0.1 to 0.81 +/- 0.06 (P less than 0.0001). The women's mean plasma testosterone and LH concentrations decreased significantly (P less than 0.001 and P less than 0.005, respectively). A significant positive correlation was found between the decreases in plasma testosterone levels and the decreases in glucose-stimulated insulin levels. Moreover, the decreases in the waist to hip ratio correlated positively with the decreases in glucose-stimulated insulin levels and inversely with the decreases in plasma 17 beta-estradiol. No relationships were found between weight loss and the changes in plasma insulin, steroid, and gonadotropin concentrations. The responsiveness to the weight reduction program was evaluated by comparing the number of menstrual cycles during the study period with the number reported before it. Eight women had significantly improved menstrual cyclicity (responders), while 12 did not (nonresponders). The clinical characteristics and hormone values were similar in responder and nonresponder women. In the group as a whole, 33% of the menstrual cycles during the study were ovulatory, and 4 pregnancies occurred. Hirsutism improved significantly in more than half of the women, as did acanthosis nigricans when present. We conclude that weight loss is beneficial in all obese hyperandrogenic women regardless of the presence of polycystic ovaries, the degree of hyperandrogenism, and the degree and distribution of obesity.
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PMID:Clinical and hormonal characteristics of obese amenorrheic hyperandrogenic women before and after weight loss. 264 85

The relationship between sex hormones and the skin is increasingly considered to be very important. The skin has appropriately been called "A peripheral endocrine gland". In this review some aspects of the cutaneous metabolism of oestrogens, progestogens and particularly androgens are analyzed. Production of skin collagen is markedly enhanced by oestrogens. Progestogens with strong androgenic activity and especially androgens have a powerful stimulating action on all skin elements particularly the epidermis and the dermis the sebaceous glands and the hair. The skin manifestations of hyperandrogenism and disturbances of reproductive functions such as anovulation, oligoamenorrhoea and polycystic ovarian disease are usually the consequences of three main aetiopathogenic factors: the first is an abnormality of GnRH pulsatility related to central nervous system dysfunction and seemingly mediated by an increase in beta Endorphin, possibly related to some extent to changes in body weight and hyperinsulinism. The second aetiopathogenic approach is hyperaestronaemia secondary to obesity. Finally adrenal hyperandrogenism caused by different types of congenital adrenal hyperplasia or by increased sensitivity to ACTH may be implicated in these various clinical manifestations.
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PMID:[Sex hormones and the skin]. 269 19

Dysfunctional uterine bleeding is classified by the character of the menstrual cycle: ovulatory or anovulatory. Anovulation can occur at any age and is physiologic in the first year or two after menarche and for several years before menopause. Anovulatory cycles are characteristically irregular and marked by prolonged episodes of bleeding unassociated with signs or symptoms of ovulation. Specific causes of anovulation such as hyperprolactinemia, thyroid disease, androgen excess, anorexia, obesity, and excess exercise can be treated specifically; otherwise, therapy depends upon patient goals. Cycle regulation can be affected by monthly courses of progestin, such as medroxyprogesterone acetate (Provera), 10 mg daily for 10 days each month. Contraception and cycle regulation can both be accomplished with oral contraceptives. Fertility, on the other hand, will require ovulation induction. Ovulatory dysfunctional uterine bleeding most prevalent in parous women between the ages of 20 and 40 is associated with regular cycle intervals and premenstrual molimina. Midcycle and perimenstrual spotting can often be treated with observation only, but depending upon patient and/or physician concerns, periodic hormonal suppression is effective. The management of menorrhagia should include the following: (1) exclusion of pathology in the genital tract; (2) reduction in activity during days of heavy flow; (3) the avoidance of aspirin in the week before and on days of flow; (4) nonsteroidal anti-inflammatory drugs; (5) cycle suppression--oral contraceptives, danazol (Danocrine), depo-progestin; (6) luteal phase progestin; and (7) surgical intervention.
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PMID:Dysfunctional uterine bleeding. 305 63

Induction of ovulation with pulsatile luteinizing hormone-releasing hormone (LH-RH) therapy was attempted in 48 women with polycystic ovary disease (PCOD) and clomiphene citrate (CC) resistant anovulation. Fourteen women ovulated regularly, 23 ovulated variably, but 11 did not ovulate at all. Fifty-two of the 108 cycles of pulsatile LH-RH therapy alone (15 mu gm per pulse, one pulse every 90 minutes) administered through the subcutaneous route were ovulatory. In patients who did not ovulate on subcutaneous LH-RH, treatment with CC (100 mg per day for 5 days) was added to the LH-RH therapy in an additional 33 cycles, of which 21 were ovulatory. In those who did not respond to the combination of treatments, the same dose of LH-RH was administered intravenously: 14 of 29 cycles of intravenous therapy were ovulatory. The overall cumulative conception rate after 6 months of therapy was 60%. When recalculated for ovulatory cycles alone it was 90%, indicating that failure of ovulation was the only cause of the failure of conception. Analysis of the clinical and endocrine findings indicated that failure to ovulate was associated with obesity and hyperandrogenization. Ten of the 23 conceptions ended in miscarriage, 8 within 4 weeks of ovulation. The authors conclude that infertility in patients with PCOD is not optimally corrected by pulsatile LH-RH therapy.
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PMID:Pulsatile luteinizing hormone-releasing hormone therapy in women with polycystic ovary syndrome. 328 91

