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PubMed1994

Relationship between insulin sensitivity and circulating sex hormone-binding globulin levels in hyperandrogenic obese women.

The aim of this work was to examine the effect of an insulin infusion on SHBG levels as well as the relationship between SHBG levels and insulin sensitivity. Acute insulin infusion was used with the insulin-glucose clamp technique. The subjects were 14 consecutive well-characterized hyperandrogenic non-diabetic obese women without biological and echographic symptoms of polycystic ovary syndrome. Adiposity and fat distribution were assessed respectively by the body mass index (BMI: 38.7 +/- 1.6 kg/m2) and by the waist hip ratio (WHR: 0.91 +/- 0.01). Hyperandrogenism was evidenced by hirsutism and serum testosterone greater than 2.8 nM. Circulating SHBG levels were determined in the fasting state by RIA. Insulin sensitivity was assessed using the euglycemic hyperinsulinemic glucose clamp technique with three incremental doses of insulin. Seven non-obese non-hyperandrogenic subjects (BMI: 21.0 +/- 0.6 kg/m2) served as controls for the study of the insulin resistance state. Because of supraphysiological insulin infusion rates (40, 100, and 350 mU/min.m2, each dose for 2 h), insulin sensitivity was mainly studied at peripheral level. We calculated the Km, i.e. the ED50 of the dose-response curve, the glucose disposal rate, and the maximal glucose disposal rate per U insulin (M/I). The hyperandrogenic obese subjects exhibited marked insulin resistance. SHBG levels, although already in the lower half of normal in the basal state, decreased from 34.8 +/- 3.4 nmol/l to 29.7 +/- 3.3 nmol/l (P = 0.001; normal values are 18-83 nmol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[Diagnostic strategy in infertility due to hyperandrogenism. Development of a decision tree].

The detection of clinical hyperandrogenism in women presenting with infertility requires detailed hormonal investigations using the decisional plan suggested here. Initial studies including measurement of plasma androgen, gonadotrophic hormones and prolactin levels, may be sufficient to reveal an adrenal origin or pure ovarian origin. Non-tumor androgenic hypercorticism is seen classically in late-presenting enzyme deficits, but also in other situations: excessive adrenarche, hyperprolactinemia, obesity, chronic stress. The immediate Synacthene test can then eliminate diagnostic uncertainties if it leads to the discovery of appearances of 21- or 11-hydroxylase or 3 beta-ol dehydrogenase blocks. Intense virilisation in a woman with a testosterone level above 2 ng/ml (7 nM/l) should lead to suspicion of an androgen-secreting tumor of the ovary or adrenal. CT scan of the abdomen and true pelvis is essential here since it may reveal the presence of an adrenal or ovarian mass. If no morphological abnormality is shown by this investigation, an endocrine lesion of a small ovary should be strongly suspected, the demonstration of which requires isotope techniques and/or catheterisation of the ovarian veins. Two situations also exist which are responsible for severe hyperandrogenism but less alarming in terms of their course and significance: certain homozygous forms of 21-hydroxylase deficit diagnosed late and ovarian hyperthecosis. It may happen that these hormonal investigations do not suffice alone to determine the precise origin of hyperandrogenism and its cause. The dexamethasone adrenal suppression test is useful in the diagnosis of type II micropolycystic dystrophy, in order to define the essentially ovarian, adrenal or mixed origin of hyperandrogenism.

Adrenal Hyperplasia, Congenital↗
PubMed1994

[Treatment of female infertility due to hyperandrogenism].

