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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Many clinical studies have shown an increased insulin response to oral glucose in patients with ischemia of the heart, lower limbs, or brain. Hyperinsulinemia also occurs in patients with angiographically proved atherosclerosis without ischemia and thus appears to be related to arterial disease and not to be a nonspecific response to tissue injury. Fasting insulin levels and insulin responses to intravenous stimuli, including glucose, tolbutamide, and arginine, are normal, suggesting a gastrointestinal factor may be involved in the increased insulin response to oral glucose. In patients with atherosclerosis, insulin sensitivity appears to be normal or enhanced with respect to both glucose and lipid metabolism. Five population studies have shown that insulin responses to glucose are higher in populations at greater risk of cardiovascular disease. Many of the hyperinsulinemic populations also had upper-body obesity, hypertriglyceridemia, lower high-density lipoprotein (HDL) levels, and hypertension. These prospective studies support an independent association between hyperinsulinemia and ischemic heart disease, although their results differ in detail. Hyperinsulinemia is associated with raised triglyceride and decreased HDL cholesterol levels. Total and low-density lipoprotein (LDL) cholesterol is less closely related to hyperinsulinemia. Upper-body adiposity is associated (in separate studies) with coronary heart disease, diabetes, hyperinsulinemia, and hypertriglyceridemia. Insulin and blood pressure are closely related in both normotensive and hypertensive people. Although obesity and diabetes are often found in hypertensive people, hyperinsulinemia also occurs in nonobese nondiabetic hypertensive people. Thus, hyperinsulinemia is closely associated with a cluster of cardiovascular risk factors, i.e., hypertriglyceridemia, low HDL levels, hypertension, hyperglycemia, and upper-body obesity. There is a possibility that insulin has a role in the sex differences in ischemic heart disease incidence and their absence in diabetes, but additional work is required for its clarification. Long-term treatment with insulin results in lipid-containing lesions and thickening of the arterial wall in experimental animals. Insulin also inhibits regression of diet-induced experimental atherosclerosis, and insulin deficiency inhibits the development of arterial lesions. Insulin stimulates lipid synthesis in arterial tissue; the effect of insulin is influenced by hemodynamic factors and may be localized to certain parts of the artery. In physiological concentrations, insulin stimulates proliferation and migration of cultured arterial smooth muscle cells but has no effort on endothelial cells cultured from large vessels. Insulin also stimulates cholesterol synthesis and LDL binding in both arterial smooth muscle cells and monocyte macrophages.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Insulin and atheroma. 20-yr perspective. 199 42

Surgically confirmed pheochromocytoma was the cause of arterial hypertension in 6 out of 668 (0.8%) children with significant hypertension admitted to Child Health Centre in Warsaw. Among clinical features most characteristic was sustained hypertension observed in all patients, often complicated by the accelerated phase of malignant hypertension and encephalopathy. Sustained tachycardia was also found in all patients. Elevated sedimentation rate and electrocardiographic changes were observed in each child while other abnormal laboratory findings such as hyperglycemia, etc. occurred at similar rate as in adults. Increased urinary excretion of catecholamines and their metabolites confirmed the diagnosis. In our study the most sensitive methods for tumor localization were ultrasonography and computed tomography of the adrenals while scintigraphy with iodo-131-metabenzylguanidine gave a high percentage of false negative results. Clinical presentation of pheochromocytomas in children is different than in adults and all pediatric patients with severe hypertension should be screened for this disease.
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PMID:Pheochromocytoma in children: difficulties in diagnosis and localization. 219 28

A population-based prospective study of insulin-dependent diabetics between the ages of 14-30 southern Wisconsin examined the relationship between oral contraceptive use and presence and severity of diabetic retinopathy, hypertension and glycosylated hemoglobin (HbA1). HbA1 is a measure of overall control of hyperglycemia. Out of 10,135 diabetic patients of 452 physicians in an 11-county area of Wisconsin, 432 were women between 14-30, and were followed from 1980-1986. The exit interview and exam consisted of pupil dilatation, stereoscopic fundus photographs, blood glucose by Chemstrip, blood pressure and determination of HbA1 with a resin microcolumn. 384 of these women provided oral contraceptive use history at follow-up. 170 ever used pills, 62 for 1yr, 59 for 2-4 yr, and 49 for 5 or more years. There was a trend toward current pill use with less severe diabetic retinopathy. There was no evidence of an association between ever using pills and the severity of diabetic retinopathy, controlling for age, duration of diabetes, systolic or diastolic blood pressure, HbA1, proteinuria or body mass index. Duration of diabetes, diastolic blood pressure, proteinuria and HbA1 were significantly associated with severity of retinopathy, while age, systolic blood pressure and body mass were not. Current, prior or duration of use of pills did not show significant effects on severity of retinopathy. Number of daily doses of insulin were inversely significantly related to HbA1.
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PMID:Oral contraceptives in women with diabetes. 220 28

