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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three girls, two of them being monozygotic twins, are affected with acanthosis nigricans and hirsutism, which worsened at the time of their puberty. The first one has primary amenorrhea and the twins complain of spaniomenorrhea. Furthermore, laboratory data concluded to diabetes, hyperinsulinism and resistance to insulin. This rare association of syndromes is not accidental but its significance remains unknown.
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PMID:[Acanthosis nigricans, hirsutism and insulin-resistant diabetes]. 49 46

Patients with dysgenetic gonads and Turner syndrome are unlikely to develop endometrial carcinoma unless they have received unopposed estrogen replacement therapy. This case describes a 54-year-old woman with Turner syndrome and primary amenorrhea who developed adenocarcinoma of the endometrium without having received hormone replacement. Vaginal bleeding, a pelvic mass, and sepsis were the presenting symptoms. The patient also had diabetes mellitus and hypothyroidism. Polyglandular endocrine patterns are known to occur with a high frequency in these patients. The woman's chromosome studies revealed a modified 46,X,i(Xq) (isochromosome X). This is the first report of an isochromosome X patient to develop endometrial cancer without receiving estrogen replacement. The etiology of this rare case may be an increased propensity for patients with X-chromosome deletions to develop neoplasms in general, or extragonadal estrogen production.
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PMID:Endometrial adenocarcinoma without prior hormone replacement in a diabetic patient with gonadal dysgenesis. 156 85

To describe the age at menarche and the prevalence of menstrual disturbances in an unselected group of women with insulin-dependent diabetes mellitus compared to controls, we identified all women having debut of diabetes mellitus before the age of 30 yr and living in the County of Funen, Denmark on July 1, 1987 and being between 18 and 49 yr old. The women received a structured questionnaire inquiring information concerning menstrual conditions. An age comparable group of nondiabetic women was used as controls; 245 (94%) diabetic women and 253 (88%) controls answered the questionnaire. Among women with debut of diabetes before the age of 10 yr, the age at menarche was delayed 1 yr when comparing to controls (P less than 0.0001). During the past 6 months before answering the questionnaire, 8.2% of the diabetic women and 2.8% of the controls had experienced episodes of secondary amenorrhea (P less than 0.01). Corresponding figures for oligomenorrhea were 10.6% and 4.8% (P less than 0.02), for polymenorrhea 7.3% and 5.2% (NS), and for all types of menstrual disturbances 21.6% and 10.8%, respectively (P less than 0.005). Episodes of secondary amenorrhea occurring more than 6 months before answering the questionnaire had been experienced by 10.7% of the diabetic population vs. 4.8% of the controls (P less than 0.05); corresponding figures for primary amenorrhea were 4.9% and 1.2%, respectively (P less than 0.05). We conclude that the age at menarche among women having developed insulin-dependent diabetes mellitus before the age of 10 yr was delayed by 1 yr when compared to controls. The overall prevalence of menstrual disturbances is increased in diabetic women compared to nondiabetic controls.
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PMID:Epidemiology of menarche and menstrual disturbances in an unselected group of women with insulin-dependent diabetes mellitus compared to controls. 163 55

From observations of female type I diabetics, we collected data on menarche, menstrual cycle and fertility. 337 women answered our questionnaire which had been published in journals for diabetic patients. The data were correlated with age, diabetes duration, and the onset of diabetes. The mean age at menarche was inversely correlated with the age of the patients; in diabetics it was 0.8-2 years higher than in the population in which diabetes developed after menarche. As compared to a population of non-diabetics we observed an increase in mean age at menarche of 0.4-1.3 years. The increase was most pronounced if diabetes developed between the age of 3-8 years. The prevalence of primary amenorrhoea in diabetics was 3.6%, in the controls and in diabetics with late onset 1.5%. Irregularities of the menstrual cycle were observed more often in diabetics than in the controls. The prevalences of oligomenorrhoea and secondary amenorrhoea were 14 and 7% in the group of patients with diabetes onset before menarche. In the group with late onset of diabetes the prevalence of secondary amenorrhoea was 12%. Irregularities of the menstrual cycle were found more frequently at the time of diabetes onset, although 76% of the patients had not remarked any change in the frequency of menstrual bleedings. With increasing diabetes duration, the frequency of bleedings normalized. 70.5% of the patients aged 35 or more had spontaneous conceptions, 2.1% were sterile. Both values are not significantly different from the data of the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Menarche, menstrual cycle and fertility in diabetic patients]. 270 25

