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

Platelet aggregates play an important role in rheology of the blood flow in microcirculation. The formation of platelet aggregates markedly raise the threshold diameter of the vessel at which the inversion of Fahraeus-Lindquist effect takes place. In different diseases (ischemic heart disease, diabetes) thromboxane A2 production by platelets is increased and, as a consequence, platelet aggregate formation is facilitated. Platelet aggregation is modulated by several mechanisms, among which thromboxane A2 and thrombin increase and prostacyclin decrease formation of platelet aggregates. Prostacyclin is able also to increase blood red cells deformability thus it appears one of the most important factors for the control of blood flow rheology in microcirculation. However, prostacyclin production is limited in time, and repeated and close periods of venous stasis induce exhaustion of prostacyclin production and increase the formation of platelet aggregates.
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PMID:Pathophysiological aspects of platelet aggregation in relation to blood flow rheology in microcirculation. 676 41

Antithrombin III activity was determined by three techniques in 58 patients with maturity onset diabetes mellitus: a spectrophotometric assay, using the chromogenic substrate Chromozym TH; evaluation of antifactor Xa activity and an immunochemical technique. Although the biological antithrombin III activity was clearly reduced in individual subjects, there was only a slight nonsignificant reduction in the mean anti-thrombin III activity values as compared to normal subjects. No difference was observed between diabetics receiving insulin and subjects taking oral hypoglycemic agents or between diabetics without vascular complications and diabetics with vascular lesions.
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PMID:Determination of antithrombin III activities by different methods in diabetic patients. 676 19

Thrombin induced thromboxane A2 and prostaglandin E2 production were significantly increased in platelets of streptozotocin induced diabetic rats as compared to non-diabetic control rats, while collagen induced thromboxane A2 production was decreased. Using exogenous arachidonic acid, prostaglandin E2 production, but not thromboxane A2 production, was increased in platelets from streptozotocin treated animals. Prostacyclin production in the diabetic aorta was significantly lowered; however, control levels of prostacyclin production resulted after incubation of the tissue with dipyridamole. Diabetic animals demonstrated a fivefold decrease in the endogenous arterial prostacyclin/platelet thromboxane A2 ration when thrombin or ADP was used to induce thromboxane A2 production. This elevated ratio could be a contributing factor to the vascular complications of diabetes. Dipyridamole, due to its ability to partially normalize this ratio, may be useful as a therapeutic agent in this and related vascular diseases.
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PMID:Alterations of the prostacyclin-thromboxane ratio in streptozotocin induced diabetic rats. 680 92

Glucose, when incubated with fibrinogen, binds covalently to that protein. The reaction is non-enzymatic in type and is directly dependant on the time of incubation, temperature and pH. Glucosylation of fibrinogen is not altered by preincubation with aspirin. No preferential glucosylation of fibrinogen, fibrinogen chains or plasmin digestion products XYDE could be demonstrated, suggesting that glucose binding occur at several different sites. No abnormality of thrombin clotting or stability of glucosylated fibrinogen could be detected. These findings are discussed in relation to the previously described abnormalities of fibrinogen metabolism in diabetes mellitus.
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PMID:Non-enzymatic glucosylation of fibrinogen. 727 78

Three parameters of coagulability--thrombin generation time (TGT), antithrombin III (AT III), and activated partial thromboplastin time (ATPP)--and two parameters of diabetic control--serial measurements of fasting serum glucose (FG) and hemoglobin A1(HbA1)--were used to study the relationship between diabetic control and hypercoagulability. Four groups of females were studied consisting of 10 young normal, 10 young insulin-dependent diabetic, 10 pregnant nondiabetic, and 8 first-trimester, insulin-dependent, pregnant diabetic subjects. Fasting serum glucose values and HbA1 were higher (P < 0.005) in nonpregnant diabetic subjects (193.1 +/- 29.1 mg/dl, 12.9 +/- 1.1%) and pregnant diabetic subjects (111.0 +/- 13.6 mg/dl, 8.2 +/- 1.7%) than in controls (64.8 +/- 4.4 mg/dl, 5.9 +/- 0.1%) and the nondiabetic pregnant females (71.6 +/- 3.8 mg/dl, 6.1 +/- 0.2%). Young diabetic females, pregnant females, and pregnant diabetic subjects had a shorter (P < 0.01) TGT than did the controls. AT III was greater (P < 0.01) for controls (99.7 +/- 2.7%) than for pregnant nondiabetic (83.2 +/- 3.8%), diabetic (79.5 +/- 2.5%), and pregnant diabetic subjects (76.2 +/- 4.4%). There was a positive correlation (r = 0.88, P < 0.005) between HbA1 and FG in the 10 young diabetic and in the 8 pregnant diabetic subjects (r = 0.74, P < 0.05). In the 10 diabetic females there was a negative correlation between AT III and FG (r = -0.76, P < 0.01) and between AT III and HbA1 (r = -0.79, P < 0.01). Thus, AT III is depressed in both diabetes and pregnancy, with pregnant diabetic subjects displaying the lowest AT III levels. Our observation that depression of AT III levels in young diabetic females was closely correlated with elevations of fasting serum glucose and HbA1 suggests that strict diabetic control may help prevent hypercoagulability in diabetes.
Diabetes Care
PMID:Plasma antithrombin III and thrombin generation time: correlation with hemoglobin A1 and fasting serum glucose in young diabetic women. 744 96

