Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mean peak systolic to end-diastolic (S/D) umbilical artery ratio was measured in 291 Doppler studies performed during pregnancy in 35 insulin-dependent diabetic women. A normal decline was observed in the umbilical artery S/D ratio, from 4.2 +/- 0.21 at 18 weeks to 2.18 +/- 0.22 at 38 weeks. There was no significant correlation between mean third-trimester S/D and either glycosylated hemoglobin (r = 0.25) or mean blood glucose levels (r = 0.15). Fetuses of women with vascular disease (class F/R or chronic hypertension) had a mean third-trimester S/D of 3.0 or higher in five of ten cases, compared with three of 25 in patients with uncomplicated diabetes (P less than .03). Mean second- and third-trimester S/D ratios differed significantly in patients with and without vascular disease: 4.34 +/- 0.7 and 3.2 +/- 0.65 versus 3.72 +/- 0.42 and 2.55 +/- 0.32, respectively (P less than .03). Two of three women without vascular disease who demonstrated an elevated mean S/D ratio developed preeclampsia and delivered appropriate for gestational age infants. In women with vascular disease, four of five with an abnormal mean third-trimester umbilical artery S/D ratio were delivered of growth-retarded infants, whereas all five with normal umbilical artery S/D ratios had appropriate for gestational age infants. In three of the abnormal cases, elevated S/D ratios were present in the second trimester before ultrasound documentation of fetal growth retardation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Doppler umbilical artery velocimetry in pregnancy complicated by insulin-dependent diabetes mellitus. 265 28

The purpose of this study was to determine whether the obese Zucker rat (OZR) develops diabeteslike peripheral vascular disease and evaluate the effects of exercise training (treadmill running, 15 m/min, 17% grade, 60 min/day, 5 days/wk, for 6 or 12 wk) on skeletal muscle vascular disease. Capillary density (CD) and capillary basement membrane (CBM) thickness were measured in the plantar muscle of sedentary and trained OZR and sedentary lean Zucker rats (LZRs). At 11 wk old, when profoundly obese, hyperinsulinemic, and insulin resistant, OZRs had lower CD and thicker CBM than LZRs. These characteristics are consistent with the expression of human diabetic microangiopathy and imply altered diffusion capacity due to increased diffusion distance and changes in the capillary wall. Between 11 and 18 wk of age, OZRs became hyperglycemic. No age-related changes in CD were observed in lean or obese animals, and OZRs had lower CDs than LZRs at 18 wk of age. CBM thickness decreased from 11 to 18 wk of age in both lean and obese animals, but the decline was proportionally greater in OZRs, and the CBM of obese animals was only slightly thicker than in lean 18-wk-old animals. Exercise training did not alter CD or CBM thickness in 11-wk-old animals. In contrast, training for 6 or 12 wk increased both CD and CBM thickness in 18-wk-old animals, normalizing CD but further increasing CBM thickness relative to LZRs. Correlational analysis revealed that CBM thickness is related to basal insulin concentration (r = .29, P less than .05) but not to basal glucose (r = .12, P greater than .05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Capillary basement membrane thickness and capillary density in sedentary and trained obese Zucker rats. 266 Dec 84

The Paris Prospective Study is a long-term investigation of the incidence of coronary heart disease in a large population of working men. The first follow-up examination involved 7,038 men, aged 43-54 years. Subjects with impaired glucose tolerance or diabetes (n = 943) were selected from the total population for a separate analysis of coronary heart disease mortality risk factors. During a mean follow-up of 11 years, 26 of these 943 subjects with abnormal glucose tolerance died from coronary heart disease. Univariate analysis showed that plasma triglyceride level (p less than 0.006), plasma cholesterol level (p less than 0.02), and plasma insulin level both fasting and 2-h post-glucose load (p less than 0.02), were significantly higher in subjects who died from coronary heart disease compared to those who did not. In multivariate regression analysis using the Cox model, plasma triglyceride level was the only factor positively and significantly associated with coronary death. The distribution of plasma triglyceride levels was clearly higher for the subjects who died from coronary heart disease compared to those who did not die from this cause or were alive at the end of the follow-up. This new epidemiological evidence that hypertriglyceridaemia is an important predictor of coronary heart disease mortality in subjects with impaired glucose tolerance or diabetes suggests a possible role of dyslipidaemia in the excessive occurrence of atherosclerotic vascular disease in this category of subjects.
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PMID:Hypertriglyceridaemia as a risk factor of coronary heart disease mortality in subjects with impaired glucose tolerance or diabetes. Results from the 11-year follow-up of the Paris Prospective Study. 266 16

