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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 37 year-old female with Kallmann syndrome and NIDDM who had two successful deliveries is reported. She had experienced no menstruation until she had treatment with gestagen in her early twenties. She had withdrawal bleeding only once. At the age of 25, she consulted her family doctor, complaining of amenorrhea. Estrogen progesterone cyclic therapy caused withdrawal bleeding, and clomiphene citrate failed to induce apparent ovulation. In January 1978, 150 IU of hMG was administered daily for 9 days, and then 3000 IU of hCG daily for the following 2 days. This therapy induced pregnancy, which failed spontaneously on June 4th. A year later, in January 1979, 150 IU of hMG was again administered daily for 7 days followed by 6000 IU of hCG for 3 days. This therapy again induced pregnancy. On September 27th, 1979, she delivered a girl vaginally, weighing 3830 g. After this delivery, she experienced no menstruation. In June 1985, she consulted her family doctor again, and she was diagnosed as being pregnant. Since her fasting blood glucose was 145 mg/dl, she was admitted to Kosei Hospital to control her blood glucose. On October 15th, she delivered a girl weighing 2600 g. On June 13th, 1989, she was referred to Kosei Hospital by her family doctor to achieve an accurate control of her blood glucose. During this admission, she was diagnosed as having Kallmann syndrome because of congenital anosmia and hypogonadotropic hypogonadism without any abnormal morphological changes. Vitamin B1 infusion test was negative.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of two successful deliveries by a woman with Kallmann syndrome and NIDDM]. 190 34

In order to determine their contraceptive practice, 209 diabetic women, aged 16-50 years, regularly attending the diabetic clinic of a University Hospital in Paris, France, were interviewed. 134 (64%) were current-users of contraception. Contraceptive use was significantly lower among patients with NIDDM compared to patients with IDDM (46% vs 70%, p less than 0.01). Methods used were: intra-uterine devices (IUD) (32% of users), hormonal compounds (27%, almost exclusively low-dose progestogen only pill), occlusive and natural methods (27%), and tubal ligation (14%). The major gynaecological side-effects were associated with the use of low-dose progestogens (39% with amenorrhoea vs 14% for other methods, p less than 0.01). A subsample (n = 165, age-range 20-44 years) of this diabetic population was compared with a representative sample of 8,899 French women of the same age. The proportion of current-users of contraception in this diabetic population was lower than in the French population (63.5% vs 72.2%, p less than 0.02). The diabetic patients tended to use more efficient methods of contraception (pill, IUD and tubal ligation), but 11% of them used no contraception without a stated reason, compared to 4% of the French population. It is suggested that contraceptive guidance should be reinforced in diabetic women, particularly with NIDDM, in order to promote family planning, since tight glycaemic control before and during pregnancy is now recommended.
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PMID:Contraceptive practice in 209 diabetic women regularly attending a specialized diabetes clinic. 367 64

Hyperandrogenism is characterized clinically by hirsutism, acne, androgens-dependent alopecia and elevated serum concentrations of androgens (testosterone and androstenedione). Polycystic ovary syndrome is the most frequent cause of hyperandrogenism. Nevertheless, the differential diagnosis includes androgen-secreting tumors of the ovary or adrenal gland. Although rare, it is important to consider this diagnosis in patients with serum testosterone concentrations greater than 7 nmol/l. A 35-year-old woman who presented with hirsutism, amenorrhea and acanthosis nigricans is described. The endocrine abnormalities included a serum testosterone concentration of 9 nmol/l and overt type II diabetes mellitus. Imaging studies, including magnetic resonance imaging and Doppler ultrasonography, did not disclose a secreting tumor. After cyproterone acetate was prescribed the serum testosterone concentration returned to normal. The recent application of modern, high-resolution diagnostic ultrasonography and magnetic resonance imaging enabled a morphologically based diagnosis in a case of severe hyperandrogenism, with no need for invasive procedures. The therapeutic response to antiandrogens is reassuring.
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PMID:A case of severe hyperandrogenism, acanthosis nigricans and over diabetes: the use of non-invasive methods for diagnosis, pathogenesis and management. 891 63

Polycystic ovary syndrome is a diagnosis made in 5%-10% of women between late adolescence and the menopause. Patients may present with oligomenorrhoea or amenorrhoea, anovulation or infertility, hirsutism or acne. Women with the syndrome have at least seven times the risk of myocardial infarction and ischaemic heart disease of other women, and by the age of 40 years up to 40% will have type 2 diabetes or impaired glucose tolerance. Polycystic ovary syndrome is associated with insulin resistance, with consequent hyperinsulinaemia and (frequently) hyperlipidaemia and obesity. Recent research has shown that the application of diabetes management techniques aimed at reducing insulin resistance and hyperinsulinaemia (such as weight reduction and the administration of oral hypoglycaemic agents) can not only reverse testosterone and luteinising hormone abnormalities and infertility, but can also improve glucose, insulin and lipid profiles. The management of polycystic ovary syndrome should now include patient education and attention to diabetes and cardiovascular risk factors such as hyperlipidaemia, obesity, physical exercise, glucose intolerance, hypertension and cigarette smoking.
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PMID:Polycystic ovary syndrome: a new direction in treatment. 986 12

