Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to investigate the factor VIII complex trend in atherosclerosis, 96 patients suffering from atherosclerosis, divided in 6 groups (angina pectoris, previous myocardial infarction, transient ischemic attacks, previous cerebral thrombosis, diabetes without symptoms of vascular injury and diabetes with vascular complications), were studied and compared to a control group of normal subjects. Plasma levels of Factor VII Coagulant (VIII C), Factor VIII-Related von Willebrand Factor (VIII-RWF) and Factor VIII-related Antigen (VIII ARg) were measured in all subjects. A significant rise of VIII RAg was noticed in all groups of patients as compared to the control group: this increase appears to be related to the severity of vascular injury. A significant rise of VIII RWF, parallel to the VIII RAg increase, was also noticed in all groups. Besides, all groups of patients showed a significant and uniform increase of VIII C. The average ratio of VIII RAg/VIII C was raised in all groups, except diabetics without complications; but the increase was statistically significant only in those patients with a heavier vascular injury which is related to the marked rise of VIII RAg in such clinical situations. The findings of this study are discussed in relation to the literature data. The significance of the determination of VIII RAg/VIII C ratio and of the VIII RAg assay as methods for monitoring the severity of the vascular injury in atherosclerosis are also discussed.
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PMID:[The factor VIII complex in atherosclerosis]. 681 35

Therapy of genetic diseases may be attempted at three different levels in the evolution of the disease process. At the first level, after clinical manifestations have appeared, methods are symptomatic and include diet, drugs, surgery, and avoidance of hazardous substances. At the second level, midway between the origin of the disease and the appearance of clinical manifestations, therapy consists of administration of a normal gene product, such as insulin in diabetes and factor VIII in hemophilia. At the third level, the origin of the disease, methods involve correcting the gene defect and are currently under investigation.
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PMID:Therapy of genetic diseases: a three-level approach. 692 69

The deterioration of the circulation in small and large vessels in diabetes seems to be related to abnormalities of the function of the endothelial cells and of the platelets. The endothelial factor VIII R:Ag, enhancing platelet adhesion, is increased, while fibrinolysis is decreased. The balance between thromboxane (platelet-aggregating) and prostacyclin (desaggregating) is also shifted in a similar way. These changes all favour increased deposition and delayed removal of platelets and fibrin on the intima, and they might contribute markedly to the development of diabetic angiopathy. Some new drugs seem to normalize the endothelial fibrinolytic activity, and long term studies are in progress to evaluate if this improvement is parallelled by a delayed or absent development of vascular complications.
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PMID:On some factors related to the pathogenesis of diabetic angiopathy. 697 42

The properties of 125I-insulin binding were assessed in endothelial cells prepared from the veins and the arteries of human umbilical cords. The endothelial nature of both the natural and venous cultures were documented by the presence of characteristic endothelial features, including Weibel-Palade bodies, factor VIII antigen, and morphology. Both arterial and venous cells possessed typical receptors for insulin on the basis of specificity of binding, curvilinear Scatchard plots, affinity profiles, pH dependency, and dissociation kinetics. Arterial cells bound at least 2.5 times more insulin than did venous cells, whether studied at 4 h, 24 h, or 72 h after in vitro plating. We conclude that (1) specific receptors for insulin are present on human arterial as well as human venous endothelial cells and (2) the concentration of insulin receptors varies among endothelial cells derived from different vascular sources.
Diabetes 1980 Dec
PMID:Differential binding of insulin to human arterial and venous endothelial cells in primary culture. 700 74

Haemostatic parameters were assessed before insulin induced hypoglycaemia and 0, 1 and 2 hr after discontinuation of insulin infusion in 7 non-diabetics, aged 28 (22-31) years (mean and range), and 8 juvenile diabetics, aged 31 (27-35) years, with a mean duration of diabetes of 4 years. The patients were normoglycaemic for at least 10 hr before the study. Platelet aggregation in vitro was induced by lower adenosine diphosphate (ADP) concentrations in the diabetics than in the controls before hypoglycaemia and 0 and 60 min after insulin infusion. Platelet counts decreased significantly in the diabetics after hypoglycaemia, whereas no changes were seen in the control group. The activated partial thromboplastin time (APTT) was reduced in both groups and significantly lower in the diabetics than in the controls 120 min after insulin infusion. Fibrinogen and factor VIII R:Ag increased after insulin infusion; highest values were seen in the diabetics. The euglobulin clot lysis time (ELT) was reduced in both groups during insulin infusion; 120 min after end of insulin infusion ELT was significantly longer in the diabetics than in the control group.
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PMID:Changes in platelet function, blood coagulation and fibrinolysis during insulin-induced hypoglycaemia in juvenile diabetics and normal subjects. 705 10

