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)

Beta-thromboglobulin (BTG) and fibrinopeptide A (FpA) were studied in 68 non-insulin dependent diabetic patients (NIDD) aged 32-81 with a mean duration of diabetes of 9 +/- 0.8 SEM years and 44 healthy controls, comparable for age and sex. Diabetic patients were subdivided into subsets according to the presence of microvascular disease, macrovascular disease or the absence of these lesions. Patients with microangiopathy (micro- and/or macrovascular disease) had higher HbA1 (a-c) (p less than 0.01), higher blood pressure (p less than 0.05) than both healthy controls and uncomplicated diabetics. Plasma BTG was higher in diabetic patients than in healthy controls (p less than 0.02), and was higher in complicated than in non-complicated diabetic subjects. Fpa was higher in complicated than in non-complicated diabetes (p less than 0.05). No differences were observed between the two subsets of complicated patients. In conclusion, we have shown that increased plasma- and platelet-BTG levels are present in non-insulin dependent diabetic subjects, with normal renal function and that plasma BTG is higher in patients with than in those without vascular disease. Fibrinopeptide A, a sensitive marker of in vivo fibrin formation, was significantly increased in NIDD with vascular complications.
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PMID:Beta-thromboglobulin and fibrinopeptide A in diabetes mellitus as markers of vascular damage. 240 34

Perisinusoidal fibrosis is a vascular lesion observed in the liver of type I diabetic patients. To investigate whether this liver lesion is secondary to hyperglycemia or whether it represents a separate collagen vascular disorder, the authors studied the structure of liver sinusoids in genetically susceptible BB rats in which a spontaneous diabetes develops similar to human type I diabetes. Seven diabetic insulin-treated BB rats, 7 nondiabetic BB rats, and 6 control non-BB rats were studied. Histologic abnormalities of the collagen network were detected on trichrome-stained sections. Perisinusoidal collagen fibers were quantified ultrastructurally by the point-counting method. All control non-BB rats had normal livers; 86% of the diabetic as well as 71% of the nondiabetic BB rats displayed localized sinusoidal thickening corresponding ultrastructurally to perisinusoidal fibrosis; in these abnormal rats the percentage of collagen fibers per sinusoid unit was significantly higher than that in controls. Fibrous septa (2 diabetic and 5 nondiabetic BB rats) and liver nodulation (3 diabetic and 1 nondiabetic BB rats) were also observed. Perisinusoidal fibrosis is a frequent liver vascular abnormality in a strain of rats genetically predisposed to the development of type I diabetes. The lesion is independent of the presence of diabetes. These observations suggest that liver perisinusoidal fibrosis in patients with type I diabetes might be linked to a genetic abnormality rather than to hyperglycemia per se.
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PMID:Liver perisinusoidal fibrosis in BB rats with or without overt diabetes. 240 8

Between 1960 and 1976 117 patients underwent pituitary implantation with yttrium-90 (90Y) for treatment of proliferative retinopathy at the Hammersmith Hospital, London. Mean age at operation was 35 +/- 11 years (mean +/- SD), and mean duration of diabetes 18.6 +/- 10.0 years. Mean insulin dosage prior to implant was 67.2 +/- 24 units, falling to 30.4 +/- 14.9 units post-implant. Thirty-two per cent of patients are still living, 60% are deceased and 8% are lost to follow-up. The 5-year survival rate was 82%. Of the causes of death, 21% died of infection, adrenal insufficiency or hypoglycaemia, 12% of renal failure, and 47% of myocardial or cerebral vascular disease. Ophthalmological follow-up was carried out on the 100 patients operated on between 1965 and 1976. The mean age of this group at implant was 35 +/- 10.5 years, and mean duration of diabetes 17.2 +/- 8.7 years. Visual acuity in the better eye at operation was 6/12 or better in 84% of patients, and this percentage remained similar at the time of the 5 and 10 year follow-up. Blindness (6/60 or worse) in both eyes was present in 12% of patients at the time of 5 and 10 year assessments. By 5 years new vessels on the disc had improved from a mean grading of 2.7 +/- 1.6 to 0.8 +/- 1.2 (p less than 0.001), and by 10 years there was no disc neovascularisation in any eye. There was a similar improvement in the grading of hard exudates, microaneurysms and haemorrhages, but there was an increase in fibrous retinitis proliferans.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term follow-up of patients who underwent yttrium-90 pituitary implantation for treatment of proliferative diabetic retinopathy. 243 1