In humans, the skin is a target tissue for androgen action; hair growth and sebum secretion are under active androgen control. An increased production or metabolism of testosterone, the main active androgen, shows up clinically in dermatological symptoms such as hirsutism, hyperseborrheic acne and alopecia. Polycystic ovary syndrome (PCOS) is the most frequent androgen disorder of ovarian function. PCOS patients have amenorrhea or severe oligomenorrhea, increased testosterone levels and most often enlarged polycystic ovaries on ultrasound examination. In addition, many PCOS patients have a tendency to accumulate abdominal fat and/or to develop obesity. Some also display a particular metabolic pattern including an atherogenic lipid profile, glucose intolerance and an increased fasting insulin level, which is known to be closely linked with an insulin resistant state. Several studies have now reported that PCOS patients show increased incidence of type 2 diabetes and cardiovascular disease. In addition to being a target for androgens the skin has abundant insulin receptors on the keratinocyte surface membrane and acanthosis nigricans is a common symptom of severe insulin resistance among patients with insulin receptor disorders. However, acanthosis nigricans could also be present in PCOS women given evidence of the intensity of their insulin resistance. This presentation will review the mutual relationship between hyperandrogenia and insulin resistance, with particular attention paid to: (1) insulin secretion and insulin sensitivity in PCOS; (2) the complexity of the molecular mechanisms involved in insulin resistance; (3) the paradoxical relationship between insulin resistance and hyperandrogenia; (4) the current genetic studies; and (5) new avenues for long-term treatment of PCOS women.
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PMID:Association of insulin resistance with hyperandrogenia in women. 1159 27

Clinical characteristics of PCOS Syndrome Two fundamental characteristics: hyperandrogenism and anovulation which lead to hirsutism and oligo-or amenorrhea. Other features include obesity, acanthosis nigricans, and metabolic disruption (insulin resistance with hyperinsulinemia, glucose intolerance, or type II diabetes mellitus). Complementary tests Serum testosterone and DHEA-S levels: to exclude androgen-producing tumors. Serum 17-hydroxyprogesterone level: to exclude congenital adrenal hyperplasia, 21-hydroxylase deficiency. Ultrasound: increased size of the ovaries and central stroma with presence of peripheral follicular cysts (8-10) measuring about 8 mm in diameter. Pathophysiology Therapeutic approaches Therapeutic approaches
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PMID:[Polycystic ovaries in 2001: physiology and treatment]. 1198 85

The classic polycystic ovarian syndrome (PCOS) was originally described by Stein and Leventhal as the association of amenorrhea with polycystic ovaries and, variably, hirsutism and/or obesity. It is estimated that 5 to 10% of women of reproductive age have PCOS. Although insulin resistance is not part of the diagnostic criteria for PCOS, its importance in the pathogenesis of PCOS can not be denied. PCOS is associated with insulin resistance, independent of total or fat-free body mass. Postreceptor defects in the action of insulin have been described in PCOS that are similar to those found in obesity and type 2 diabetes. Treatment with insulin sensitizers, metformin, and thiazolidinediones (TZDs) improve both metabolic and hormonal patterns and also improve ovulation in PCOS. Recent studies have shown that women who have PCOS have higher circulating levels of inflammatory mediators such as C-reactive protein, tumor necrosis factor, tissue plasminogen activator, and plasminogen activator inhibitor-1 (PAI-1). It is possible that the beneficial effect of insulin sensitizers in PCOS may be partly due to a decrease in inflammation.
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PMID:Insulin resistance in polycystic ovarian disease. 1621 83

