Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The action of estrogens on glucose metabolism has been proven more than 30 years ago. Estroprogestational agents do not modify sensibly glucose metabolism in normal women, but they do have a serious diabetogenic effect on women with hereditary antecedents of diabetes. These women can use oral contraception only under strict surveillance. Estroprogestinic agents should never be administered to women with latent diabetes; they can be administered to women with diabetes only if glycemia and vascular conditions are constantly checked. It is possible that minipills can cause fewer glucose metabolism complications. Steroids used as male contraceptives have no influence on lipid and glucose metabolism. Natural estrogens administered during and after menopause can improve the glucose tolerance in diabetic patients. It is still not clear what mechanism governs the diabetogenic effects of estroprogestinic agents. The article contains a detailed review of the literature on the subject, and a very useful table listing all combined oral contraceptives available in France.
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PMID:[Diabetes and estro-progestins]. 88 24

In a search for possible hormonal reasons for the loss of protection from myocardial infarction seen in diabetic women, serum levels of estradiol, progesterone, and luteinizing hormone were compared throughout a menstrual cycle (17 points) in eight healthy nonsmoking women and five otherwise healthy nonsmoking insulin-dependent diabetic women. The total length of the menstrual cycle and the lengths of the follicular and luteal phases did not differ between the groups. During the periovulatory and luteal phases, there was no significant intergroup difference with respect to any of the three hormones. During the follicular phase, in both groups, there was a plateau in serum progesterone concentration, with the level approximately 42% lower in the diabetic group (12.0 +/- 6.6 ng/dl versus 20.7 +/- 5.7; P less than 0.0001). Follicular-phase serum estradiol showed a rising curve in both groups; day-by-day comparison (days -10 to -3 before the luteinizing hormone peak) showed consistently higher levels in the diabetic group (mean, 108 pg/ml versus 95 pg/ml; P less than 0.001). The follicular-phase serum estradiol to progesterone ratio was nearly twice as high in the diabetic group as in the normal group (8.9 versus 4.6), a difference that was highly significant. The finding of elevated serum estradiol and subnormal serum progesterone concentrations during the follicular phase is so far unique to women with insulin-dependent diabetes mellitus. The possibility that this pronounced abnormality in diabetic women may be related to coronary disease merits testing in suitable in vivo and in vitro models of atherogenesis.
Steroids 1990 Dec
PMID:Subnormal follicular-phase serum progesterone levels and elevated follicular-phase serum estradiol levels in young women with insulin-dependent diabetes. 208 47

A male to female ration of coronary disease of 2:1 has been a consistent finding. This differential persists event when the classic risk factors for coronary disease--hypertension, smoking, obesity, diabetes, and hyperlipidemia--are controlled for gender. The most likely ultimate cause of this phenomenon is male-female differences in sex hormone patterns. Clinical studies in this area have either compared the sex hormone profiles of men and women with and without coronary disease or computed the relative prevalence of disease in populations that differ in their sex hormone patterns. In general, research findings have disputed the hypothesis that persons with coronary disease have low levels of a protective factor such as estrogen or progesterone and high levels of testosterone. Coronary disease patients actually have elevated estrogen levels and low testosterone levels; endogenous progesterone levels are normal before infarction but show a stress-mediated increase in the immediate postinfarction period. Findings of a low prevalence of coronary disease in premenopausal women, a loss of protection after menopause, and a low prevalence of coronary disease in men with cirrhosis-related hyperestrogenemia suggest that natural estrogens are antiatherogenic. The protective effect of pregnancy against myocardial infarction, despite concomitant potentially thrombogenic levels of estrogen at the time, seems to indicate that progesterone, whose levels are also extremely high during pregnancy, plays a major anti-infarction protective effect distinct from that of estrogen. Studies of women oral contraceptive (OC) users and men taking estrogens for brief periods have found that these exogenous hormones produce coronary thrombosis but not atherosclerosis. Finally, the finding of increased coronary disease risk in long-term OC users indicates that synthetic estrogens favor coronary atherosclerosis by suppressing natural estrogen and progesterone production.
Steroids 1990 Aug
PMID:Sex hormones and coronary disease: a review of the clinical studies. 223 42

