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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The use of insulin by diabetics has largely removed the threat of death from ketotic coma but cardiovascular dysfunction remains a major cause of death in patients with diabetes. Recent research has indicated a generalized membrane defect, which may cause abnormalities of calcium metabolism in nerves, cardiac and smooth muscle as well as endothelial cells and thus may lead respectively to the development of neuropathy, primary cardiomyopathy, microangiopathy and atherosclerosis in the diabetic population. Each of these pathogenic processes, which are associated with insulin deficiency, alone or in combination with others, may result in cardiac dysfunction in chronic diabetes. Activation of the sympathetic nervous system and abnormalities in catecholamine metabolism have been identified in diabetes; their involvement in the genesis of cardiac pump failure as well as large and small vessel disease is likely. The membrane defects as indicated by changes in both plasma membrane and glycocalyx in diabetic cardiomyopathy appear to be complex and may involve alterations in the metabolism of lipids and pyrimidine nucleotides. It seems that intracellular calcium overload is intimately involved in the development of diabetic cardiomyopathy; however, a concentrated research effort is required to understand the primary biochemical lesion in the pathogenesis of cardiac dysfunction in diabetes. In the meantime, a heightened awareness on the part of clinicians concerning the susceptibility of diabetic patients to cardiovascular problems may help in reducing mortality and morbidity in the diabetic population.
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PMID:Pathogenesis of cardiac dysfunction in diabetes mellitus. 385 Jul 73

A 30-year-old man presented at the diagnosis of an insulin dependent diabetes mellitus with pronounced and multiple complications, such as retino-, nephro-, dermo- and neuropathy. His diabetes had a malignant course and he died from uremia within one year after diagnosis. There were no signs of atherosclerosis at autopsy but in several organs there were pronounced diabetic small vessel lesions.
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PMID:Malignant diabetes mellitus--a case report. 400 39

This review examines the pathology, clinical effects and physiological disturbances produced by vascular disease and autonomic neuropathy in the lower limb in diabetic subjects. Atherosclerosis is a major factor in causing foot lesions in diabetics. The distribution of the disease frequently makes vascular reconstructive surgery difficult or impossible but an aggressive approach to reconstruction is justified because the results of major amputations are bad. Arterial calcification probably has no significant effect on the blood supply to the foot. There is some evidence that disease of arteries in the foot may be associated with the development of ulcers or gangrene. Disease of the arterioles and capillaries is frequent, but there is little evidence that this microangiopathy causes lesions. Autonomic neuropathy affecting the limb is also common, and although there are several mechanisms by which this might predispose to ulcers or gangrene, there is little evidence of such a direct relationship. In a patient presenting with ulceration or gangrene of the foot it is often impossible to determine the relative roles of vascular disease, affecting large or small vessels, and neuropathy, either somatic or autonomic, in the development of the lesion. Further progress depends on the development of more direct methods for assessing microvascular and autonomic nervous function.
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PMID:Vascular disease and vascular function in the lower limb in diabetes. 652 89

Patients with Type I, i.e., insulin-deficient diabetes, Type II or non-insulin-deficient diabetes, and impaired glucose tolerance or so-called chemical diabetes are variably predisposed to develop macroangiopathy, i.e., atherosclerosis, microangiopathy or basement membrane thickening, and neuropathy. Once these morphologic changes appear, they in all probability will remain irreversible even when precise regulation is attained. Hence prevention is the only realistic goal.
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PMID:Diabetic complications and their prevention or reversal. 740 16

Human serum paraoxonase is physically associated with HDL and has been implicated in the detoxification of organophosphates and possibly in the prevention of LDL lipid peroxidation. We investigated the serum activity and concentration of paraoxonase in 78 patients with type 1 diabetes mellitus, 92 with type 2 diabetes, and 82 nondiabetic control subjects. Paraoxonase activity was generally lower in diabetics than in control subjects. This decrease was unrelated to differences in paraoxonase phenotype distribution or its serum concentration. Rather, the difference in paraoxonase activity was explained by its specific activity, which was lower in diabetics, indicating either the presence of a circulating inhibitor or disturbance of the interaction of paraoxonase with HDL affecting its activity. Paraoxonase specific activity was lowest in patients with peripheral neuropathy, suggesting an association of paraoxonase with neuropathy. In control subjects but not patients with diabetes, paraoxonase correlated with HDL cholesterol and apolipoprotein A-1. Our results indicate that the low paraoxonase activity in diabetes is due to decreased specific activity. In other studies low serum paraoxonase activity has been associated with increased susceptibility to atherosclerosis, and the present results also suggest an association with peripheral neuropathy, which could be due to reduced capacity to detoxify lipid peroxides in diabetes.
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PMID:Serum paraoxonase activity, concentration, and phenotype distribution in diabetes mellitus and its relationship to serum lipids and lipoproteins. 758 60

Human cytomegalovirus (HCMV) can establish lifelong persistence after primary infection with reactivation occurring as a result of immunosuppression. There is much evidence that molecular interactions between the immune system and the HCMV are responsible for immune escape. HCMV in many cells especially in mononuclear blood cells during latency are frequently the source of transmission and spreading and results in a variety of disorders. In this review some data about acute infection in immunocompetent host (mononucleosis, hepatitis), about intrauterine HCMV infection, about infection and endogenous reinfection in bone marrow and solid organ transplant recipients (pneumonitis) and about HCMV disease in AIDS patients (encephalitis, neuropathy, retinitis, colitis) are investigated. Moreover, HCMV associated vasculitis is described in patients with myocarditis, rheumatoid arthritis or polyradiculopathy. HCMV could play an important role in atherosclerosis. Several types of human malignancy have been linked to HCMV and it has been shown that HCMV ie genes upregulate expression of cellular oncogenes. The diagnosis of HCMV infection is carried out by viremia in cell culture using immediate early antigen staining, by antigenaemia which appears to be an early quantitative and predictive tool, by HCMV DNA detection using hybridization and PCR, and by IgM and IgG antibody evaluation. Two antiviral drugs are used for treatment: ganciclovir and phosphonoformic acid; few resistant clinical isolates have been reported. Specific gammaglobulin activity is discussed. HCMV vaccine is not available.
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PMID:[Current status of human cytomegalovirus disease]. 759 23