The chronic hyperglycemia of non-insulin-dependent diabetes mellitus (NIDDM) evolves gradually and is usually preceded by more transient hyperglycemia, classified as impaired glucose tolerance (IGT). Already in this phase, there is an increased risk of cardiovascular complications, and many IGT subjects, like NIDDM patients, often display several of the metabolic and circulatory disturbances that are associated with hyperglycemia, e.g., insulin resistance, hyperinsulinemia and/or hyperproinsulinemia, delayed insulin release, dyslipidemia, and hypertension. Therefore, and because untreated hyperglycemia is a self-perpetuating condition, early detection and early intervention may be necessary to prevent the progression and complications of NIDDM. This in turn would necessitate screening procedures, and the therapeutic goal should include both euglycemia and normalization of plasma insulin, plasma lipids, and blood pressure. A study in the German Democratic Republic indicated that the mortality in screening-detected NIDDM patients did not differ from that in patients detected in routine care. In a Swedish study on screening-detected NIDDM subjects, only those who had IGT rather than manifest NIDDM could maintain fasting blood glucose less than or equal to 6 mM for 5 yr by hypocaloric dietary regulation alone. In those with screening-detected NIDDM, the delayed acute insulin release and net postprandial hyperglycemia were improved by addition of glipizide, and most managed to attain and maintain fasting blood glucose less than or equal to 6 mM for approximately 2 yr after such addition. However, after 4 yr, there was an increase in blood glucose, suggesting that preventive intervention either may not be possible or may have to start in the IGT phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Will sulfonylurea treatment of impaired glucose tolerance delay development and complications of NIDDM? 220 45

We have studied the effect of acute hyperglycemia on glomerular function in seven insulin-dependent diabetics with overt nephropathy during hyperglycemic or euglycemic clamp. In all patients glomerular filtration rate (GFR) was higher during hyperglycemia than during euglycemia (35.0 +/- 15.5 vs. 21.4 +/- 10.3 ml.min-1.1.73 m-2, P less than 0.01), whereas renal plasma flow did not change significantly. To establish which determinant of GFR is altered by hyperglycemia, fractional clearances of neutral dextrans of graded molecular size were determined in both glycemic states, and data were analyzed by a theoretical model of hindered transport of macromolecules through a porous membrane. Hyperglycemia significantly increased sieving coefficients of small dextran molecules (28-40 A in radius), whereas fractional clearances of large macromolecules (greater than 44 A) did not change. Theoretical analysis suggested that the ultrafiltration coefficient (Kf) and membrane permeability to small dextrans (less than 40 A) increased in hyperglycemia in respect to euglycemia. Because these results have been obtained in patients with severe renal failure and hypertension, our conclusions do not necessarily apply to the early phase of diabetic nephropathy.
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PMID:Glomerular response to hyperglycemia in human diabetic nephropathy. 222 Oct 91

There are three major obstacles to a recommendation for screening the elderly for NIDDM. The first is the conflicting evidence as to whether early detection and treatment reduce complications. The second is that treatment of hyperglycemia with attainment of euglycemia is difficult to achieve in the elderly. Nondrug therapy often fails because of lifelong eating habits, denture problems, fixed income, and physical handicaps. Drug therapy is fraught with the dangers of hypoglycemia and drug interactions. Compliance with therapy often is poor and leads to conflicts between physician and patient that may be detrimental in the treatment of other diseases in which intervention has proven worthwhile. The third obstacle is the lack of data regarding the adverse effects of labeling and noncompliance issues in the face of a positive screening test. Because obesity is a risk factor for NIDDM and hypertension in conjunction with NIDDM leads to atherosclerosis, screening and treatment for these two conditions are warranted whether or not NIDDM is present concurrently. Medicine is in a dynamic state of flux and, undoubtedly, conflicts over the benefits of early treatment and patient compliance will be resolved. Until then, there is no justification for screening for NIDDM in the elderly.
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PMID:Screening for non-insulin-dependent diabetes mellitus in the elderly. 222 50

