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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood and plasma viscosities were determined using respectively a Couette type micro-viscometer (LS 30) and an automatic capillary viscometer (FICA). Plasma beta-thromboglobulin (beta-TG) levels were determined by radioimmunoassay. These parameters were measured in a group of 11 poorly controlled insulin requiring diabetics before and after blood glucose normalization using an artificial pancreas (Biostator GCIIS). Before connection to the artificial pancreas, blood and plasma viscosity and beta-TG levels were significantly higher in diabetics than in controls. The strict metabolic control obtained by the artificial pancreas resulted in a normalization of the hemorheological parameters and in a significant reduction of plasma beta-TG levels after 48 h. These results suggest that the metabolic control of diabetes influences the rheological behavior of blood and the metabolism of platelets.
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PMID:[Influence of metabolic control on blood viscosity and platelet activity in insulin requiring diabetics]. 621 23

37 type 2 diabetic patients with no clinical evidence of retinopathy or vascular disease were studied at diagnosis and following control of hyperglycaemia for evidence of abnormalities of coagulation, fibrinolysis and platelet behaviour. 38% showed hyperactive platelets, demonstrating either in vitro hyperaggregability, circulating platelet aggregates, or raised plasma beta-thromboglobulin levels. 36% showed abnormally raised factor VIII coagulant activity (FVIIIc) levels, though this was mainly in female patients. The mean level of FVIIIc decreased with treatment. Anti-thrombin III (AT-III) levels were decreased, and 33% of the patients had levels less than 80%. In this group AT-III increased following treatment. No abnormalities of fibrinolysis were demonstrated. These findings support the concept that diabetes can be associated with a hypercoagulable state, which is not necessarily dependent on the presence of overt vascular disease, or correlated with the degree of chronic hyperglycaemia (HbA1c levels).
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PMID:Diabetes, a hypercoagulable state? Hemostatic variables in newly diagnosed type 2 diabetic patients. 621 31

Haemostasis was studied in 34 diabetic patients with and without detectable vascular complications (micro- and macroangiopathy). Information on platelet functions was obtained by beta-thromboglobulin determination, and of heparin-thrombin coagulation time, platelet aggregation in vivo, and on the condition of the vessel walls by estimation of factor VIII-protein (VIIIR:Ag). The results were suggestive of an increased platelet activity, the most marked abnormalities having been found in cases of angiopathy. Attention is drawn to the therapeutic possibilities offered by studies of the pathogenetic role of the abnormalities of haemostasis in diabetes.
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PMID:Haemostasis in diabetics. 623 79

Investigations on the platelet function in diabetes mellitus were performed on 28 patients with insulin-dependent diabetes and in 33 healthy controls of similar age. In the diabetic patients it was possible to induce 50% of maximal aggregation by lower concentrations of adenosine diphosphate or arachidonic acid than in the controls. In the presence of N-ethyl maleimide, platelets from diabetic patients produced significantly more malondialdehyde than those from normal controls. After addition of arachidonic acid the platelets from the diabetic patients also synthesized more thromboxane B2. This synthesis of thromboxane was inversely correlated to the minimal concentration of arachidonic acid necessary to induce 50% platelet aggregation. Circulating platelet aggregates were more common in the diabetic patients than in the controls. Plasma levels of beta-thromboglobulin and platelet factor 4 were raised in parallel in the diabetic patients and correlated with the increased production of thromboxane B2 by the platelets from the same patients. Platelets from patients with diabetes thus demonstrated signs of hyperreactivity both in vivo and in vitro. This may be of clinical importance for the development of vascular complications in this disease.
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PMID:Investigations on platelet function in diabetes mellitus. 623 82

It has been postulated that abnormal platelet and endothelial function may contribute to microangiopathy in diabetes mellitus. If this proposal is correct, alterations in platelet and endothelial function should be found before the appearance of vascular disease in insulin-dependent patients and in animal models of diabetes mellitus. This appears to be the case for the following: platelet aggregation, increased platelet production of the proaggregatory prostaglandin metabolite thromboxane, decreased endothelial production of the antiaggregatory prostaglandin prostacyclin, and decreased platelet survival. Insulin therapy will return some of these findings to normal. Platelet-plasma interactions that promote platelet aggregation and increased plasma levels of the platelet-specific protein beta-thromboglobulin have been reported in insulin-dependent diabetic patients who have not manifested vascular complications as well as in those with vascular complications. It has now been demonstrated in animal models that platelet microthrombi are found in small retinal vessels after months of experimental diabetes. Collectively, these findings demonstrate that alterations in platelet and endothelial function that favor thrombosis occur early in the diabetic state and may contribute to microvascular disease. There are several ongoing studies of antiplatelet agents in diabetic vascular disease that will provide clinical evidence bearing on the major postulate. Until these and other studies are completed, the platelet-endothelial story remains an attractive hypothesis in the genesis of diabetic microvascular disease.
Diabetes 1983 May
PMID:Do platelets have anything to do with diabetic microvascular disease? 624 36

At present there is no simple, reliable and non-invasive method for monitoring progression and improvement in diabetic microangiopathy. However, some diabetic patients with severe microvascular complications show a fairly specific pattern of impaired left ventricular function (abnormal relaxation, cavity filling and wall thinning) and abnormalities of haemorheology (increased viscosity, erythrocyte rigidity and beta-thromboglobulin and decreased threshold for platelet ADP aggregation). A single-blind, 6-months' crossover study of an antiplatelet agent, ticlopidine, was conducted in 20 diabetics with clinical evidence of microvascular disease. Response to therapy was monitored by digitised M-mode echocardiographic analysis of left ventricular diastolic function and haemorheology. All patients had abnormal basal values with no significant change during the 3-month placebo run-in period but, although significant alterations in viscosity, erythrocyte deformability, beta-thromboglobulins and ADP threshold were observed, no change in left ventricular function was detected. It is concluded that, while it may be possible to alter abnormal haemorheology in diabetes, there was no change in one parameter of microvascular end-organ damage.
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PMID:Clinical trials of an antiplatelet agent, ticlopidine, in diabetes mellitus. 635 6