Anticoagulant response to activated protein C (APC) was studied in 40 healthy subjects and 67 patients with insulin-dependent diabetes mellitus (IDDM) using a modified activated thromboplastin time assay. Results are expressed in terms of the APC sensitivity ratio (APC SR). In addition, plasma levels of protein C, total and free protein S (PS), coagulation factors V and VIII, and prothrombin fragment 1+2 (F1+2) were measured. Patients with IDDM and a urinary albumin excretion rate (UAER) < 30 mg/24 h showed a median APC SR of 2.5 (interquartile range 2.3-2.9). In patients with a UAER between 30 and 300 mg/24 h, the median APC SR was 2.7 (2.7-2.9). Both values were significantly greater than the median APC SR of 2.1 (2.0-2.5) observed in healthy control subjects (P < 0.001). Also, the percentage of subjects with an APC SR < or = 2.0 was markedly smaller in both patient groups. Factor V and VIII levels were not significantly different between IDDM patients and healthy subjects. Grouping of IDDM patients according to the APC SR revealed significantly enhanced levels of total PS (P < 0.05) and factor VIII (P < 0.01) in patients with a poor anticoagulant response to APC (APC SR < or = 2.0) compared with those with an APC SR > 2.7. The negative correlation of the APC SR in diabetic patients with both coagulation and anticoagulation factors indicates a complex role of this parameter in regulating the coagulation system in IDDM.
Diabetes 1995 Sep
PMID:Enhanced anticoagulant response to activated protein C in patients with IDDM. 765 25

A 77-year-old man was diagnosed to have diabetes. He was hospitalized for appetite loss, weight loss (6 kg/3 months) and right femoral pain. An abnormal shadow was noted on chest X-P. On admission, he was alert and there were no abnormal physical findings except limitation in the range of motion in the right lower extremity. His femoral pain was treated by a non-steroid anti-inflammatory drug (NSAID). Right femoral bone biopsy revealed angiosarcoma and staining for factor VIII, with negative staining for epithelial membrane antigen on enzyme assay. Therefore, he received systemic administration of recombinant interleukin-2 (rIL-2). rIL-2 was administered intravenously twice daily at a dose of 40 x 10(4) JRU. The total dosage of rIL-2 amounted to 1200 x 10(4) JRU, but renal failure deteriorated and he died on the 50th hospital day of his second admission. Combination of rIL-2 and NSAID may cause progression of nephropathy.
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PMID:[A case of angiosarcoma with renal failure caused by recombinant interleukin-2 (rIL-2) and non-steroid anti-inflammatory drug (NSAID)]. 777 36

The clinical efficacy of the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMGCoA) reductase inhibitor simvastatin in the treatment of hypercholesterolaemia in non-insulin-dependent diabetes (NIDDM), was examined in a double-blind placebo-controlled study of 6 months in 70 patients with NIDDM (age 25-70 years), of whom 57 were randomised to placebo (29 patients) or simvastatin for 6 months, following a 3-month run-in on diet. Patients were hypercholesterolaemic (7.8 (7.6-8.0) (mean (95% confidence intervals)) mmol/l simvastatin vs. 8.0 (7.7-8.5) mmol/l placebo) and mildly hypertriglyceridaemic (2.6 (2.2-3.0) simvastatin vs. 2.9 (2.3-3.5) placebo). Other lipid measures and estimates of glycaemic control and haemostasis were similar in both groups. There were no significant changes in lipids, haemostatic factors, or measures of glycaemic control in the placebo treatment group. Conversely by the end of 24 weeks, simvastatin produced a 28% reduction in cholesterol (to 5.6 (5.0-6.2) mmol/l (P < 0.001)), a 38% reduction in LDL cholesterol (from 5.5 (5.4-5.6) mmol/l to 3.4 (2.8-4.0) mmol/l, P < 0.001), a 15% reduction in triglyceride (to 2.2 (1.8-2.6) mmol/l, P < 0.05, and a 9% rise in HDL (from 1.16 (1.07-1.25) to 1.23 (1.14-1.32) mmol/l, P < 0.05). Improvements in apolipoprotein B (apo B) (-28%, P < 0.001), the LDL cholesterol to apo B ratio (-20%, P < 0.001), and apo A1 (+15%, P < 0.001) were recorded. There were no effects upon fibrinogen, factor VII activity, factor VIII activity, or measures of glycaemic control (fasting glucose, insulin, C-peptide, or HbA1).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Res Clin Pract 1994 Mar
PMID:Simvastatin in non-insulin-dependent diabetes mellitus: effect on serum lipids, lipoproteins and haemostatic measures. 807 Mar 2