In the present study the effects of a short term intensive glycaemic control obtained with subcutaneous insulin therapy on lipids and apoprotein levels, platelet aggregation, platelet sensitivity to prostacyclin and platelet thromboxane production were investigated in 20 patients with type 2 diabetes and vascular disease. In 11 out of the 20 patients there was a significant improvement of glycaemic control (fructosamine reduction). Only with tight improvement of glycaemic control there was significant change in the concentration of ADP and collagen required to produce 50% of the maximum aggregation wave response, in the responsiveness of platelet to PGI2 and in the TxB2 synthesis. Lower Apo B levels were also shown in the tight control group suggesting that Apo B changes may have influenced platelet aggregation and thromboxane synthesis.
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PMID:Platelet function in patients with type 2 diabetes mellitus: the effect of glycaemic control. 266 42

The prevalence of smokers among patients with diabetes is found to be lower than in the population as a whole. Diabetic patients have increased morbidity and mortality from cardiovascular diseases and, in the majority of investigations, smoking is found to be a risk factor in this relationship which does not differ quantitatively from that found in non-diabetics. On the basis of the literature, it has not proved possible to quantitate smoking as a risk factor for the development of peripheral arteriosclerotic vascular disease. Smoking involves hormonal and metabolic changes which are of particular interest in relation to diabetes mellitus. Thus, smoking stimulates the secretion of the antiinsulin hormones, particularly catecholamines, resulting in subcutaneous vasoconstriction which may be unfortunate as it influences insulin absorption. Patients who smoke do not, however, appear to present poorer glycaemic control than non-smokers. A few investigations have shown that smokers have greater insulin requirements than non-smokers. In type 1 (insulin-dependent) diabetes, there is evidence to suggest that diabetic nephropathy and proliferative retinopathy occur more frequently in smokers than in non-smokers. Smoking aggravates the pre-existing more pronounced osteoporosis which occurs in female insulin-dependent patients. It is therefore advantageous to advise diabetic patients against smoking from the point of view of diabetes as such.
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PMID:[Smoking and diabetes mellitus]. 268 32

This review summarized aspects of the widening scope, phenotypic expression, natural history, recognition, pathogeneses, and heterogenous nature of maturity-onset diabetes of the young (MODY), an autosomal dominant inherited subtype of NIDDM, which can be recognized at a young age. There are differences in metabolic, hormonal, and vascular abnormalities in different ethnic groups and even among Caucasian pedigrees. In MODY patients with low insulin responses, there is a delayed and decreased insulin and C-peptide secretory response to glucose from childhood or adolescence, even before glucose intolerance appears; it may represent the basic genetic defect. The nondiabetic siblings have had normal insulin responses for decades. The fasting hyperglycemia of some MODY has been treated successfully with sulfonylureas for more than 30 years. In a few, after years or decades of diabetes, the insulin and C-peptide responses to glucose are so low that they may resemble those of early Type I diabetes. The rate of progression of the insulin secretory defect over time does distinguish between these two types of diabetes. In contrast are patients from families who have very high insulin responses to glucose despite glucose intolerance and fasting hyperglycemia similar to those seen in patients with low insulin responses. In many of these patients, there is in vivo and in vitro evidence of insulin resistance. Whatever its mechanism, the compensatory insulin responses to nutrients must be insufficient to maintain normal carbohydrate tolerance. This suggests that diabetes occurs only in those patients who have an additional islet cell defect, i.e., insufficient beta cell reserve and secretory capacity. In a few MODY pedigrees with high insulin responses to glucose and lack of evidence of insulin resistance, an insulin is secreted which is a structurally abnormal, mutant insulin molecule that is biologically ineffective. No associations have been found between specific HLA antigens and MODY in Caucasian, black, and Asian pedigrees. Linkage studies of the insulin gene, the insulin receptor gene, the erythrocyte/Hep G2 glucose transporter locus, and the apolipoprotein B locus have shown no association with MODY. Vascular disease may be as prevalent as in conventional NIDDM. Because of autosomal dominant transmission and penetrance at a young age, MODY is a good model for further investigations of etiologic and pathogenetic factors in NIDDM, including the use of genetic linkage strategies to identify diabetogenic genes.
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PMID:Maturity-onset diabetes of the young (MODY). 268 21