Hyperglycemia is only one of several metabolic derangements that are prevalent in diabetes mellitus. Of these, hyperlipidemia, obesity, and co-existent hypertension may make more important contributions to complications than persistently elevated blood sugars. The role of hyperglycemia in the genesis of diabetic complications is uncertain and there is little evidence from prospective randomized controlled studies to support rigorous hypoglycemic treatment. Adverse consequences of pharmacologic therapy can be severe, including death, and are most frequent in the elderly. The group of elderly diabetic ambulatory patients is markedly heterogeneous and individualization of therapy is required. Obese persons require dietary therapy, and additional dietary manipulations are needed for patients with the complications of hyperlipidemia, hypertension, and nephropathy. Pharmacologic hypoglycemic therapy may be required to control symptoms, but its use in asymptomatic diabetic persons is for the most part unwarranted.
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PMID:Glycemic control in elderly people with diabetes. 222 56

1969 subjects underwent albumin index [A.I., urine microalbumin (mg/liter)/creatinine (g/liter)] in early morning urine, 75 g oral glucose tolerance test (OGTT), determination of plasma lipids (total cholesterol, triglyceride and high density lipoprotein-cholesterol) and a resting electrocardiogram. There was no history of treatment for diabetes mellitus and hypertension. The relationship between microalbuminuria, and hyperglycemia or high blood pressure at non-diagnostic level was examined. Then, plasma lipid levels or changes in electrocardiogram were correlated with the degree of microalbuminuria. Subjects were divided into 4 groups according to 75 gOGTT and into 3 groups according to blood pressure based on WHO definition, and A.I. was divided into 4 categories (0-9.9, 10.0-19.9, 20.0-49.9, and 50.0-199.9 mg/gCr). Mildly or moderately enhanced microalbuminuria (A.I.) was found in subjects with hyperglycemia or high blood pressure at non-diagnostic level. In normotensive subjects, neither hyperglycemia in fasting nor after glucose challenge increased urine microalbumin above normal range, while in borderline hypertensives, diabetic glucose intolerance produced 2 and 3 fold increases respectively compared with normotensives. There was a linear increase in urine microalbumin in relation to the glucose intolerance in newly diagnosed hypertensives. No correlation could be found between microalbuminuria and plasma lipid levels, while the prevalence of electrocardiographic changes increased 3 folds in group with the heaviest microalbuminuria compared with the other 3 groups excreting less microalbumin.
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PMID:Microalbuminuria in subjects with no history of diabetes mellitus and hypertension: the relationship with hyperglycemia and high blood pressure at non-diagnostic level. 222 27

In 102 patients with ischemic heart disease the severity of stenosis was classified into 7 grades (0, 25, 50, 75, 90, 99, 100%) in accordance with the AHA reporting system. The coronary angiograms were compared at first and second catheterization (intervals 2-84 months) and progression was considered present if the stenosis in the second study showed more than one grade increase in comparison with the first study. Fifty six patients met criteria for progression. Risk factors were obtained within the first second catheterization. Drug and diet therapy were evaluated by interview. No significant difference could be found between the progression (P) group and the nonprogression (N) group in relation to family history and obesity. A history of hypertension was more common in the P group. In respect to blood sampling, the values of total cholesterol, Apo B, CII, E and Apo B/AI were significantly higher in the P group than those in the N group at first and second catheterization. The percentage of patients showing abnormal levels of blood sugar and lipid were higher in the P group than the N group although the percentage of patients with drug and diet therapy were higher in the P group than in the N group. The percentage of patients with diet therapy for hyperglycemia and hyperlipidemia were higher in the P group, however weight increase was more common in the P group. These data suggest that sufficient diet and drug therapy is necessary for patients with risk factors.
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PMID:[Prevention of progression of coronary atherosclerosis by drug and diet therapy]. 223 14

When insulin was introduced in medical therapy in 1922, it permitted to save diabetics from premature death; however, it has allowed, after a certain period of time, for the appearance of a cohort of chronic complications connected more or less specifically to the degree of hyperglycemia. After a short review of the pathophysiology of the microangiopathy, the authors have tried to demonstrate, on the basis of numerous prospective and retrospective studies in the human as well as in the animal, that an important relationship exists between the degree of glycemic control and the severity of the classical complications, retinopathy, neuropathy and nephropathy. However, the most recent studies have stressed the role of some other factors, not well established in the past, as for example the potential negative impact on retinopathy of rapid normalization of glycemia, following a long period of poor metabolic control. Likewise, high blood pressure, smoking, genetic background, as well as probably also excess of protein intake, do play an important etiopathogenic role. Thus, the simplistic equation hyperglycemia = complications is not completely valid. Microangiopathic risk in insulin-dependent diabetics seems to be low as long as their HbAlc is below 7.5%, and they do not have hypertension and do not abuse tobacco. Finally, the general approach to therapy is redefined: Try to get as close as possible to near-normoglycemia by multiple insulin injections, without causing, however, major hypoglycemia; this should be done very early after the onset of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Control of diabetes and late complications]. 223 45


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