This study reviews the various types of treatment used in infertility due to hyperandrogenism, with the aim of answering the following three questions: How should these drugs be prescribed? What are their side-effects? What are the best diagnostic indications? Possibilities include ovulation inducers but also all types of treatment capable of improving the fertility of these women. The treatment of infertility due to adrenal hyperandrogenism is based upon glucocorticoids. This treatment must be continued for 3 months after conception, to attempt to avoid early spontaneous abortion. The first-line inducer in ovarian hyperandrogenism is clomiphene citrate. The good results obtained using the combination of dexamethasone and clomiphene citrate are explained by an adrenal participation in this type of hyperandrogenism. In case of failure, and in addition to classical menotrophins:--pre-treatment using LHRH agonists avoids the onset of premature luteinisation but does not prevent the possibility of multiple pregnancies;--use of purified FSH reduces, though not sufficiently, the risks of multifollicular maturation but does not greatly increase the overall pregnancy rate;--the "slow" protocol with purified FSH reduces the incidence of multifollicular maturation. Should this fail, prior treatment with an LHRH agonist and if not the pulsed administration of LHRH in non-obese women can be suggested. Surgical treatment provides useful results in severe forms of sterility due to polycystic ovaries syndrome, with new per-celioscopic techniques.

Clinical Protocols↗
PubMed1994

Hyperandrogenism, insulin resistance and acanthosis nigricans. 10 years of progress.

Polycystic ovary disease is a heterogeneous endocrinopathy with many interacting causal factors. One potential such factor is chronic hyperinsulinemia. Multiple, independent lines of evidence support the contention that chronic hyperinsulinemia causes ovarian hyperandrogenism. This evidence includes: (1) mutations in the insulin receptor gene that cause severe hyperinsulinemia appear to be associated with ovarian hyperandrogenism, (2) insulin stimulates ovarian thecal and stromal androgen secretion in vitro, and (3) in some experimental models, manipulation of circulating insulin concentrations results in changes in circulating androgens. Although the association between hyperinsulinemia and hyperandrogenism remains to be fully explained at the molecular level, chronic hyperinsulinemia appears to be an important cause of hyperandrogenism.

Acanthosis Nigricans↗
PubMed1997

[Biochemical markers and methods to assess insulin resistance in normal, obese and hyperandrogenic women].

BACKGROUND: Euglycemic or hyperglycemic clamp and the frequently sampled i.v. glucose tolerance test are the most frequently used methods to assess insulin resistance. However, both are expensive and cumbersome. AIM: To evaluate the relative or discriminatory usefulness of sex hormone binding globulin (SHBG), dehydroepiandrosterone sulphate (DHEAS) and insulin like growth factor binding protein 1 (IGFBP-1) as markers of insulin resistance and to estimate the tissue sensitivity to insulin by means of the insulin tolerance test (ITT) and the frequently sampled i.v. glucose tolerance test (IVGTT) in normal, obese and hyperandrogenic women. SUBJECTS AND METHODS: Six normal, 6 obese and 12 hyperandrogenic women of similar ages, were studied. In two consecutive days, the ITT and the IVGTT were performed and a basal blood sample was obtained to measure SHBG, DHEAS and IGFBP-1. Insulin sensitivity was calculated as the blood glucose slope in the ITT and with the minimal model of Bergman in the IVGTT. RESULTS: Insulin sensitivity, measured with ITT was 0.58 (0.53-0.63) in normal, 0.38 (0.05-0.59) in obese and 0.20 (0.0-0.36) in hyperandrogenic women. The figures for the IVGTT were 7.97 (4.1-15.4), 2.41 (0.81-4.89) and 1.1 (0.46-1.88), respectively. Both methods had a positive correlation coefficient of 0.792 (p < 0.001). SHBG was 87.0 m 37.9 and 18.3 nmol/l in normal, obese and hyperandrogenic women, respectively (p < 0.09). IGFBP-1 values were 3.0, 2.1 and 1.6 ng/ml respectively (p < 0.05). DHEAS values were 132, 190 and 206 ug/dl, respectively (ND). CONCLUSIONS: ITT is a simple and reliable method to assess insulin sensitivity. SHBG discriminates subjects with different levels of insulin sensitivity. Since it is easy to measure, it could be used as a marker on insulin sensitivity.

Adult↗
PubMed1997

[Effects of metformin on insulin resistance in obese and hyperandrogenic women].