A study has been made of hypertension and its associated vascular risk in 2319 male and 2412 female participants in the WHO Multinational Study of Vascular Disease in Diabetics. Rates of hypertension were higher in non insulin-dependent diabetics (NIDDs) compared with insulin-dependent diabetics (IDDs). On average, diastolic blood pressures were lower in IDDs than NIDDs. The frequency of isolated systolic hypertension varied between 2.5% and 5.6%. In a 6 to 7 year mortality follow-up, hypertension was significantly associated with an increased risk of circulatory death, even allowing for its association with proteinuria.
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PMID:Blood pressure, proteinuria and their relationship with circulatory mortality: the WHO Multinational Study of Vascular Disease in Diabetics. 269 43

Long-term hyperglycemia is the main cause of diabetic late complications (angiopathy, neuropathy). The problem of lifelong management of diabetes is to guarantee near-normal glycemia. Since the introduction of self-monitoring of blood glucose by means of extracorporeal devices on the basis of strips, an important improvement of metabolic management of diabetic patients has become possible. In order to further improve the control of glycemia, the following steps of an evolving system of electrochemical glucose sensing and monitoring should be envisaged: (1) fast-acting extracorporeal glucometers for incidental analyses, (2) intracorporeal sensors for short-term but easily repeated use to follow any kind of open-loop insulin therapy and to provide appropriate hypoglycemia-warning signals, (3) intracorporeal sensors as an essential part of automated feedback-controlled systems for insulin delivery. Approximately 4000 patients per million of the population might benefit from the latter version of intracorporeal glucose sensors. In closed-loop blood glucose control, however, pathophysiological problems may arise from the sole application of negative feedback control in the glucose-insulin algorithm.
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PMID:Implications of an intracorporeal glucose sensor in the management of diabetic patients. 270 67

Among 163 insulin-dependent (type I) diabetics (average age 43.5 years; average duration of diabetes 17.5 years), 40 (24.5%) died within ten years from the consequences of micro- and (or) macro-angiopathies. The death-rate among hypertensives was twice that among normotensives: 21 of 53 patients (39.6%) with blood pressures above 160/95 mmHg, but 19 of 110 patients (17.3%) with normal pressures. Proliferative retinopathy at the onset of the study was also a predictive marker of a poor prognosis. The death-rate increased threefold for patients with retinopathy if they also had hypertension: 13 of 30 (43.3%) with background retinopathy and hypertension died, compared with 9 of 68 without hypertension (13.2%; P less than 0.01). Independently of hypertension the death-rate for patients with persistent proteinuria (greater than 0.5 g/24 h) was about threefold that among those without it. The highest death-rate (56.7%) was among the 30 patients with proteinuria and hypertension. Stepwise linear regression analysis demonstrated that the correlation between death from micro- and macro-vascular disease and the known risk factors was entirely determined by blood pressure and proteinuria.
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PMID:[Significance of proteinuria and hypertension in the prognosis of type 1 diabetes. Results of a 10-year follow-up study on micro- and macrovascular disease mortality]. 276 53

The major surfactant protein with a molecular weight of 35 kd and also saturated phosphatidylcholine and phosphatidylglycerol were analyzed in specimens of amniotic fluid; 68 were from cases of maternal diabetes, 41 from preeclampsia or maternal hypertension, 26 from premature rupture of the fetal membranes, and 45 from normal pregnancies. The relationship between the individual surfactant components was studied after covariance adjustment for the length of gestation. In severe early-onset preeclampsia, the 35 kd surfactant protein/saturated phosphatidylcholine ratio was significantly higher than in the other pregnancies. In diabetic pregnancies (classes B to D without preeclampsia), the phosphatidylglycerol/saturated phosphatidylcholine ratio was lower than in the other pregnancies. Isolated surfactant complex showed similar abnormalities. In severe early-onset preeclampsia and insulin-dependent diabetes without vascular disease, the phosphatidylglycerol/saturated phosphatidylcholine ratio correlated negatively with fetal growth. In four samples of amniotic fluids from cases of severe early-onset preeclampsia, the 35 kd protein falsely predicted lung maturity. All had abnormally high 35 kd protein/saturated phosphatidylcholine ratios (greater than 2 SD of controls). According to the present results, the 35 kd protein may give a false mature test result in severe preeclampsia.
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PMID:Surfactant proteins in the diagnosis of fetal lung maturity. II. The 35 kd protein and phospholipids in complicated pregnancy. 280 45


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