Eight hundred and seventy-nine patients with Bell's Palsy were seen over a 10-year period. There was a distinct female preponderance and the peak incidence occurred in the second to fourth decades. There did not appear to be an increased incidence of either hypertension or diabetes but there was a definite increased risk during pregnancy. Half of the patients had an incomplete palsy and they all recovered within a few weeks of onset. Those patients with complete palsy but without evidence of degeneration also all recovered but took longer to do so. If degeneration was evident the chance of recovery was only 50 per cent. Steroids did not appear to influence the outcome of Bell's Palsy.
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PMID:Idiopathic facial nerve palsy (the effect of treatment with steroids). 339 32

Glucocorticoid treatment was performed in 31 patients with diabetes mellitus (41 examinations). The therapy was effective in the patients with the labile form of the disease, in diabetic nephropathy not accompanied by stable azotemia and after administration of allergenic insulin drugs. Steroids should be combined with divided doses of short-acting insulin drugs within 24 hours. The adrenocortical drugs are absolutely contraindicated in pronounced ketosis. The treatment above can be aggravated by a chronic inflammatory process, especially by cholecystitis.
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PMID:[Interrelations between blood coagulation and lipid metabolism in patients with diabetes mellitus]. 685 93

Sporadic acute brachial plexus neuropathy occurs in approximately 1.64/100,000 population, but may present in epidemic form. Sporadic lumbosacral plexus neuropathy is far less common and has to be distinguished from more common disorders affecting the plexus and roots such as diabetes. Early this century, when serum therapy became popular to treat or prevent prevalent infectious diseases, it became apparent that a plexopathy could follow treatment. It has thus been assumed that many of the cases are due to an autoimmune or inflammatory lesion of the plexus. A wide variety of vaccines, infections and medications seem able to precipitate the disorder. Recent work has shown that cultured lymphocytes from affected patients, but not controls, are able to mount a blastogenic response to components of cadaver brachial plexus. This response seems to be selective not only to the brachial plexus, but also to discrete components of the plexus. The recovery rate in brachial plexus neuropathy is good, being almost 90% at 3 years. Recovery with lumbosacral disease is less satisfactory. Histological material and descriptions of acute brachial plexus neuropathy are rare. There is some evidence that an inflammatory process is present, but the role of demyelination and axonal atrophy in producing the observed clinical signs, is still uncertain. Virtually nothing is known about the histological changes in lumbosacral plexus neuropathy. Treatment is mainly supportive, but important in limiting disability. Steroids may help relieve pain in the acute stages, but do not seem to alter the prognosis.
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PMID:Brachial and lumbar neuropathies. 792 88

This review examines the relationship between renal transplantation and two important metabolic consequences: hyperlipidemia and glucose intolerance. Before cyclosporine, hypertriglyceridemia and hypercholesterolemia were common abnormalities that worsened in the cyclosporine era. In addition to obesity, steroid use, and reduced renal function, cyclosporine plays an independent role in elevating cholesterol levels, with particular reference to the modulation of the low-density lipoprotein receptor. Management includes maintaining low levels of steroid, manipulation of cyclosporine appropriately, diets low in fat and cholesterol, and an exercise program. Pharmacologic management in general revolves around the HMG-COA reductase drugs, which can be used safely if liver function tests and muscle enzymes are monitored. The unmasking of clinically important glucose intolerance occurs in 5 to 10% of patients in the cyclosporine era, not different from the earlier experience. Steroids and cyclosporine independently can worsen glucose tolerance to unmask a genetic predisposition to Type II diabetes in some and to even create glucose intolerance in otherwise normal individuals. Management is based on dietary and immunosuppressive drug dosing manipulations and the judicious use of oral hypoglycemic agents. Half of these recipients may ultimately need insulin. In summary, hyperlipidemia and glucose intolerance remain important metabolic consequences of renal transplantation that affect long-term patient survival unless recognized and treated.
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PMID:Hyperlipidemia and glucose intolerance in the post-renal transplant patient. 819 94