BACKGROUND: Metformin is a biguanide often used in obese diabetics that improves tissue sensitivity to insulin. AIM: To assess the effects of metformin on tissue insulin sensitivity in obese and hyperandrogenic women. PATIENTS AND METHODS: Eight obese and eight obese and hyperandrogenic women received metformin 850 mg orally during 12 weeks. Before and at the end of the treatment period, an insulin tolerance test to measure insulin sensitivity was performed and blood was drawn to measure sex hormone binding globulin (SHBG), dehydroepiandrosterone sulphate (DHEAS), testosterone, triglycerides, total and HDL cholesterol. The free androgen index was calculated for each sample. RESULTS: After metformin treatment, the insulin sensitivity index improved from 0.38 (0.05-0.5) to 0.43 (0.25-0.59) in obese women and from 0.2 (0-0.36) to 0.3 (0.06-0.4) in obese and hyperandrogenic women. SHBG increased and total cholesterol and triglycerides decreased significantly in both groups. No other significant changes were observed. CONCLUSIONS: Metformin has a favorable effect on tissue sensitivity to insulin, SHBG and serum lipids in obese and hyperandrogenic women.

Adult↗
PubMed1998

[Influence of weight and distribution of adipose tissue in functional hyperandrogenism].

Approximately half the women with the polycystic ovary syndrome (PCOS) are obese or overweight. Obesity and body fat distribution have independent roles in the development of hyperandrogenism in PCOS. Most obese and normal weight PCOS are insulin resistant and hyperinsulinemic. Moreover, a significant positive correlation exists between the degree of hyperandrogenism and that of hyperinsulinism. The pathogenetic role of obesity may involve different mechanisms, the major one being the hyperinsulemic state, since insulin is capable of stimulating ovarian androgen secretion and controlling androgen metabolism and transport in peripheral tissues. Abdominal body fat distribution in obese women with PCOS amplifies the degree of hyperandrogenism and related clinical symptoms and signs. Both loss of body weight and/or the reduction of the degree of hyperinsuliemia, induced by diet or insulin-sensitizing drugs, have important effects, since they reduce blood androgen levels and can improve ovulation and clinical signs of hyperandrogenism.

Adipose Tissue↗
PubMed1991

Late-onset congenital adrenal hyperplasia in a group of hyperandrogenic women.

The aim of this study was to determine the prevalence of late-onset congenital adrenal hyperplasia (LOCAH) in a group of hyperandrogenic women presenting with menstrual disturbances and/or infertility. Thirty-five women were evaluated by basal hormonal profiles and underwent ACTH stimulation testing. In this study, 17.1% of women showed evidence of partial 21-OH deficiency (21-OHD), and 5.7% 3 beta-HSD deficiency. Neither basal hormonal levels nor clinical characteristics distinguished women with LOCAH from other hyperandrogenic women. And although the mean basal 17-OH progesterone (17-OHP) level in women with 21-OHD (152 +/- 66 ng/dl) was significantly higher than levels in other hirsute women, 4 of 6 (67%) women with 21-OHD had normal 17-OHP levels. Thus, to identify all affected individuals with partial 21-OHD, our data suggest that hyperandrogenic women with basal unsuppressed 17-OHP levels greater than 100 ng/dl should undergo dynamic testing. With regard to partial 3 beta-HSD deficiency, basal DHEA-S levels greater than the 95th percentile of other hirsute women may be used to screen for this deficiency. In conclusion, LOCAH due to partial steroid enzyme deficiencies are a frequent occurrence in women who present with symptoms of hyperandrogenism and ACTH stimulation remains an important tool in making the diagnosis of enzyme deficiencies.

Adrenal Hyperplasia, Congenital↗
PubMed1978

Adrenal hyperandrogenism: detection by adrenal scintigraphy.

Hyperandrogenism is a common endocrinopathy in women. Localization of the source of excess androgen production is mandatory for proper management. Ovarian hyperandrogenism has been implicated in the majority of patients studied, though the true prevalence of adrenal hyperandrogenism is not yet known. Adrenal scintigraphy is a simple non-invasive technique which detects adrenal functional abnormalities. The detection of adrenal hyperandrogenism by adrenal scintigraphy in three women with mild hirsutism is discussed.

