Overt non-insulin-dependent diabetes mellitus (NIDDM) is the end of a continuum in metabolic insulin resistance with decreasing compensation by insulin production from the beta cell [1]. Risk factors for ischaemic heart disease, the most importance cause of death and disability in elderly patients with diabetes, like carbohydrate intolerance or manifest diabetes, visceral obesity, hypertriglyceridaemia [2], low HDL-cholesterol content in plasma [3] and hypertension [2] are often clustered in a more or less complete profile of interdependent metabolic abnormalities, called the insulin resistance syndrome [4]. The balance between coagulation and fibrinolysis is intimately linked with this profile [5][6][7]. In patients with NIDDM the cardiovascular risk is increased 2 Diabetologia (1997) b -estradiol during 6 weeks in 40 postmenopausal women with NIDDM. Glycated haemoglobin (HbA 1c ), insulin sensitivity, suppressibility of hepatic glucose production, lipoprotein profile and parameters of fibrinolysis were determined. The oestrogen treated group demonstrated a significant decrease of HbA 1c and in the normotriglyceridaemic group a significantly increased suppression of hepatic glucose production by insulin. Whole body glucose uptake and concentrations of non-esterified fatty acids did not change. LDL-cholesterol-and apolipoprotein B levels decreased, and HDL-cholesterol, its subfraction HDL 2 -cholesterol and apolipotrotein A1 increased. The plasma triglyceride level remained similar in both groups. Both the concentration of plasminogen activator inhibitor-1 antigen and its active subfraction decreased. Tissue type plasminogen activator activity increased significantly only in the normotriglyceridaemic group. Oestrogen replacement therapy improves insulin sensitivity in liver, glycaemic control, lipoprotein profile and fibrinolysis in postmenopausal women with NIDDM. For a definite answer as to whether oestrogens can be more liberally used in NIDDM patients, long term studies including the effect of progestogens are necessary. [Diabetologia (1997) 40: 843-849] Keywords Oestrogen therapy, non-insulin-dependent diabetes mellitus, glucose regulation, insulin sensitivity, hepatic glucose production, lipoprotein profiles, coagulation factors, fibrinolysis.Received: 12 November 1996 and in revised form: 21 March 1997Corresponding author: H. E. Brussaard, M. D., Virga Jesse Hospital, Stadsomvaart 11, B-3500 Hasselt, Belgium Abbreviations: Apo A1 and apo B, Apolipoprotein A1 and B; ERT, oestrogen replacement therapy; FSH, follicle stimulating hormone; HDL-chol, high density cholesterol; HGP 1 and HGP 2 , hepatic glucose production basal (first step) and second step; HGP suppr , suppression of HGP from the first to the second step; LDL-chol, low-density cholesterol; LH, luteinising hormone; NEFA, non-esterified fatty acids; NEFA suppr , percentage suppression of NEFA from the first to the second step; t-PA-ag, tissue type plasminogen activator antigen; PAI-1, plasminogen activator inhibitor; VLDL-TG, very low density ...

The objective of this study was to present the long-term results of total adrenalectomy for Cushing's disease. Forty-four patients undergoing total adrenalectomy for Cushing's disease between 1953 and 1989 at Leiden University Medical Center, The Netherlands, were studied retrospectively. Remission was achieved in 42 patients (95%), with a mean duration of 19 years. Adrenal remnants were observed in 12 patients (27%), and were without clinical consequence in the majority of patients, but caused early recurrent disease in 2 patients. Nine patients (20%) experienced Addisonian crises up to 30 years following treatment. Nelson's syndrome developed in 10 patients (23%) 7-24 years following total adrenalectomy. Prior pituitary irradiation was a protective factor against Nelson's syndrome as it delayed its onset (p = 0.025). On the other hand, subnormal dose or noncontinuous glucocorticoid replacement therapy was associated with increased risk of development of Nelson's syndrome (p = 0.047). The incidence of Nelson's syndrome increased with prolonged follow-up, and female patients seemed to be at increased risk. Quality-of-life assessment showed less favorable scores on mental health and health perception scales, for which no explanation can be found except the long-lasting metabolic effects of Cushing's disease, even when successfully treated. In conclusion, total adrenalectomy remains the final treatment for Cushing's disease. The presence of adrenal remnants which can cause recurrent disease and the development of Nelson's syndrome during prolonged follow-up enhance the need for continued regular follow-up. Pituitary irradiation prior to total adrenalectomy delays the onset of Nelson's syndrome.