Several coagulation proteins have been implicated as possible risk factors for the development of atherosclerotic diseases, among which are factor VIII and von Willebrand factor. As part of the Atherosclerosis Risk in Communities (ARIC) Study, a prospective study designed to assess risk factors for the development of atherosclerotic diseases, baseline measurements of factor VIII and von Willebrand factor (vWF) were performed to determine their relationship to the development of atherosclerosis. We herein report the associations of factor VIII and vWF with constitutional, lifestyle, and biochemical factors. Factor VIII and vWF were strongly correlated with each other (r = 0.73), and, therefore, had similar associations with risk factors. Mean levels of both factors were higher in women than in men, in blacks than in whites, and increased with age. In univariate analysis, both were positively associated with diabetes, body mass index, waist-to-hip ratio, serum insulin, and plasma triglycerides. Both were negatively associated with alcohol intake, educational level, physical activity (with some exceptions), and HDL-cholesterol. No correlations were observed between factor VIII or vWF and plasma LDL-cholesterol or lipoprotein(a). Although factor VIII was negatively associated with smoking in both sexes, vWF was not associated with smoking status. Most of these associations were confirmed in multivariate analysis. The strongest associations observed were of factor VIII and vWF with race and diabetes. In multivariate analysis, blacks had factor VIII and vWF levels 15 to 18 percentage points higher than whites, and diabetics had factor VIII and vWF levels 11 to 18 percentage points higher than non-diabetics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Associations of factor VIII and von Willebrand factor with age, race, sex, and risk factors for atherosclerosis. The Atherosclerosis Risk in Communities (ARIC) Study. 806 42

Increased plasminogen activator inhibitor-1 (PAI-1) activity has been reported in Type 2 (non-insulin-dependent) diabetes and is a recognized risk factor for coronary artery disease. Fourteen newly diagnosed Type 2 diabetic patients were studied before and 3 months after standard clinical dietary modification. To assess the effect of improved metabolic control on PAI-1 activity, nine Type 2 diabetic patients established on diet therapy and with previous stable glycaemic control served as controls. In the newly diagnosed patients diet therapy resulted in a significant decrease in HbA1c levels (8.3 +/- 0.5 vs 5.2 +/- 0.3% (mean +/- SEM); p < 0.001), and this was accompanied by a fall in fibrinogen (4.3 +/- 0.3 vs 3.0 +/- 0.2 g.l-1; p < 0.01) concentration, and PAI-1 (18.7 +/- 2.3 vs 12.2 +/- 0.9 arbitrary units ml-1; p < 0.02) and factor VIII (147 +/- 17 vs 115 +/- 13%; P < 0.01) activities. PAI-1 activity was correlated with triglyceride levels at the first assessment in the newly diagnosed patients (r = 0.66; p < 0.01), and this was the only independent association by multiple regression analysis when all patients (n = 23) were considered (r = 0.62; p < 0.002). However, there was no association between the changes in PAI-1 activity and the changes in HbA1c BMI, and serum triglyceride levels following treatment in the newly diagnosed patients. Serum triglyceride concentrations, HBA1c, PAI-1 activity, and the coagulation factors remained unchanged in the control group over the same treatment period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased plasminogen activator inhibitor-1 activity in newly diagnosed type 2 diabetic patients following dietary modification. 828 22


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