Repeated ultrasound imaging was performed in 23 cases of polycystic ovary syndrome (PCO). Diagnosis was established on the basis of the clinical picture, the endocrine parameters and on that of ultrasonographic findings. Almost all patients presented with oligomenorrhoea and also hirsutism, and obesity appeared in more than half of the cases. The hormonal picture was characterized by elevated LH and testosterone, by a higher than the upper limit of the normal range of oestradiol and low progesterone levels. In 18 cases, ultrasonography documented enlarged bilateral ovaries containing several small cysts. Repeated examinations proved the permanent absence of follicular maturation and ovulation. In additional five patients, the size of ovaries was slightly larger than normal with no microcystic change being present. According to the authors, ultrasonography is particularly useful in the noninvasive diagnostics of PCO syndrome, in judging better the borderline cases and in adjusting the ovulation induction therapy. If a combined chemotherapy administered in a gradually increasing dose keeps on being ineffective in eliminating chronic anovulation, the only possible procedure is surgical solution, that is bilateral wedge resection of the ovaries.
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PMID:The role of ultrasonography in treating polycystic ovary syndrome. 329 36

We have reviewed the role of insulin in ovarian physiology. Clinical observations and experimental data strongly support the hypothesis that insulin possesses gonadotropic activity, when acting alone or with FSH or LH. This idea is further supported by the recent discovery of insulin in follicular fluid. The idea that insulin has gonadotropic function can explain a variety of clinical observations, which otherwise are difficult to understand. For example, manifestations of ovarian hypofunction (primary amenorrhea, late menarche, anovulation, low pregnancy rate, and early menopause) in IDDM can be understood if it is accepted that insulin is necessary for the ovary to reach its full steroidogenic potential. The idea that insulin affects ovarian steroidogenesis also helps to understand the observation that hyperandrogenism frequently accompanies each of the various insulin-resistant states, regardless of the latter's etiology (e.g. genetic deficiency in the number of insulin receptors, antiinsulin receptor antibodies, obesity, etc.). The explanation for this association is based on the idea that hyperinsulinemia intensifies ovarian steroidogenesis, which manifests clinically as hyperandrogenism. Continuous stimulation of the ovary by insulin over a long period of time possibly produces morphological ovarian changes, such as hyperthecosis or polycystic changes; these changes commonly are observed among women with insulin resistance. The effects of insulin on ovarian cells are mediated possibly through binding of the peptide to its own receptor or to the IGF-1 receptor (the specificity spillover phenomenon). The latter could be an important mechanism in cases of insulin resistance. Potential mechanisms underlying the gonadotropic activity of insulin include direct effects on steroidogenic enzymes, modulation of FSH or LH receptor number, synergism with FSH or LH, or nonspecific enhancement of cell viability. The gonadotropic function of insulin adds yet another note to what has been termed a symphony of insulin action. Further investigation into this new area may yield greater insights not only into normal ovarian physiology, but also into the pathogeneses of such diverse entities as PCO, obesity, diabetes mellitus, and the syndromes of insulin resistance and acanthosis nigricans.
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PMID:The gonadotropic function of insulin. 330 17

This article reviews current knowledge of the effect of obesity on ovulation and reproductive potential. Although only a minority of obese women are affected, it seems certain that there is a link between obesity and anovulation. This interrelationship is suggested by the apparent effectiveness of weight reduction in suppressing the hyperandrogenemia observed with obesity and restoring ovulation. The increased aromatase activity and hyperinsulinemia observed in obese women is believed to play a major role in causing the hyperandrogenemia, either by stimulating luteinizing hormone secretion or directly stimulating the ovary. In addition to ovarian hyperandrogenemia, pituitary hypothalamic dysfunction has been observed in response to obesity. Inadequate central serotonin stimulation, excessive dopamine stimulation, and insensitivity to endorphins may all be involved in the pituitary hypothalamic dysfunction, as well as resistance to weight reduction. Few data are available on the efficacy of weight loss in restoring ovulatory function in obese women; nonetheless, weight reduction should be regarded as a central component of any attempt to induce ovulation. In terms of fertility, even a short-term weight loss can be beneficial. Ileal jejunal bypass surgery to effect weight reduction appears to place a fetus at risk; thus, avoidance of pregnancy for at least 2 years after such surgery is advised.
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PMID:Obesity and its effect on reproductive function. 390 6

Polycystic ovarian disease represents a poorly defined spectrum of clinical disorders having oligo-ovulation or anovulation as a common feature. There is no single, universally accepted biochemical or clinical definition. Clinical findings usually include anovulation resulting in irregular uterine bleeding and infertility, androgen excess resulting in hirsutism and acne, and obesity. The patho-physiology involves altered functions of the hypothalamus, pituitary, ovary and adrenal glands, resulting in failure of folliculogenesis to regularly proceed to ovulation. The cause of the initiating event in this disease process remains enigmatic. Therapy for the various abnormalities in polycystic ovarian disease is tailored to a patient's needs and may include preventing endometrial hyperplasia, controlling irregular uterine bleeding, controlling hirsutism and inducing ovulation.
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PMID:Polycystic ovarian disease. 392 38


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