Prednisone is widely used by most heart transplantation units despite its frequent side effects. Deflazacort, an oral synthetic steroid with fewer side effects, has been successfully used in patients after heart transplantation, but a prospective study comparing deflazacort and prednisone in transplant patients is lacking. We have carried out, in the last year, a prospective trial of deflazacort versus prednisone involving 35 consecutive heart transplant patients. Two of these patients died perioperatively (surgical mortality, 5.7%), and another two were excluded from the protocol because of diabetes mellitus in one patient and active infection before transplantation in the other patient. Thus 31 patients were enrolled in the 3-month study. All of them were treated with antithymocyte globulin, 10 mg/kg/day for 3 days after transplantation, azathioprine, and cyclosporine; patients were randomly assigned groups: 15 patients to receive deflazacort therapy, 1.5 mg/kg/day, and 16 patients to receive prednisone therapy, 1 mg/kg/day, starting the first day after transplantation. Steroids were rapidly tapered, reaching the maintenance dose at 2 to 3 weeks after transplantation (prednisone, 0.15 mg/kg/day; deflazacort, 0.25 mg/kg/day). Both groups were similar in terms of age, gender, ABO identity, serum cyclosporine levels, azathioprine dosage, and pretransplantation serum glucose and lipids levels. Seven endomyocardial biopsies were performed on each patient, at 1, 2, 3, 5, 7, 10, and 13 weeks after transplantation. Incidence of acute rejection was similar between prednisone and deflazacort groups; 33% of patients receiving prednisone therapy and 42% of patients receiving deflazacort therapy had one episode of 3A or higher rejection (not significant).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A randomized study comparing deflazacort and prednisone in heart transplant patients. 824 Dec 29

We prospectively withdrew prednisone in 28 adult patients who had stable graft function more than 2 years after orthotopic liver transplantation (OLTx) and had been on 5 mg/d prednisone for at least 6 months. Prednisone was decreased from 5 mg/d to 2.5 mg/d for 1 month then stopped completely. Cyclosporine monotherapy was maintained at a level of approximately 200 ng/mL (TDX). Nineteen patients had prednisone withdrawn without complications. Four (14.2%) had modest elevations in liver function tests (two biopsy proven mild rejections and two were not biopsied). These four were treated with methylprednisolone boluses and then withdrawal of steroids again. Prednisone was restarted in five patients because of generalized fatigue and body aches (n = 4) and colitis (n = 1). Steroids later were successfully withdrawn in two of these patients. After prednisone withdrawal, three of five insulin-dependent diabetic patients were able to discontinue insulin therapy and their glycosylated hemoglobin levels improved. Four of fourteen hypertensive patients were able to discontinue antihypertensive medicines. Mean serum cholesterol decreased from 222.6 +/- 43.3 to 188.3 +/- 33.3 mg/dL (P < .001). The number of patients with serum cholesterol levels > 220 mg/dL decreased from 13 to 4. A control group of 24 patients maintained on 5 mg/d prednisone at least 2 years after liver transplantation also was studied. In this group during the study period, no diabetic became normoglycemic, no patient decreased their antihypertensive medicine, and the mean serum cholesterol levels did not change significantly. We conclude that prednisone withdrawal using cyclosporine monotherapy late after liver transplantation does not lead to graft loss and decreases the prevalence of diabetes, hypertension, and hypercholesterolemia. Symptoms occurring during withdrawal may be minimized by earlier or slower tapering.
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PMID:Prednisone withdrawal late after adult liver transplantation reduces diabetes, hypertension, and hypercholesterolemia without causing graft loss. 898 86

Increasing human epidemiological data suggest that events that subtly retard intrauterine growth may determine common disorders, such as hypertension and non-insulin-dependent diabetes, in adult life. The underlying mechanisms are unknown. However, excessive fetal exposure to glucocorticoids retards growth and "programs" adult hypertension in rats. 11 beta-Hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) catalyzes the rapid inactivation of cortisol and corticosterone to inert 11 keto-products. Normally, 11 beta-HSD2 in the placenta and some fetal tissues is thought to protect the fetus from excess maternal glucocorticoids. In both rats and humans there is considerable natural variation in placental 11 beta-HSD2, and enzyme activity correlates with birth weight. Moreover, inhibition of feto-placental 11 beta-HSD2 in the rat reduces birth weight and produces hypertensive and hyperglycaemic adult offspring, many months after prenatal treatment; effects are dependent upon intact maternal adrenals, suggesting a direct action on the fetus or placenta. Maternal protein restriction during pregnancy also produces hypertensive offspring and selectively attenuates placental 11 beta-HSD2 activity. These data suggest that feto-placental 11 beta-HSD2, by regulating fetal exposure to maternal glucocorticoids, crucially determines fetal growth and the programming of later disorders. Deficiency of the barrier to maternal glucocorticoids may represent a common pathway between the maternal environment and feto-placental programming of later disease. These data may, at least in part, explain the human observations linking early life events to the risk of subsequent disease.
Steroids 1997 Jan
PMID:Glucocorticoids, feto-placental 11 beta-hydroxysteroid dehydrogenase type 2, and the early life origins of adult disease. 902 21


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