Adenoma↗
PubMed1984

Evolution of the hyperandrogenism-polycystic ovary syndrome from isosexual precocious puberty: report of two cases.

Two girls who presented initially with isosexual precocity later developed the hyperandrogenism-polycystic ovary syndrome. We propose that the pathogenesis of the hyperandrogenism-polycystic ovary syndrome in these two children is related to an abnormal release of hypothalamic gonadotropin-releasing hormone, a subsequent sustained secretion of luteinizing hormone, and a consequent excessive secretion of ovarian androgens that results in hyperandrogenism. The clinical findings in these patients suggest that the dysfunction of the hypothalamic-pituitary regulation of luteinizing hormone secretion that leads to the hyperandrogenism-polycystic ovary syndrome may occur prior to puberty.

Adolescent↗
PubMed1990

Endocrine and behavioral responses to psychological stress in hyperandrogenic women.

Stress has been implicated in the physiopathology of the ovarian androgenic syndrome. To explore further this notion, we compared the behavioral and endocrine responses to a mental stressor between women with hyperandrogenism (n = 13) and normals (n = 11). The standardized psychological stimulus produced higher levels of anxiety in the hyperandrogenic group than in controls. The endocrine (cortisol, prolactin, growth hormone, beta-endorphin) responses poststressor were definitely dissociated. Both groups showed a comparable anticipatory stress cortisol-secretion response. The cortisol release was greater following the mental stressor in the hyperandrogenic group than in the normals. Thus, hyperandrogenic women appear to have an abnormally affected pituitary-adrenal activation, which may play a role in the pituitary-ovarian disruption characteristic of the ovarian androgenic syndrome.

Adult↗
PubMed1998

Role of the ovary in the adrenal androgen excess of hyperandrogenic women.

OBJECTIVE: To test the hypothesis that ovarian hormones in women with hyperandrogenism alter adrenocortical steroidogenesis. DESIGN: Combination of two prospective studies. SETTING: Academic medical centers. PATIENT(S): Eighteen hyperandrogenic patients demonstrating hirsutism with either hyperandrogenemia, oligomenorrhea, or both. Eighteen healthy nonhirsute eumenorrheic untreated women served as controls. INTERVENTIONS: Blood sampling basally and after acute adrenal stimulation with ACTH, before and after 20-24 weeks of leuprolide administration. Nine patients also received 0.625 mg/d of oral conjugated esterified estrogens and 10 mg of medroxyprogesterone acetate days 1-12 of the month (i.e., estrogen replacement therapy [ERT]), whereas the remaining nine did not. MAIN OUTCOME MEASURE(S): Before and after the administration of the GnRH agonist (GnRH-a), the basal concentrations of DHEAS; and the levels of androstenedione (A4), DHEA, androstenediol, 11 beta-hydroxyandrostenedione (11-OHA4), and cortisol before and 60 minutes after acute adrenal stimulation, were measured. RESULT(S): Levels of DHEAS, androstenediol, and 11-OHA4 decreased by 15%-30%, regardless of whether patients initially had or did not have DHEAS excess. However, only hyperandrogenic patients with elevated levels of DHEAS showed a significant decrease in basal DHEA levels. No statistically significant difference in the response of either androgen to ACTH (1-24) stimulation was noted with ovarian suppression, regardless of initial DHEAS level or use of ERT. CONCLUSION(S): We found no evidence that ovarian hormone secretion affected adrenal steroidogenesis, and those women with the highest adrenal androgen levels had the least response to GnRH-a suppression. These findings further support the concept of an intrinsic, and possibly primary, abnormality of adrenocortical steroidogenesis in a subset of hyperandrogenic women that is independent of ovarian abnormalities.

Adolescent↗
PubMed1990

Hyperandrogenism in peripubertal girls.

