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)

The aim of our study was to evaluate the fibrinolytic system in patients with retinal branch vein occlusion (RVO). The following tests were carried out: prothrombin time, partial thromboplastin time (PTT), fibrinogen degradation products, euglobulin lysis time, fibrinogen, pasminogen, antithrombin III, alpha 2-antiplasmin and alpha 2-macroglobulin. Comparing the results of patients with those of normal controls, only the fibrinogen increase and PTT shortening were significantly different. All other tests taken into account were within normal limits. Only the patients without other associated diseases (diabetes or hypertension) showed a significant activation of fibrinolysis (either with respect to normal or to other RVO patient groups). In conclusion, no important fibrinolytic impairment was seen in our longstanding RVO patients. Fibrinolytic activation seen in patients without verified associated diseases may be related to the presence of a sound endothelium, still able to release plasminogen activators in response to RVO. The fibrinogen and PTT changes in RVO were probably due to other associated diseases.
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PMID:Fibrinolytic behavior in long-standing branch retinal vein occlusion. 369 97

The effects of induced hyperglycemia on both antithrombin III (ATIII) biologic activity and plasma concentration in normal subjects are reported. A decrease in ATIII activity parallel to hyperglycemia was observed, while ATIII concentration was unchanged. When the glycemia returned to basal values ATIII activity concomitantly showed values in the basal range. Heparin infusion was able to significantly preserve ATIII activity from glycemia-induced alterations. These data demonstrate that hyperglycemia by itself may alter ATIII biologic activity. Moreover, the effect of heparin administration suggests that both glucose and heparin compete in vivo for the same functional site. Our study, showing the possible role of hyperglycemia in altering the biologic function of some proteins, stresses the role of increased blood glucose in the development of some complications in diabetes.
Diabetes 1987 Mar
PMID:Induced hyperglycemia alters antithrombin III activity but not its plasma concentration in healthy normal subjects. 380 39

The effects of metabolic control on both antithrombin III (AT III) activity and AT III plasma concentration in 20 insulin-treated diabetic subjects have been evaluated. Basal AT III activity was significantly lower in diabetic subjects versus healthy controls (P less than 0.001), whereas no difference was found in AT III concentration. A good correlation was found between AT III activity and AT III concentration (r = 0.81; P less than 0.001) in healthy controls, but this correlation was not significant in diabetic subjects (r = 0.12; P = NS). In those subjects a linear inverse correlation was found to exist between AT III activity and level of glycosylated proteins (r = -0.43; P less than 0.05). Diabetic subjects were also examined after 1 and 2 mo of restored metabolic control, obtained by human insulin (DNA-recombinant) therapy. Improved metabolic control was characterized by an increase of AT III activity (P less than 0.05), a decrease of mean daily blood glucose, and stable HbA1 and glycosylated proteins (P less than 0.05), while AT III concentration did not vary. On the other hand, a significant inverse correlation between AT III activity and glycosylated proteins was found during both the first and second months (r = -0.54 and r = -0.53, respectively; P less than 0.01). Moreover, no correlation between AT III activity and AT III concentration was found. These data suggest that impaired metabolic control may alter the biologic activity of AT III in diabetes, but not its plasma concentration.
Diabetes Care
PMID:Metabolic control may alter antithrombin III activity but not its plasma concentration in diabetes: a possible role for nonenzymatic glycosylation. 394 45

The presence of soluble fibrin complexes (SFC) measured by gel filtration of plasma on 4% agarose columns, fibrinogen heterogeneity on 3.5% SDS-polyacrylamide gels and the concentrations of several plasma proteins were evaluated in 39 patients with diabetes mellitus (DM) and 19 matched control subjects. A small but significant increase of SFC was found in DM (p less than 0.01). On individual basis 51.2% of the patients had increased SFC (greater than M + 2 SD of the controls). Polyacrylamide gel electrophoresis of the SFC showed no evidence of cross-linking or proteolysis. Plasma clots formed in the presence of EDTA and trasylol were analysed in SDS-polyacrylamide gels in a normal and two lower molecular weight fibrin bands (band I, II, III). The percentage of band I fibrinogen was in diabetics (65.3 +/- 4.7%) lower than that of the controls (71.8 +/- 4.5%) (p less than 0.01). Fibrinogen levels, antithrombin III, alpha 1-antitrypsin, alpha 2-macroglobulin and plasminogen were significantly increased in DM. We suggest that in DM there is an enhancement of intravascular fibrin formation and accelerated fibrinogen degradation to lower molecular weight forms.
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PMID:Soluble fibrin complexes and fibrinogen heterogeneity in diabetes mellitus. 616 8