Spontaneous platelet aggregation (SPA), a phenomenon observed in vitro, was noted in 29 of 74 (39%) children and adolescents with insulin-dependent diabetes. Its occurrence was independent of age of onset, duration of diabetes, HbAI levels or presence of background retinopathy but varied between normal and abnormal in given individuals tested repeatedly over some time. Plasma beta-thromboglobulin, the platelet protein specific for Phase II of the release reaction, was elevated in the diabetic subjects but was independent of the occurrence of SPA. SPA in the diabetic children and adolescents, in contrast to SPA in other conditions, was not suppressed by either acute or chronic administration of aspirin adequate to suppress ADP induced second wave aggregation. SPA was uniformly suppressed by addition to the in vitro system of EDTA, adenosine, antisera to human fibrinogen or vitamin E. The data suggest that SPA is ADP induced and reflects either abnormal platelet membrane permeability to the nucleotide or its abnormal release, or abnormal platelet sensitivity to normal plasma levels of ADP.
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PMID:Some characteristics of spontaneous platelet aggregation in young insulin-dependent diabetic subjects. 645 81

Many diseases in children are associated with thrombotic tendencies either as a complication or as part of the pathophysiologic process. Disorders in which platelet consumption and/or activation occur include myeloproliferative syndromes, sickle cell disease, cardiac prostheses, arteriovenous shunts, vasculitis, diabetes mellitus, and hemolytic-uremic syndrome and other renal diseases. Platelet involvement can be demonstrated by several indicators, including an increase in platelet release product levels in the plasma (beta-thromboglobulin, platelet factor 4, and thromboxane B2). The agents that have the greatest success in thrombotic disorders where platelet involvement is prominent include the prostaglandin pathway cyclo-oxygenase inhibitors aspirin and sulfinpyrazone, as well as dipyridamole. Although indications and dosages for the use of antiplatelet agents in children can be suggested, the treatment of each patient should be individualized in light of current knowledge.
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PMID:Use of antiplatelet agents in pediatric hypercoagulable states. 670 78

Stimulation of human platelets to release results in decreased buoyant density. This decreased density provides a tool to detect circulating platelets which have participated in a thrombotic process. Platelet density gradient centrifugation using Stractan was standardized and the effects of anticoagulation, temperature, and osmolarity were investigated. In 7 out of 32 patients with thrombotic disease less dense platelets were found. Platelet activation in the patient group was also indicated by spontaneous aggregation (10/32), decreased circulating platelet aggregate ratios (5/24) and elevated plasma beta-thromboglobulin levels (2/ 11). Several of these tests were also abnormal in diabetes mellitus thrombocytosis, leukaemia and several systemic diseases with thrombotic complications. The platelet density test using Stractan is reproducible and independent of other tests for platelet activation and is therefore potentially a useful extension of platelet function testing in patients with thrombotic disease.
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PMID:Determination of the density distribution of human platelets--methodological aspects and comparison with other tests for platelet activation. 711 98

Increased plasma levels of beta-thromboglobulin, a platelet activation marker, are observed in coronary artery disease. Urinary albumin excretion, a marker of endothelial cell perturbation, is related to cardiovascular disease in diabetes. To test the value of these markers in predicting forthcoming coronary disease, the relations between urinary excretions of high molecular weight beta-thromboglobulin (HMW-beta TGf) and albumin and subsequent coronary disease in a cohort of 15,484 middle-aged women were investigated in a nested case-control study. Baseline questionnaire data and urine samples were available from a breast cancer screening program in Utrecht during 1982-1985. Cases were Utrecht hospital admissions for myocardial infarction (n = 50) or angiographically confirmed coronary disease (n = 28) from 1982-1985 to 1990-1991. Classifying events occurred a median of 5.1 years after baseline. Controls were a random sample from the cohort, individually case matched for baseline examination date and age, at a 1:2 ratio. HMW-beta TG/creatinine ratios (ng/mmol, mean +/- standard error) were 5.3 +/- 0.3 in cases and 4.7 +/- 0.3 in controls; albumin/creatinine ratios (mg/mmol, median) were, respectively, 0.37 and 0.22. Crude odds ratios for classification in the highest compared with the lowest tertiles of HMW-beta TG/creatinine and albumin/creatinine distributions were elevated for cases compared with controls: HMW-beta TG/creatinine odds ratio = 2.4, 95% confidence interval 1.1-5.0; albumin/creatinine odds ratio = 2.1, 95% confidence interval 1.0-4.1. These relations persisted after adjustment for smoking, hypertension, Quetelet index, and menopausal status. Both urinary HMW-beta TG and albumin excretion are markers of coronary disease risk in middle-aged women, indicating that increased platelet activation and endothelial cell perturbation precede coronary heart disease events in women.
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PMID:Urinary excretions of high molecular weight beta-thromboglobulin and albumin are independently associated with coronary heart disease in women, a nested case-control study of middle-aged women in the Diagnostisch Onderzoek Mammacarcinoom (DOM) Cohort, Utrecht, Netherlands. 748 62


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