Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is clearly recognized that patients with NIDDM have an increased risk for CHD. Recent data indicate that persons with glucose concentrations in the nondiabetic range also may be at higher risk for CHD. These associations may not represent cause and effect, however. Emerging data suggest that hyperglycemia and CHD may both arise from hyperinsulinemia/insulin resistance. In support of this hypothesis are studies showing that NIDDM and CHD have many risk factors in common, including age, elevated blood pressure, dyslipidemia, adiposity, and a central pattern of fat distribution. Moreover, these risk factors are frequent concomitants of hyperinsulinemia, itself a risk factor for CHD and perhaps for NIDDM. Although the duration of NIDDM has been infrequently related to risk of CHD, the authors hypothesize that duration of hyperinsulinemia/insulin resistance would be a more sensitive marker for risk of CHD. The relation of IDDM to CHD is a different situation. The etiological process leading to IDDM, namely the destruction of beta-cells in genetically predisposed persons, is not related to cardiovascular risk. However, IDDM patients still have an excess of CVD, the risk factors for which may vary according to the location of the diseases (e.g., LEAD vs. CHD). There is a strong relationship between proteinuria and CVD, which has led to a general theory of vascular complications in IDDM based on defective heparan sulfate metabolism (Steno hypothesis). Recent evidence challenges parts of this hypothesis, and the possibility is raised that a higher case-fatality rate in a subgroup of patients with both renal and CVD explains part of the renal connection, as does the general worsening of CVD risk factors.
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PMID:Diabetes mellitus and macrovascular complications. An epidemiological perspective. 139 12

A review of the putative risk factors associated with the development of coronary heart disease in diabetes is presented. Emphasis is given to the effect of nephropathy (persistent proteinuria) and hypertension on cardiovascular mortality in IDDM. Risk factors associated with CHD in NIDDM are also reviewed. Finally, possible reasons to explain the increased incidence of CHD associated with proteinuria in IDDM patients, including lipoprotein abnormalities, increased fibrinogen levels, increased platelet adhesiveness, and altered hemostatic variables, are discussed.
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PMID:Risk factors for coronary heart disease in diabetes mellitus. 152 26

Currently our knowledge of the role of lipid abnormalities as risk factors for CHD in diabetes is insufficient. We need to define exact risk parameters to target correctly the therapy of lipid disorders and to outline optimum therapeutic strategies. Therefore it is necessary to identify quantitative and qualitative abnormalities of lipoproteins and apoproteins which signify the risk of CHD and to define their predictive power in prospective trials. Obviously we need to know more about the pathophysiology of lipid abnormalities and the action of insulin. Because diabetic patients carry a high inherent risk of CHD, target values recommended for non-diabetic populations may not be optimal for diabetic populations, but should be lower. To date no primary or secondary intervention trials in diabetic populations have been carried out to show that the lowering of lipid values (serum and LDL cholesterol) will reduce the risk of CHD morbidity or mortality or will prevent the progression of CHD in diabetes. Since hypertriglyceridaemia and low HDL levels are typical abnormalities in NIDDM it is a unique target group to test whether lowering of triglycerides and raising of HDL cholesterol levels will reduce the risk of CHD. Therefore there is a pressing need for clinical trials in both IDDM and NIDDM to provide adequate information on the benefits of lipid-lowering therapy and to confirm treatment strategies.
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PMID:Hyperlipidaemia in diabetes. 208 5

The paper is concerned with quantitative characterization of lipoprotein (LP) spectrum, including the determination of the content of apoproteins A1 and B, in 69 women aged 40 to 59 with normal body mass, suffering from types I and II diabetes mellitus in the state of compensation of carbohydrate metabolism, with CHD and without signs of it, using a method of quantitative rocket immunoelectrophoresis. Atherogenic dyslipoproteinemia was observed in the presence of CHD in women with types I and II diabetes mellitus. In patients without clinical signs of CHD (in type I diabetes mellitus) serum atherogenic shifts were absent whereas in type II in spite of the absence of clinical signs of CHD disorders in the content and cholesterol transport function of HDLP particles were found.
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PMID:[The content of basic apoproteins A1 and B and lipids in the blood serum of women with type-I and -II diabetes mellitus and ischemic heart disease]. 251 68

On the basis of the available data (much of which is contradictory), I suggest that the following might summarize the role of Lp(a) in diabetes currently. 1. Lp(a) in IDDM: Concentrations are probably elevated. Concentrations are probably related to metabolic control. Concentrations are increased with microalbuminuria. 2. Lp(a) in NIDDM: Concentrations are not elevated. Concentrations do not change with metabolic control. Too few data exist to make an assessment of relation of Lp(a) to microalbuminuria in NIDDM. 3. Lp(a) and CHD in diabetes: Little current evidence shows that Lp(a) is a risk factor for CHD in diabetes. More studies--especially prospective studies with larger numbers of subjects--need to be done.
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PMID:Lipoprotein(a) and diabetes. An update. 849 27