Patients suffering from the severe complications associated with both insulin- (IDDM) and non-insulin-dependent diabetes mellitus (NIDDM): nephropathy, retinopathy, neuropathy, and atherosclerosis are still largely left without a prospect of an efficient treatment. This is the case even if it has been assumed for decades and now finally proved by the results from the Diabetes Control and Complications Trial (DCCT) that hyperglycemia is the single main cause of these complications. Improved glycemic control as a result of intensive insulin treatment has the potential to reduce the incidence and progression of complications, but implementation and monitoring of improved glycemic control in all groups of IDDM and NIDDM patients in different communities will be difficult and expensive. Results from the recently terminated DCCT have shown that even with intensive insulin treatment, there will be a significant burden of complications on the diabetic population. It will, therefore, still be of immense importance for the long-term quality of life for the diabetic patient that additional possibilities are developed for prevention and intervention against diabetic complications. Almost two decades of research, animal model testing, and clinical trials have been conducted on various efficient aldose reductase inhibitors. Now the concept of inhibition of formation of advanced glycosylation endproducts on proteins and lipids resulting from extra- and intracellular hyperglycemia is entering the scene as an alternative or perhaps supplementary approach to reduce the occurrence of diabetic complications. An overview of the results from these two fields of research and associated drug-development programs will be presented along with thoughts on possible future developments.
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PMID:Diabetic late complications: will aldose reductase inhibitors or inhibitors of advanced glycosylation endproduct formation hold promise? 759 49

The prevalence of diabetic microangiopathy (retinopathy, microalbuminuria, and neuropathy) and macroangiopathy (ischemic changes in EKG) in patients with diabetes mellitus was compared between patients newly found on occasion of mass-screening without any symptoms and signs in Funagata, Japan, and patients who visited the outpatient clinic of our university hospital. The mean fasting blood glucose level in the Funagata group was lower, and the mean duration of diabetes was shorter. The prevalence of every microangiopathic complication was significantly lower in the Funagata group than in the outpatient clinic group. However, the prevalence of ischemic changes in EKG was not different between the two groups. The conclusion that prevalence of diabetic microangiopathic complications was primarily related to the degree and duration of hyperglycemia seemed to be in accordance with the results of the Diabetes Control and Complications Trial (DCCT). The role of hyperglycemia for pathogenesis of macroangiopathy and atherosclerosis has been controversial. Not only hyperglycemia but also hypertension, dyslipoproteinemia, and other factors due to insulin resistance resulting from visceral fat syndrome, might be responsible for the occurrence of atherosclerosis.
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PMID:[Risk factor: diabetes mellitus]. 769 23

The Diabetes Control and Complications Trial (DCCT), a multicenter, randomized, controlled clinical trial, demonstrated that intensive diabetes therapy delays the onset and slows the progression of retinopathy, nephropathy, and neuropathy in patients with insulin-dependent diabetes mellitus. This study presents the effect of intensive therapy on atherosclerosis-related events and associated risk factors. Patients (n = 1,441) between the ages of 13 and 39 years with insulin-dependent diabetes mellitus were randomly assigned to conventional or intensive diabetes treatment. The patients were free of cardiovascular disease at baseline. Patients with hypertension, hypercholesterolemia, or obesity were excluded. Average length of follow-up was 6.5 years (range 3.5 to 9). The study used standardized definitions of macrovascular events, verification of such events, and central laboratories for determination of lipids and the grading of electrocardiograms. The number of combined major macrovascular events was almost twice as high in the conventionally treated group (40 events) as in the intensive-treatment group (23 events), although the differences were not statistically significant (p = 0.08). There were no differences in the cumulative incidence of hypertension. Mean total serum cholesterol, calculated low-density lipoprotein cholesterol, and triglycerides were significantly reduced in the intensive-treatment group (p < or = 0.01), as was the development of low-density lipoprotein cholesterol levels > 160 mg/dl. Weight gain was significantly increased in the intensive-treatment group (p < 0.001). There were no differences in cigarette smoking habits, consumption of alcohol, or aspirin use between treatment groups. The reduction in some, but not all, cardiovascular risk factors suggests a potential beneficial effect of intensive therapy on macrovascular disease in insulin-dependent diabetes mellitus.
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PMID:Effect of intensive diabetes management on macrovascular events and risk factors in the Diabetes Control and Complications Trial. 773 97

Small concentrations of albumin detected in the urine predict renal dysfunction and reflect vascular abnormalities such as atherosclerosis, retinopathy and, probably, neuropathy. Although microalbuminuria is not specific for diabetic complications, it has been most extensively studied in diabetics. The rate of urinary albumin excretion can also be used to determine therapeutic response to pharmacologic and lifestyle interventions such as diet, smoking cessation and physical activity. The pathophysiology of microalbuminuria and its clinical significance in diabetes is presented, along with a discussion of measurement issues and implications for clinical management. An algorithm for the evaluation of diabetic patients is included.
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PMID:Microalbuminuria and diabetes mellitus. 824 73


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