These are the same for all types of diabetes: Relief of symptoms. 0 Reduction of mortality. Treatment of accompanying disorders. This desktop guide is a quick source of information for the day-to-day care of persons with NIDDM. It should be used together with the booklet, Your Guide to better Diabetes Care', and the International Care Card, Diabetes.2 Improvement of the quality of life. Prevention of acute and chronic (long-term) compl ications.

. Retention of estradiol negative feedback relationship to LH predicts ovulation in response to caloric restriction and weight loss in obese patients with polycystic ovary syndrome. Am J Physiol Endocrinol Metab 286: E615-E620, 2004. First published December 16, 2003 10.1152/ajpendo.00377.2003.-The present study tests the hypothesis that specific endocrine, metabolic, and anthropometric features distinguish obese women with polycystic ovary syndrome (PCOS) who resume ovulation in response to calorie restriction and weight loss from those who do not. Fifteen obese (body mass index 39 Ϯ 7 kg/m 2 ) hyperandrogenemic oligoovulatory patients undertook a very low calorie diet (VLCD), wherein each lost Ն10% of body weight over a mean of 6.25 mo. Body fat distribution was quantitated by magnetic resonance imaging. Hormones were measured in the morning at baseline, after 1 wk of VLCD, and after 10% weight loss. To monitor LH release, blood was sampled for 24 h at 10-min intervals before intervention and after 7 days of VLCD. Responders were defined a priori as individuals exhibiting two or more ovulatory cycles in the course of intervention, as corroborated by serum progesterone concentrations Ն18 nmol/l followed by vaginal bleeding. At baseline, responders had a higher sex hormonebinding globulin (SHBG) concentration but were otherwise indistinguishable from nonresponders. Body weight, the size of body fat depots, and plasma insulin levels declined to a similar extent in responders and nonresponders. Also, SHBG increased, and the free testosterone index decreased comparably. However, responders exhibited a significant decline of circulating estradiol concentrations (from 191 Ϯ 82 to 158 Ϯ 77 pmol/l, means Ϯ SD, P ϭ 0.037) and a concurrent increase in LH secretion (from 104 Ϯ 42 to 140 Ϯ 5 U⅐l Ϫ1 ⅐day Ϫ1 , P ϭ 0.006) in response to 7 days of VLCD, whereas neither parameter changed significantly in nonresponders. We infer that evidence of retention of estradiol-dependent negative feedback on LH secretion may forecast follicle maturation and ovulation in obese patients with PCOS under dietary restriction. fertility; ovarian cycle; sex hormones; body fat distribution; gonadotropins POLYCYSTIC OVARY SYNDROME (PCOS) is a heterogeneous disorder of female reproduction characterized by hyperandrogenism and chronic oligo-or anovulation in the absence of specific disease of the adrenal glands, ovaries, or pituitary gland (41). If these criteria are applied to establish the diagnosis, PCOS occurs in 4-8% of premenopausal women (2,5,19).The etiology of the disease remains uncertain. It is thought that various environmental factors interact with genes that predispose women to the development of PCOS (8, 21). A number of features that are often, but not always, present in PCOS may provide mechanistic clues: obesity, peripheral insulin resistance, and chronic hyperinsulinemia (6, 11). More than 30% of women with PCOS are obese (body mass index Ͼ30 kg/m 2 ), reflecting primarily visceral adiposity (11). Intraabdominal obesity is freque...

No abstract