Polycystic ovary syndrome (PCOS) is a common heterogenous endocrine disorder associated with amenorrhoea (or oligomenorrhoea), hyperandrogenism, hirsutism, obesity, insulin resistance, and an approximately 7-fold increased risk of type 2 diabetes mellitus (NIDDM - non-insulin dependent diabetes mellitus). It is a leading cause of female infertility. The prevalence of PCOS among reproductive-age women has been estimated at 4%-12%. Familial aggregation of this syndrome is well established. There are also ethnic and racial variations in the prevalence of the syndrome and its symptoms. Multiple biochemical pathways have been implicated in the pathogenesis of PCOS. Several genes from these pathways have been tested include genes involved in steroid hormone biosynthesis and metabolism (StAR, CYP11, CYP17, CYP19 HSD17B1-3, HSD3B1-2), gonadotropin and gonadal hormones action (ACTR1, ACTR2A-B, FS, INHA, INHBA-B, INHC, SHBG, LHCGR, FSHR, MADH4, AR), obesity and energy regulation (MC4R, OB, OBR, POMC, UCP2-3), insulin secretion and action (IGF1, IGF1R, IGFBPI1-3, INS VNTR, IR, INSL, IRS1-2, PPARG) and many others. Most women with PCOS, both obese and lean, have a degree of insulin resistance. The minisatellite of insulin gene (INS VNTR), especially class III alleles and III/III genotypes might not only determine the predisposition to anovulatory PCOS but also the concomitant risk for development of type 2 diabetes. The function of the insulin receptor (IR) is probably normal in woman with PCOS. However abnormal serine phosphorylation in the receptor may impair signal transduction accounting for a post-binding defect in insulin action. Serine phosphorylation is also involved in the postranslational regulation of 17,20-lyase activity (CYP17). There may be a common aetiology for both insulin resistance and hyperandrogenism. Polymorphic alleles of both IRS-1 and IRS-2 (insulin receptor substrate 1 - 2), alone or in combination, may have a functional impact on the insulin-resistant component of PCOS. There is no evidence to suggest that follistatin gene polymorphisms play a role in the pathogenesis of insulin resistance in PCOS women. PCOS appears to be associated with the absence of the four-repeat-units allele in a polymorphic region of pentanucleotide (TTTTA)n repeats within CYP11A gene, which encodes cytochrome P450scc. It has been hypothesized that up-regulation of this enzyme could lead to increased androgen production. There is no evidence of any association of alleles of CYP19 gene (encoding cytochrome P450arom) with PCOS. Association exists between androgen receptor gene (AR) polymorphisms an androgens action in PCOS. Increased hirustism and decreased CAG repeat length within AR gene has been also demonstrated in women with normal testosterone levels. Expression of estrogen receptor (ERs) as well as 5-alpha-reeducates (SRD5A1-2 genes) activity was analysed in granulosa (GC) and theca cells (TC). The results of this study demonstrate that there are significant alterations in the expression of ERalpha and ERbeta in PCOS that may be related to abnormal follicular development. On the other hand elevated SRD5A activity in polycystic ovaries supported the hypothesis that 5-alpha-reduced androgens may play a role in the pathogenesis of the syndrome. The genetic aetiology of PCOS remains unknown. There are a number of interlinking factors that affects expression of PCOS. Single cause of PCOS is unlikely. Other possible mechanisms in pathogenesis of PCOS are discussed.
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PMID:[Genetic aspects of polycystic ovary syndrome]. 1635 Jul 21

Epilepsy in women is relatively often linked with reproductive disorders which include polycystic ovarian syndrome, hypothalamic amenorrhea and functional hyperprolactinaemia. These disorders have a significant share in a high incidence of infertility and premature menopause while the polycystic ovarian syndrome, also manifested by the metabolic syndrome, places the affected patients at risk of later consequences such as type 2 diabetes mellitus, cardiovascular diseases including arterial hypertension, gynaecological neoplasias (the breast and the endometrium), and in the case of pregnancy, a higher incidence of pregnancy induced hypertension. Apart from epilepsy as such, also antiepileptic treatment may have negative impact on the female's reproductive functions. In many cases, adverse effects of treatment complicate the patient's life more than the attacks alone. Medication induced weight gain might be responsible for different endocrine diseases (menstruation disorders, polycystic ovarian syndrome, hyperandrogenism). The article analyses the influence of side effects of the different antiepileptic drugs on the development of metabolic and endocrine anomalies. The role of antiepileptic drugs in the development of reproductive and endocrine disorders was first described by Isojarvim in 1993. A high incidence of polycystic ovarian syndrome and/or hyperandrogenism (43%) was observed in women taking valproat, which was clearly higher than in women taking other antiepileptics. Results reported in literature are rather controversial. The article gives an overview of current knowledge with respect to the influence of epilepsy and antiepileptics on the incidence ofpolycystic ovarian syndrome, which is considerably higher in women with epilepsy (10-25%) than in the unaffected population (4-7%), and of the related metabolic syndrome. The article concludes with recommendations for clinical practice in the treatment of epilepsy in women in reproductive age.
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PMID:[Epilepsy and disorders of reproduction]. 1747 15

Extreme forms of insulin resistance are a rare cause of type 2 diabetes. However, individuals with severe insulin resistance pose unique diagnostic and therapeutic challenges, and have often acted as 'experiments of nature' providing important novel information regarding endocrine physiology and mechanistic insights relevant to the study of more common disorders. Progress in understanding the molecular pathogenesis of such syndromes is also beginning to yield novel therapeutic options. Severe insulin resistance typically presents in 1 of 3 ways: (1) disordered glucose metabolism including both diabetes and/or paradoxical hypoglycaemia; (2) acanthosis nigricans, a velvety hyperpigmentation of axilliary and flexural skin often associated with skin tags; or (3) hyperandrogenism in girls (hirsutism, oligo-/amenorrhoea and polycystic ovaries). Lipodystrophy is a major cause of severe insulin resistance and needs to be looked for very carefully, particularly in the patients with significant dyslipidaemia and fatty liver. Specific treatments are now available for some forms of severe insulin resistance; for example, leptin replacement in patients with generalized lipodystrophy. In the absence of a specific diagnosis and therapy, metformin is a useful insulin sensitizer and should be used in conjunction with aggressive diet and exercise interventions.
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PMID:A clinical approach to severe insulin resistance. 1798 32


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