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

A case is presented of congenital lipodystrophy and diabetes coexistent with severe polycystic ovarian disease characterized by primary amenorrhea and pronounced virilization. The relationship of these two disease entities is unknown. This case strengthens the suggestion that isochronia may not be coincidental.
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PMID:Congenital lipodystrophy and polycystic ovarian disease. 723 Jan 51

The status of oocytes, the follicular fluid concentrations of steroids, and the in vitro steroidogenic capacities of stromal tissue, thecal tissue, and granulosa cells from a 15-yr-old girl with primary amenorrhea, ovarian hyperandrogenism, insulin-resistant diabetes mellitus, and acanthosis nigricans were compared to those from normal adult human ovaries. Most oocytes (95%) in the antral follicles recovered from the hyperandrogenic ovaries were degenerative, and the antral fluid levels of testosterone were 30- to 200-fold higher than those in normal ovaries. Granulosa cells from the hyperandrogenic ovaries produced mainly estradiol as did those from normal healthy follicles. The thecal tissues produced 2- to 6-fold more androgen than similar tissues from normal ovaries. However, the stroma from the hyperandrogenic ovaries produced 49- to 250-fold more testosterone than that generated by normal tissues. These data suggest that the removal of stromal tissue as well as follicular tissue from patients with certain types of hyperandrogenism may sometimes contribute to a reduction in androgen secretion.
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PMID:The intraovarian sites of androgen and estrogen formation in women with normal and hyperandrogenic ovaries as judged by in vitro experiments. 736 31

A 47-year-old woman was evaluated for congenital dwarfism, primary amenorrhoea due to hypogonadotrophic hypogonadism, severe hyperlipidaemia with pancreatitis, and overt diabetes mellitus associated with severe insulin resistance requiring 2.5-3 units of insulin per kilogram body weight. Chromosomal analysis with trypsin banding was normal and biochemical evaluation revealed low oestrogen levels, inappropriately low gonadotrophins, very low IGF-I concentrations and GH concentrations unresponsive to insulin or L-dopa administration. Prolactin, pituitary-adrenal and pituitary-thyroid axes were normal. Dynamic testing with GnRH and GHRH produced increases in FSH, LH and GH concentrations. A MRI of the brain revealed no discernible hypothalamic abnormalities and a small pituitary. The presence of congenital combined growth hormone and gonadotrophin deficiency on the basis of a suprapituitary defect suggests the existence of common or related pathways regulating GnRH and GHRH synthesis or secretion and may have contributed to the ultimate development of insulin resistance and hyperlipidaemia.
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PMID:Isolated combined growth hormone and gonadotrophin deficiency due to hypothalamic dysfunction, associated with insulin resistance. 755 20

A 37-yr-old woman was admitted to our hospital for evaluation of diabetes mellitus, liver cirrhosis and primary amenorrhea. Serological and hematological examinations revealed that she suffered from hemochromatosis secondary to congenital dyserythropoietic anemia (CDA), characterized by ineffective hematopoiesis and erythropoietic dysplasia. Iron deposition was suggested by MRI on the pancreas, liver and pituitary gland. Endocrinological examinations demonstrated that she had isolated gonadotropin deficiency and ovarian failure, resulting in hypogonadotropic hypogonadism. In addition, despite normal responses of serum cortisol and plasma aldosterone to ACTH and furosemide-standing tests, respectively, serum dehydroepiandrosterone (DHEA) responded poorly to ACTH test, suggesting selective damage of zona reticularis in adrenocortical steroidogenesis in association with hemochromatosis.
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PMID:[Isolated gonadotropin deficiency and secretory discrepancy of cortisol and adrenal androgen by hemochromatosis secondary to congenital dyserythropoietic anemia]. 795 84

A 56-year-old woman of short stature (148 cm) was medically examined after applying for a disability pension on account of chronic back-pain. She gave a history of primary amenorrhoea (not examined further), slowly increasing deafness, type IIb diabetes mellitus, hyperlipoproteinaemia, hypothyroidism and osteoporosis. Physical examination showed hypoplasia of both breasts, shield chest and slight webbing of the neck. Ultrasonography of the thyroid revealed late stage of Hashimoto thyroiditis. Vaginal ultrasonography confirmed absence of uterus and adnexae. All these findings were compatible with the diagnosis of Turner's syndrome, which was confirmed by chromosomal examination of 50 analysable metaphases showing chromosomal mosaic 45,X/46,X, i(Xq), as well as two cells with 47 chromosomes, two with isochromosomes for the long arm of the X-chromosome. Treatment consisted of administration of L-thyroxin (75 micrograms/d) and oestrogen. There was no follow-up.
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PMID:[Diagnosis of an Ullrich-Turner syndrome in pension evaluation]. 807 Mar 32


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