It is well known that subjects with type 1 diabetes are at an increased risk of death from coronary heart disease in comparison to non-diabetic age-matched individuals because hyperglycaemia is believed to be a key risk factor for the development of micro- and macrovascular complications. On the other hand there is increasing evidence about the role of inflammatory mediators in the pathogenesis of atherosclerosis and the development of acute coronary syndromes. It has been recently suggested that IL-18 and sICAM-1 have a strong predictive value for cardiovascular diseases and deaths in patients with coronary artery disease and/or in apparently healthy men. The aim of our study was to estimate the serum levels of IL-18 and sICAM-1 in subjects with type 1 diabetes and their relatives, who share HLA diabetic susceptibility genes (with or without pancreatic autoantibodies), but still without glucose level disturbances, as an evaluation of the possible role of genetic predisposition to the presence of IL-18 in diabetic families. The study was carried out in 35 type 1 diabetic subjects, their 101 healthy first-degree relatives: 36 siblings and 65 parents and the control group consisted of 31 healthy volunteers. We have found increased IL-18 and sICAM-1 levels in subjects with type 1 diabetes and their first degree relatives, who share diabetic HLA haplotypes: DRB1*03/DRB1*04 or DRB1*03/*04/DQB1*02 independently of their autoimmune status. There was a strong positive correlation between IL-18 and sICAM-1 levels in diabetic subjects and their first degree relatives without glucose level disturbances. To our knowledge this is the first study, which suggests that sICAM-1 elevations could be a result of IL-18 overproduction in type 1 diabetic subjects and their first degree relatives. Since in previous studies IL-18 and sICAM-1 were found to be predictors of death in subjects with CHD, one could speculate that high levels of IL-18 observed in subjects with genetic predisposition, but still with normal glucose levels, are an in addition to hyperglycaemia, pathogenic factors responsible for a higher risk of acute coronary events in subjects with diabetes type 1.
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PMID:Interleukin 18 and sICAM-1 serum levels in families with type 1 diabetes mellitus. 1635 56

Modified lipoproteins induce autoimmune responses including the synthesis of autoantibodies with pro-inflammatory characteristics. Circulating modified lipoprotein autoantibodies combine with circulating antigens and form immune complexes (IC). We now report the results of a study investigating the role of circulating IC containing modified lipoproteins in the progression of carotid intima-media thickness (IMT) in patients enrolled in the Epidemiology of Diabetes Interventions and Complications (EDIC) Trial, a follow-up study of the Diabetes Control and Complications Trial (DCCT). This cohort includes 1229 patients with type 1 diabetes in whom B-mode ultrasonography of internal and common carotid arteries was performed in 1994-1996 and in 1998-2000. Conventional CHD risk factors, antibodies against modified forms of LDL and modified lipoprotein IC were determined in 1050 of these patients from blood collected in 1996-1998. Cholesterol and apolipoprotein B content of IC (surrogate markers of modified ApoB-rich lipoproteins) were significantly higher in patients who showed progression of the internal carotid IMT than in those showing no progression, regression or mild progression. Multivariate linear and logistic regression modeling using conventional and non-conventional risk factors showed that the cholesterol content of IC was a significant positive predictor of internal carotid IMT progression. In conclusion these data demonstrate that increased levels of modified ApoB-rich IC are associated with increased progression of internal carotid IMT in the DCCT/EDIC cohort of type 1 diabetes.
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PMID:Immune complexes containing modified lipoproteins are related to the progression of internal carotid intima-media thickness in patients with type 1 diabetes. 1653 Jul 70

Measurement of coronary artery calcium score (CACS) by electron beam tomography has been shown to a powerful predictor of coronary heart disease events in asymptomatic non-diabetic subjects. In type 2 diabetes, measurement of CACS was found to be a powerful predictor of cardiovascular events which could enhance prediction provided by established risk models. 23% of type 2 diabetic subjects with low CACS were found to be at low risk for cardiovascular events. Moreover mortality was similar for type 2 diabetic and non-diabetic subjects with undetectable coronary artery calcification. Conversely type 2 diabetic subjects with high CACS were identified who were at high cardiovascular risk. Thus not all those with type 2 diabetes are at similar cardiovascular risk. Measurement of CACS enables cardiovascular risk in type 2 diabetes to be stratified so that the level of preventive therapy could be reduced in some and intensified in others. Although prospective data for the power of CACS to predict CHD events in type 1 diabetes are lacking, measurement of CACS could help in deciding on preventive therapy in type 1 diabetes.
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PMID:Coronary artery calcium and cardiovascular risk in diabetes. 1996

The C-allele of rs266729 is associated with CHD, while the G-allele of rs17300539 is associated with metabolic traits. We examined these in type 1 diabetes. For rs266729, the C-allele was associated with 8-fold increase in CHD. For rs17300539, the G-allele was associated with increases in triglycerides and waist circumference.
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PMID:Association of the adiponectin rs266729 C>G variant and coronary heart disease in the low risk 'Golden Years' type 1 diabetes cohort. 2120 76