Plasminogen activator inhibitor-1 (PAI-1) is an important physiological inhibitor of fibrinolysis. It circulates in blood both in free active form and in inactive form complexed with tissue type plasminogen activator (t-PA). Control mechanisms for its synthesis and release from hepatocytes and endothelial cells are important in the pathogenesis of thrombosis. Possible risk factors for myocardial infarction include high insulin and PAI-1 levels, which correlate with one another in healthy subjects, and fibrinogen, which together with PAI-1, is an acute-phase reactant. We therefore studied the interrelationships between PAI-1, plasma insulin, and acute-phase proteins in 67 patients with angina pectoris. Plasma insulin correlated strongly (r = 0.59, p less than 0.001) with PAI activity, free PAI-1 antigen (r = 0.60, p less than 0.001), and total PAI-1 antigen (r = 0.58, p less than 0.001). The acute-phase proteins, fibrinogen and C-reactive protein, correlated significantly with t-PA antigen, total PAI-1 antigen, and PAI-1/t-PA complexes but not with PAI activity or free PAI-1. The results suggest that insulin stimulates synthesis and release of free PAI-1 (probably via hepatocytes as previously shown with cell culture) and that endothelial cell synthesis and release of t-PA, together with PAI-1, reflects a nonspecific acute-phase response to chronic vascular disease. Hyperinsulinemia found in patients with angina pectoris could play a role in the development of myocardial infarction via the induction of high plasma PAI-1 activity.
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PMID:Plasma plasminogen activator inhibitor-1 in angina pectoris. Influence of plasma insulin and acute-phase response. 247 Mar 43

Scanning Electron Microscopy (SEM) was used to study vascular casts of twenty-four autopsy eyes taken from patients with long-standing insulin-dependent Diabetes Mellitus. These casts were compared to casts of ten 'normal' autopsy eyes from patients without a history of diabetes or other vascular disease. The SEM findings in the choroidal vessels of the diabetic eyes included: increased tortuosity, focal vascular dilations and narrowings, hypercellularity, vascular loops and microaneurysm formation, 'drop-out' of choriocapillaries, and sinus-like structure formation between choroidal lobules in the equatorial area. In the iris, neovascularization was evident in the vascular casts in cases with clinically recognized rubeosis iridis. These findings indicate that there is significant involvement of the uveal tract in diabetic eyes. The present study strongly supports the Hidayat and Fine light microscopic observation that the diabetic choroid demonstrates significant vascular changes (e.g. narrowed vessels with possible 'drop-out' of capillaries and neovascularization). Changes in the diabetic choroid, especially in the choriocapillaris, may be a contributing factor in diabetic retinopathy, resulting in decreased oxygenation of the outer layer of the retina. Short reviews and updated information of diabetic eye disease provide some additional insights into the vascular problems in the eye.
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PMID:Diabetic choroidal and iris vasculature scanning electron microscopy findings. 248 64

The present prospective follow-up study was made to study the effect of glycaemic regulation on levels of factor VII, protein C and protein S in 15 insulin-dependent diabetic patients without manifestations of vascular disease. Patients were tested before and after 8 weeks of 'metabolic' intervention, whereby a near-normoglycaemic state was achieved. At baseline, values of cross-linked fibrin degradation products (XL-FDP) and levels of 'total' protein S were significantly increased and protein C values were decreased in the diabetic patients when compared to control subjects, whereas levels of factor VII and 'free' protein S were near normal. After 'metabolic' intervention a decrease of all haemostatic parameters were recorded, however XL-FDP levels did not decline to control levels and the imbalance of factor VII and protein C persisted. When patients with newly diagnosed diabetes (n = 8) were compared to those with long-term disease (n = 7) higher levels of factor VII, protein C and protein S were recorded in the latter group before and after metabolic intervention; at baseline the differences reached statistical significance for factor VII and protein S, and remained significant for factor VII after metabolic intervention. Before and after intervention XL-FDP levels were higher in patients with newly diagnosed disease than in patients with long-term diabetes. The correlation analysis revealed positive correlations of factor VII, protein C and protein S to cholesterol and triglycerides, of protein S to all glycaemic control parameters, negative correlations of protein C to glucose, and of XL-FDP to factor VII, protein C and protein S. The results indicate an imbalance of haemostasis towards thrombophilicity in insulin-dependent diabetic patients, not completely correctable by glycaemic control.
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PMID:The effect of near-normoglycaemic control on plasma levels of coagulation factor VII and the anticoagulant proteins C and S in insulin-dependent diabetic patients. 253 36

We report on unobserved, sudden, and unexpected deaths that occurred in a randomized multicenter trial. The long-term effects of aspirin plus dipyridamole on major vascular outcome variables were studied in 231 non insulin-dependent diabetic men with either a recent amputation for gangrene or active gangrene. Depending upon the definition of sudden death used, there were 14, 22, or 17 deaths in the drug group versus 6, 6, or 3 deaths in the placebo group (p = 0.04, 0.001, or 0.001, respectively). Total deaths from atherosclerotic vascular disease or deaths from all causes did not differ in the two treatment groups. Since this finding of a secondary end point is found only after multiple analyses of the data, it must be interpreted with caution. However, it is suggested that further studies on effects of antiplatelet agents on sudden deaths should be performed.
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PMID:V.A. Cooperative Study of antiplatelet agents in diabetic patients after amputation for gangrene: unobserved, sudden, and unexpected deaths. 253 10