Plasma beta-thromboglobulin, platelet factor 4, fibrinogen, fibrinopeptide A, antithrombin III, factor VIII related antigen, alpha 2-macroglobulin, platelet count, and total glycosylated haemoglobin were measured in three well matched groups of subjects: non-diabetic controls, diabetics without retinopathy, and diabetics with proliferative retinopathy. beta-thromboglobulin and platelet factor 4 concentrations were significantly higher in the diabetics with retinopathy than in the controls and platelet factor 4 was also increased in the diabetics without retinopathy compared with controls. Fibrinogen concentration was raised in diabetics without retinopathy compared with controls, diabetics with retinopathy compared with controls, and diabetics with retinopathy compared with those without. Fibrinopeptide A concentration did not differ significantly between groups. Antithrombin III levels were increased in diabetics with retinopathy compared with controls, and in diabetics with retinopathy compared with those without. Factor VIII related antigen values were higher in both the diabetic groups when compared with the controls. Fibrinopeptide A concentration correlated with both beta-thromboglobulin and platelet factor 4 in each of the three groups. Haemostatic abnormalities in diabetes have been shown, although a hypercoagulable state has not been confirmed. These changes in platelet and coagulation function may be secondary to the development of microvascular disease and their role in the pathogenesis of retinopathy remains uncertain.
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PMID:Platelet and coagulation factors in proliferative diabetic retinopathy. 620 21

To determine the effect of improved, short-term glycemic control on various functions of hemostasis in insulin-dependent diabetes, we measured changes in plasma fibrinogen, fibrinopeptide A (FPA), functional antithrombin III (AT-III), factor VIII:ristocetin cofactor ( VIIIRCoF ), beta-thromboglobulin (BTG), platelet factor 4 (PF4), and platelet aggregation responses to ADP and collagen in 12 patients with low or undetectable stimulated (postprandial) serum C-peptide levels during 4-8 wk (median, 6 wk) of treatment with constant subcutaneous insulin infusion. Mean plasma fibrinogen, FPA, AT-III, VIIIRCoF , and BTG at baseline were elevated compared with normal. Three patients had heightened platelet responses to ADP that did not correlate to other indicators of a hypercoagulable state; the affected patients, in fact, had significantly lower plasma BTG (25.5 +/- 5.3 [SEM] versus 44.6 +/- 4.6 ng/ml, P less than 0.05) and FPA (1.1 +/- 0.1 versus 2.5 +/- 0.5 ng/ml, P less than 0.05) than the remaining patients. Patients with clinically evident vascular disease had higher baseline plasma BTG and FPA than those without vascular disease (44.6 +/- 5.4 versus 30.2 +/- 4.6, and 2.6 +/- 0.6 versus 1.3 +/- 0.2 ng/ml, P less than 0.05, respectively). During treatment, all patients had declining blood glucose (200 +/- 18 to 102 +/- 5 mg/dl, P less than 0.001) and HbA1 (11.8 +/- 0.6 to 10.2 +/- 0.4%, P less than 0.005). No statistically significant changes in hemostatic functions were noted. During treatment, one patient had an acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Care
PMID:Plasma beta-thromboglobulin, platelet factor 4, fibrinopeptide A, and other hemostatic functions during improved, short-term glycemic control in diabetes mellitus. 620 89

Twenty control subjects, 12 insulin treated and 10 non-insulin treated diabetics were studied. All diabetics had retinopathy documented by fluorescein angiography and fluorophotometry. Factor VIIIR:Ag and plasma fibrinogen concentrations were elevated in both diabetic groups, but more so in the insulin treated patients. Within this latter group the plasma fibrinogen was also correlated with the degree of retinopathy. Platelets separated on linear isosmolar Percoll gradients showed an increase in intraplatelet beta TG content and concentration and a slight increase in volume of the lightest platelets in the insulin treated diabetics. Plasma platelet factor 4 and antithrombin III concentrations were normal and plasma beta TG levels were elevated only in those patients with renal insufficiency. Platelet aggregometry was performed in 18 diabetic subjects and found to be normal. It is concluded that abnormalities of coagulation and platelets in diabetes are determined by metabolic factors rather than the severity of microvascular disease per se.
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PMID:Platelets, coagulation and fibrinolysis in patients with diabetic retinopathy. 622 3

In order to compare the metabolic and hemobiological properties of two sulfonylureas, thirty-five non-insulin-dependent diabetics were randomly assigned to two groups. Each group was given either gliclazide (n = 20) or glibenclamide (n = 15) for six months. Metabolic control was improved in both groups, as evidenced by the decrease in HbA1 concentrations. A significant fall in ADP (1 and 4 microM)--induced platelet aggregation was recorded in the gliclazide group, while antithrombin III levels remained normal throughout the trial and plasminogen activator levels increased. These hemobiologic changes may be effective in preventing the vascular complications of diabetes. In contrast, glibenclamide did not alter platelet aggregation. Furthermore, a significant decrease in both antithrombin III levels and basal and venostasis-stimulated plasminogen activator levels were seen in glibenclamide patients. The beneficial changes in hemostasis seen in gliclazide patients probably result from a direct effect of the drug since hemobiological parameters and metabolic control parameters were not correlated.
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PMID:[Effects of gliclazide and glibenclamide on platelet function, fibrinolysis and metabolic control in diabetic patients with retinopathy (author's transl)]. 628 3