Androgens arise from either adrenal or ovarian secretion or by peripheral conversion of secreted precursors. The adrenals and ovaries normally contribute about equally to testosterone and AD production. DHAS is the major adrenal 17-KS. Testosterone is the major circulating form of androgen. More than 96% of plasma testosterone is bound to SHBG; the free testosterone seems to be the bioavailable fraction. Hyperandrogenism must be considered in any girl with premature or excessive development of public hair or acne, menstrual irregularity (whether it be oligo-amenorrhea or dysfunctional uterine bleeding), or obesity. The most common cause of premature public hair development (pubarche) is premature adrenarche. The most common cause of hyperandrogenism presenting in a teenage girl is polycystic ovary syndrome. However, the differential diagnosis includes "exaggerated adrenarche," late-onset congenital adrenal hyperplasia, virilizing tumors, Cushing's syndrome, hyperprolactinemia, acromegaly, and abnormalities of androgen action or of metabolism. The plasma free testosterone is a more sensitive indicator of hyperandrogenism than is the total testosterone concentration. The pattern of response of plasma free testosterone, DHAS, and cortisol to dex-suppression testing is diagnostic of the source of androgen excess. Most hyperandrogenic adolescents will be found to have PCOS. The treatment is chosen according to particular symptoms, such as menstrual irregularity, hirsutism, or obesity.

Adolescent↗
PubMed1990

Glucocorticoid therapy in hyperandrogenism.

Hyperandrogenism is a common disorder in the reproductive age female. It is associated with cutaneous manifestations and ovulatory dysfunction. The degree of hyperandrogenaemia is directly related to the severity of ovulatory dysfunction. The ovulatory dysfunction frequently leads to infertility. The most common form of hyperandrogenism is idiopathic glucocorticoid-suppressible hyperandrogenism (IGSH). The management of this disorder involves appropriate use of physiological doses of glucocorticoids. This treatment leads not only to normalization of serum androgen levels but also to amelioration of cutaneous symptoms and improvement in ovulatory function. In infertile women with ovulatory dysfunction secondary to IGSH, occurrence of pregnancy after treatment with glucocorticoids is directly related to the degree of the suppression of serum androgen levels. In other words, this treatment does not 'induce ovulation', but its effectiveness in improving ovulatory function is a result of a correction of the hyperandrogenic state. At physiological doses glucocorticoid therapy does not appear to be associated with significant side-effects. With appropriate management, androgen levels can be maintained within the normal range indefinitely. Furthermore, in a majority of patients, androgen levels remain within the normal range for a long time (years) after discontinuation of chronic glucocorticoid therapy.

Androgens↗
PubMed1983

Investigative strategy of hyperandrogenism in women.

Investigative procedures in the assessment of female hyperandrogenism are reviewed. Based on their experience, the authors suggest an inexpensive investigative strategy in hyperandrogenic females consisting of the following: the first step depends upon the clinical symptoms--in cases of hirsutism with regular menstrual cycles, plasma testosterone (T) and plasma dehydroepiandrosterone sulfate (DHA-S) are assayed, and the basal body temperature chart is recorded. In cases of hirsutism with irregular or anovulatory menstrual cycles, in addition to T and DHA-S, plasma 17-hydroxyprogesterone and urinary-free cortisol are assayed. In case of anovulation without hirsutism, T and DHA-S are assayed, and the LHRH test is performed. The results of this first investigation allow to attribute to the woman one of the six following hormone profiles: (1) metabolic hyperadrenalism; (2) tumoral hyperandrogenism; (3) 21-hydroxylase defect; (4) nontumoral DHA-S increase; (5) nontumoral ovarian hyperandrogenism; (6) idiopathic hirsutism. The additional investigative procedures required in each of these groups are detailed.

Adrenal Hyperplasia, Congenital↗
PubMed2005

Phenotypic variation in hyperandrogenic women influences the findings of abnormal metabolic and cardiovascular risk parameters.