Diabetes mellitus is a multi-component syndrome that is often complicated by angiopathy which is partly due to enhanced platelet functions. Using fluorescent dyes 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF) and Fura-2 AM, changes was evaluated in the concentration of baseline and thrombin-stimulated increases in intracellular ionized calcium (Ca2+i) relative to hydrogen ions in the platelets from control, insulin-treated, and non-treated diabetic rats. The cytosol of platelets from the diabetic rats were more acidic compared to the insulin-treated and normal control rats. The increased intracellular hydrogen ion concentration [H+] or decreased pH (pH) in the diabetic rat platelets is associated with an increased baseline [Ca2+]i. Upon stimulation with thrombin, the mean peak [Ca2+]i for the insulin-treated (309 +/- 97 nmol/L) and untreated (339 +/- 135 nmol/L) diabetic rats was significantly higher than the concentration for the normal rats (213 +/- 101 nmol/L). Treatment with insulin attempts to correct the diabetes-induced elevation in the baseline of [Ca2+]i and intracellular H+. These results suggest that the relationships between Ca2+ and H+ relative to binding sites are similar in the intra- and extracellular compartments. It is our conclusion that the enhanced platelet activity and associated development of vascular diseases in diabetes may be due to an increased intracellular H+ that caused an increased baseline [Ca2+]i in diabetes mellitus.
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PMID:Intracellular calcium and hydrogen ions in diabetes mellitus. 748 14

To assess the risk factors for atherosclerosis in Werner's syndrome (WS), coagulation/fibrinolytic system parameters and lipid levels were investigated in 9 non-smoker patients with WS and compared with normal control values (N). The levels of thrombin antithrombin III complex (p < 0.05), D-dimer (p < 0.05), tissue plasminogen activator (p < 0.005) and PA inhibitor 1 (p < 0.01) were significantly increased, while the level of thrombomodulin (p < 0.005) in the fasting plasma was significantly decreased in the WS cases compared with N. Lipid profiles confirmed that 8 of the 9 patients were of hyperlipidemia type IIb, 7 had hyperinsulinemia and 5 fulfilled the criteria for clinical diabetes mellitus. The hypercoagulable condition suggested the existence of multiple risk factors for atherosclerosis in WS in addition to the previously reported hyperinsulinemia and hyperlipidemia.
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PMID:Hypercoagulable state indicates an additional risk factor for atherosclerosis in Werner's syndrome. 749 61

The fibrinolytic resistance of platelet-rich arterial thrombi received much attention. Clot lysis method was used to assess the in vitro fibrinolytic properties in diabetes mellitus. Platelet rich (PRP) clots were formed by addition of thrombin, and lysis was induced by tissue-plasminogen-activator. The coagulation and lysis was followed by the light scattering properties. A special pattern of good initial lysis followed by a second clotting phase was observed in more than half of insulin dependent diabetic patients, while a similar pattern of clot-lysis was only occasionally found in non-insulin dependent diabetes mellitus or in the healthy control group. Following the thrombin activation of washed, gel-filtered platelets, the supernatants possessed an inhibitory action on in vitro lysis of PPP-clots. This suppression was remarkably stronger in IDDM, along with the highest PAI-1 activity concentration ratio of the platelet lysates, compared to plasmatic levels. The relation of this special type of PRP clot-lysis resistance to diabetic vascular complications needs further clarifying and investigations.
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PMID:Altered lysis resistance of platelet-rich clots in patients with insulin-dependent diabetes mellitus. 749 4

In this study, human platelets were used as a cellular model for exploring cytosolic free Ca (Cai) regulation in non-insulin-dependent diabetes mellitus (NIDDM). Cai levels were monitored in resting and thrombin-stimulated platelets from obese females with NIDDM; obese, nondiabetic women, and nonobese, nondiabetic women. All subjects were black. Significant and marked elevation of basal Cai levels was observed in platelets from the diabetic subjects when no aspirin was used during platelet isolation. However, no significant differences were observed in Cai between aspirin-treated platelets from women with NIDDM and platelets from nondiabetic women. The rate of the Cai return to basal level after thrombin stimulation was significantly lower in platelets from the diabetic subjects, suggesting an abnormality in platelet Ca extrusion or sequestration in NIDDM. Platelet Cai levels positively correlated with low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio (LDL/HDL) and fasting blood glucose. These findings suggest abnormalities in platelet Cai homeostasis in NIDDM that are influenced by the serum lipid profile and perhaps glucose.
J Diabetes Complications
PMID:Cytosolic Ca profile of resting and thrombin-stimulated platelets from black women with NIDDM. 759 51

Diabetes is characterized by the existence of a thrombosis-prone condition, possibly related to hyperglycemia. However, the mechanism linking hyperglycemia to the activation of the coagulation cascade is still unclear. It has been recently suggested that diabetes is accompanied by increased oxidative stress. In this work, the possibility that oxidative stress may be involved in the hyperglycemia-induced coagulation activation has been evaluated. Prothrombin fragment 1 + 2 (F1 + 2), which represents a reliable marker of the amount of thrombin released in the circulation, has been chosen for studying thrombin formation in vivo. In nine type II diabetic patients and in seven healthy control subjects, matched for age and body mass index, three different experiments were performed: oral glucose tolerance test (OGTT), intravenous antioxidant glutathione (GSH) administration for 2 h, and OGTT plus intravenous GSH administration. Samples were drawn at -15 min and every 30 min from 0 to 180 min. During the OGTT, F1 + 2 significantly increased in both diabetic and healthy subjects. GSH administration during OGTT normalized this phenomenon. GSH administration alone significantly decreased F1 + 2 in diabetic patients, while no effect was observed in the normal subjects. These data suggest that hyperglycemia may induce thrombin activation, possibly inducing an oxidative stress, and that antioxidant GSH may counterbalance this effect.
Diabetes 1995 Aug
PMID:Hyperglycemia-induced thrombin formation in diabetes. The possible role of oxidative stress. 762 98


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