A case of acute intestinal vascular necrosis in a 19-year-old user of oral contraceptives (OCs) is described, and hypotheses explaining the digestive complications of synthetic estrogens are reviewed. The patient had originally presented with a violent gastric pain that subsequently spread to the entire abdomen. An abrupt worsening of her condition involved cardiovascular collapse associated with a peritoneal syndrome, vomiting and dehydration, and hyperleukocytosis. Emergency opening of the peritoneum was followed by evacuation of a large quantity of fetid gas and alimentary debris, and observation of a completely necrosed stomach. A careful lavage of the entire intestinal cavity led to temporary improvement, but it became clear during an attempt at gastrectomy that further treatment would be unavailing and the patient died shortly thereafter. Estrogens were believed to be responsible for the digestive necrosis because it occurred in a young woman who had used an estrogen-rich OC for 3 years and who smoked; a hapatic biopsy confirmed the diagnosis. No traces of other risk factors such as hypertension, hyperlipidemia, diabetes, neoplasia, or obesity were observed. Recent publications indicate that OCs are responsible for a certain number of digestive problems, which may include acceleration of intestinal transit, severe diarrhea, rectorrhagia, ischemic or ulcerative colitis, intestinal infarct which is usually localized, and hepatocellular problems ranging from moderate hepatic insufficiency to malignant tumor and Budd-Chiari syndrome. OCs do not modify hemodynamic regimes, but they may cause elevation of fibrinogen and thrombin, diminution of antithrombin III acitivty, increased platelet adhesivity, and decreased fibrinolysis leading to hypercoagulability. These modifications in hemostasis occur in all OC users and are not statistically correlated with occurence of thrombotic accidents. OCs are probably responsible for parietal vascular lesions; experimental injection of synthetic estrogens is associated with both arterial and venous lesions. The most characteristic anomaly is at the level of the intima, with proliferation of smooth muscle cells and increased conjunctive tissue fibers associated with proliferation of the media or the endothelium. The absence of lipid deposits, the simultaneous appearance of arterial and venous lesions, and other evidence argues against and atheromatous origin of parietal lesions. A significant correlation has been found between high levels of anti-synthetic ethinyl estradiol antibodies and the presence of vascular lesions. It is hypothesized that these circulating immune complexes penetrate the vascular walls of OC users and produce lesions, which may depend on factors such as smoking.
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PMID:[Digestive complications of oral contraceptives: a case of extensive digestive necrosis in a young woman]. 647 54

To counter the paucity of documention on thromboembolic disorders caused by oral contraceptives (OC), a case study is presented describing the incidence of occlusion of arteria centralis retinae in a 24-year old woman after prolonged use of an OC, Bisecurin. She had taken Bisecurin for 4.5 years and had gained 20 kg during that time, but stopped usage 1 month before admission. She was hospitalized with severe deterioration of vision in the left eye. An eye examination indicated an edematous condition of the retina and reddening of the macula. Acuity of vision value for the left eye was .01 vs. 1.0 for the right, which was confirmed by fluorescein fundus angiography. Moderately decreased antithrombin III (AT III) activity was also ascertained. Treatment consisted of immediate retrobulbar injection with Tolazolin followed by Rheomacrodex, Cavinton infusions, B1 and B12 injections, Oradexon subconjunctival injection as well as vitamin B complex, Cavinton, and Colfarit tablets and a fat-free diet. Significant improvement of the left eye condition appeared 4 weeks later. Periodic follow-ups showed the healing of the condition around the macula; however, the patient suffered permanent damage to the retina due to the arterial occlusion above and below the macula. The disturbed lipid values of metabolism were also returned to normal, as borne out by normal dextrose loading results 8 months later (glucose tolerance was abnormal during examination at admission). The estrogen and progesterone components of OCs have been shown to reduce AT III levels, shorten heparin-thrombin coagulation time, increase fibrinogen levels, decrease HDL cholesterol levels, and produce excess TXA2 (thromboxan) resulting in vasoconstriction and thrombocyte aggregation. The risk of thrombosis is 6 times higher in OC users than in nonusers, although other susceptibility factors (obesity, diabetes, hypertension) also contribute to thrombosis.
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PMID:[Arterial occlusion in the ocular fundus induced by oral contraceptives]. 651 54


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