In hyperandrogenic women, several phenotypes may be observed. This includes women with classic polycystic ovary syndrome (C-PCOS), those with ovulatory (OV) PCOS, and women with idiopathic hyperandrogenism (IHA), which occurs in women with normal ovaries. Where other causes have been excluded, we categorized 290 hyperandrogenic women who were seen consecutively for this complaint between 1993 and 2004 into these three subgroups. The aim was to compare the prevalence of obesity, insulin resistance, and dyslipidemia as well as increases in C-reactive protein and homocysteine in these different phenotypes with age-matched ovulatory controls of normal weight (n = 85) and others matched for body mass index (BMI) with women with C-PCOS (n = 42). Although BMI affected fasting serum insulin and the Quantitative Insulin-Sensitivity Check Index, these markers of insulin resistance were greatest in C-PCOS (n = 204), followed by OV-PCOS (n = 50) and then IHA (n = 33). Androgen levels were similar in OV-PCOS and IHA but were higher in C-PCOS, whereas gonadotropins were similar in all groups. Lipid abnormalities were highest in C-PCOS and OV-PCOS and were normal in IHA. C-reactive protein was elevated in C-PCOS and OV-PCOS but not IHA. Homocysteine was elevated only in C-PCOS. Overall, the prevalence of obesity (BMI > 30) was 29% in C-PCOS, 8% in OV-PCOS, and 15% in IHA and insulin resistance (Quantitative Insulin-Sensitivity Check Index < 0.33) was 68% in C-PCOS, 36% in OV-PCOS, and 26% in IHA. The prevalence of having at least one elevated cardiovascular risk marker was 45% in C-PCOS 38% in OV-PCOS and was not increased on IHA (6%). These results suggest that among hyperandrogenic women the prevalence of abnormal metabolic and cardiovascular risk parameters is greatest in C-PCOS, followed by OV-PCOS and then women with IHA. Moreover, in that in OV-PCOS and IHA, ages and weights were similar yet the prevalence of metabolic and cardiovascular risk was greater in OV-PCOS, the finding of polycystic ovaries may be a significant modifying factor.

Body Mass Index↗
PubMed1987

The effects of hyperinsulinemia on serum testosterone, progesterone, dehydroepiandrosterone sulfate, and cortisol levels in normal women and in a woman with hyperandrogenism, insulin resistance, and acanthosis nigricans.

Insulin may mediate the hyperandrogenism that frequently occurs in patients with insulin-resistant states. To test this hypothesis, we studied five normal women and one woman with hyperandrogenism, insulin resistance, and acanthosis nigricans with the hyperinsulinemic-euglycemic clamp technique. Each woman received a 0.1 U/kg insulin bolus dose, followed by a 10 mU/kg X min insulin infusion for 12-16 h. In the normal women, an average insulin level of 1832 +/- 292 (+/- SEM) microU/ml was achieved; serum glucose was clamped at 116 +/- 5 mg/dl. At this level, insulin may bind to the insulin-like growth factor I receptor as well as to its own receptor. Contrary to our working hypothesis, a rise in serum testosterone did not occur in any women during insulin infusion, and in one women, serum testosterone levels decreased. When analyzed as a percentage of the basal value, serum progesterone levels fell 20% in the normal women within the first 2 h of insulin infusion, but did not change thereafter. Dehydroepiandrosterone sulfate (DHEA-S) levels, however, uniformly and progressively decreased by 39% after 12 h of insulin infusion in the normal women and by 31% at 14 h in the woman with hyperandrogenism, insulin resistance, and acanthosis nigricans. The fall in serum DHEA-S levels was not due to diurnal rhythmicity, as the changes in serum DHEA-S levels did not correlated with those in serum cortisol. Suppression of PRL release also was excluded as a cause of the fall in DHEA-S levels. These results indicate that acute hyperinsulinemia of 12- to 16-h duration does not increase serum testosterone or DHEA-S concentrations and, indeed, can cause a decline in serum DHEA-S levels in both normal women and the single woman studied with hyperandrogenism, insulin resistance, and acanthosis nigricans.

Acanthosis Nigricans↗
PubMed1989

Clinical and hormonal characteristics of obese amenorrheic hyperandrogenic women before and after weight loss.

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.

Adult↗