Individuals with diabetes mellitus may have increased in vivo platelet activity. Abnormal platelet function could contribute to the increased incidence of vascular disease in diabetes mellitus. The biochemical mechanism(s) for platelet hyperactivation is unknown. We examined the hypothesis that platelet phosphoinositide turnover, a key signal-transducing mechanism involved in platelet activation, was abnormal in diabetic subjects. Platelets were harvested from 16 subjects with insulin-dependent diabetes mellitus (IDDM) and 19 healthy, nondiabetic control subjects of comparable age. Plasma beta-thromboglobulin (beta-TBG), a specific marker of platelet activity in vivo, was increased in IDDM (67.1 +/- 7.3 ng/ml) compared with control (41.0 +/- 6.0 ng/ml) subjects (P less than .005). [32P]orthophosphate (32Pi) incorporation into the individual phosphoinositides and phosphatidic acid (PA) reached isotopic equilibrium by 120 min for IDDM and control subjects. Specific activity (dpm 32P/micrograms phosphorus) of phosphatidylinositol 4-phosphate (PIP) and phosphatidylinositol 4,5-bisphosphate (PIP2) was not different between IDDM and control subjects. Under these conditions, basal 32Pi incorporation into PIP2 and PIP but not phosphatidylinositol (PI) or PA was significantly lower in IDDM subjects. There was significantly decreased [32P]PIP2 and [32P]PIP hydrolysis and decreased [32P]PA formation in IDDM after platelet stimulation with 4 U/ml human thrombin. There were no differences in [32P]PI hydrolysis between the two groups. The mass of PIP2 was reduced (P less than .005) in the platelets from IDDM (0.71 +/- 0.23 nmol/10(9) platelets) compared with control (1.65 +/- 0.53 nmol/10(9) platelets) subjects. Similarly, PIP was lower (P less than .001) in IDDM (0.66 +/- 0.09 nmol/10(9) platelets) than in control (2.92 +/- 0.43 nmol/10(9) platelets) subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased platelet phosphoinositide turnover and enhanced platelet activation in IDDM. 254 8

We measured simultaneous plasma beta-thromboglobulin (BTG) and adhesion of 51Cr-labelled, washed platelets to confluent, bovine aortic endothelial monolayers in 50 insulin-dependent diabetic patients and 30 normal subjects (respective mean ages (+/- SD) = 45.1 +/- 16.4 and 45.8 +/- 17.2 years). Compared to normal subjects without arteriosclerotic complications, diabetic patients had higher plasma BTG (34.8 +/- 1.8 (SEM) vs. 21.3 +/- 1.8 ng/ml) and platelet adhesiveness to endothelium (PAE) (3240 +/- 170 vs. 2430 +/- 120 X 10(3) platelets per well) (p less than 0.0002, respectively). Results in diabetic patients did not correlate with plasma glucose, hemoglobin AIa-c, known duration of disease, or sex; plasma BTG correlated with age (r = +0.36), and PAE correlated with plasma creatinine (r = +0.39). Those with clinically evident vascular disease, who were also older (47.8 +/- 2.6 (SEM) vs. 37.3 +/- 4.5 years, p less than 0.05), showed trends to higher plasma BTG (36.7 +/- 2.2 (SEM) vs. 28.8 +/- 3.4 ng/ml, p = 0.06) and PAE (3400 +/- 200 vs. 2800 +/- 280 X 10(3) platelets per well, p = 0.09). A strong correlation was found between plasma BTG and PAE in diabetic patients (r = +0.62, p less than 0.0001) either with or without vascular disease, which remained strong after statistical correction (partial Pearson correlation) for age and plasma creatinine, but not in normal subjects (r = +0.08, p greater than 0.1). These studies demonstrate that platelets in some diabetic patients are excessively adhesive to vascular endothelium, and that plasma BTG and platelet adhesiveness are intercorrelated.
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PMID:Plasma beta-thromboglobulin is correlated with platelet adhesiveness to bovine endothelium in patients with diabetes mellitus. 257 51

Numerous studies have demonstrated that poor glycemic control is associated with elevated plasma cholesterol levels in diabetic patients. Experiments have shown that cholesterol synthesis is increased in the small intestine of various diabetic animals. This increase is a generalized phenomenon occurring in all segments of the small intestine. Insulin therapy that normalizes blood glucose levels markedly decreases intestinal cholesterol synthesis in diabetic animals to a level similar to that observed in control animals. Studies have suggested that the hyperphagia that accompanies poorly controlled diabetes is the chief stimulus for the increase in intestinal cholesterol synthesis. However, the direct contact of the intestinal mucosa with nutrients is not the sole trigger for increasing cholesterol synthesis in the small intestine, suggesting that circulating and/or neurological factors play a role. The transport of newly synthesized cholesterol, most of which is in the chylomicron lipoprotein fraction, from the intestines to the circulation is increased in diabetic rats. The sterols associated with these chylomicrons are rapidly cleared from the circulation and delivered to the liver. The increased transport of chylomicrons from the intestine to the circulation in diabetic patients could potentially result in several alterations in lipid metabolism that may increase the risk of atherosclerotic vascular disease.
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PMID:Importance of small intestine in diabetic hypercholesterolemia. 264 36


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