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

Fibrinolysis treatment with urokinase was successfully undertaken in two patients, aged 71 and 76 years, with phlegmasia coerulea dolens. In the first case, with necrosis in the fore-foot, there was significant regression of the necrotic area, but a later limited amputation was still necessary. In the second, with severe heart failure, recurrent pulmonary emboli and hyperosmolar uncontrolled diabetes mellitus, complete healing was achieved. Venous thrombectomy was not possible in these two patients because of the duration of the thrombosis in the veins of the pelvic region, necrosis had already occurred, and the patients' general condition was so serious. The advanced age and arteriosclerotic changes argued against streptokinase treatment. Mean urokinase maintenance dosage of 1000-1500 IU/kg X h, with simultaneous administration of heparin at about 20 U/kg X h, produced no significant side-effects. Minor gastro-intestinal bleeding did not require stoppage of urokinase administration.
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PMID:[Urokinase treatment of phlegmasia coerulea dolens (author's transl)]. 31 5

Hyaline membrane disease (HMD) is leading single cause of death of newborn, premature infants. The "hyaline membranes" consist chiefly of fibrin. The clinical manifestation of HMD is the respiratory distress syndrome (RDS). Infants with RDS were treated with urokinase-activated human plasmin in a previous clinical trial. Survival rate was increased in the plasmin treated group as compared to the placebo recipients. However, cost and difficulty in the preparation of the enzyme made this treatment impractical. We, as well as others, have shown the premature infants lack serum plasminogen; thus they are unable to develop effective fibrinolysis and are defenseless against pulmonary fibrin deposition. Therefore, plamsinogen was tested as a possible preventive agent in RDS due to HMD. In a double blind, randomized study, infants between 1 and 2.5 kg birth weight received plasminogen or placebo shortly after birth, and were then followed for development of RDS. After 100 infants were entered into the study, the code was broken and results were evaluated to assure safety of the procedure. Among the 100 infants, 51 received placebo, 49 received plasminogen. Among the infants who received placebo, seven developed mild, and ten developed severe respiratory distress; of these ten, five died with histopathologically documented HMD. Two infants died from causes other than HMD. Among the 49 infants treated with plasminogen, 13 developed mild and three developed severe respiratory distress. There was no death due to HMD. Two deaths were due to other causes. Factors placing the infant at risk from HMD (degree of prematurity, sex, cesarean section, bleeding episodes during pregnancy, maternal diabetes) were found to be evenly distributed between control and treated groups. Since completing the first phase of the study, data of an additional 277 infants has become available. Although the code was not broken in this series, a preliminary look at mortality data in comparison with mortality data of the first series of 100 (in which the code was broken) suggests that preventive activity of plasminogen has been maintained in the second phase of the study.
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PMID:Studies on the prevention of respiratory distress syndrome of infants due to hyaline membrane disease with plasminogen. 79 69

Long-term effects of urokinase on the preservation of renal function in patients with diabetic nephropathy were evaluated. Twenty-nine adult patients with non-insulin-dependent diabetes mellitus and overt proteinuria were randomly divided into two groups. One group was treated with daily oral administration of dipyridamole or dilazep dihydrochloride and weekly intravenous administration of urokinase; the other group was treated with dipyridamole alone. There was a significant decrease in the amount of proteinuria in the first group after 3 months of the treatment compared with the second group. There was also a significant preservation of renal function in the first group after three years of treatment compared with the second group. It was concluded that continuous administration of urokinase in addition to antiplatelet agents is useful in the treatment of patients with diabetic nephropathy.
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PMID:Effect of urokinase on preservation of renal function in patients with diabetic nephropathy. 177 66

In order to evaluate precisely the fibrinolytic states in clinical disorders, plasma levels of D dimer (cross-linked fibrin degradation products) were measured by a newly developed, rapid quantitative method based on the latex photometric immunoassay in patients with hematological malignancies, diabetes mellitus, collagen disease, liver disease, thrombotic disease and disseminated intravascular coagulation (DIC). Plasma levels of D dimer were elevated in a variety of diseases, especially in DIC. Patients with hematological malignancies, liver disease and thrombotic disease also had relatively high levels of D dimer. On the whole, D dimer values were positively correlated with plasmin-alpha 2-plasmin inhibitor complex and thrombin-antithrombin III complex. In addition, plasma D dimer was measured during fibrinolytic therapy with urokinase or tissue-type plasminogen activator; its elevation was detected in some patients. These findings indicate that accelerated fibrinolysis is frequently observed in a variety of diseases, and that a rapid quantitative measurement of D dimer would be valuable for the precise assessment of fibrinolysis in these disease states.
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PMID:[Evaluation of clinical usefulness of a rapid quantitative measurement of D dimer (cross-linked fibrin degradation products)]. 177 52

Acute fatal pulmonary embolism is one cause of sudden death which should be guarded against. It is the most often missed diagnosis in sudden death cases within the hospital. Clinical pictures of 10 patients with acute fatal pulmonary embolism proved by autopsy were examined to elucidate the problems of diagnosis, and to look for an effective treatment, and a method of prevention. Common risk factors were old age and immobility due to stroke or postoperative state. Common past histories were hypertension, diabetes mellitus, obesity, atrial fibrillation and hyperlipidemia. Electrocardiogram and echocardiogram showed that in these patients there was definite evidence of acute right ventricular overload. High doses of intravenous urokinase should be given whenever acute cardiovascular collapse develops in such high risk patients. Emergent pulmonary angiogram and pulmonary embolectomy could be life-saving in patients with acute massive pulmonary embolism. Prevention is, however, the best treatment. In addition to anticoagulation medication, frequent change of body position and early mobilization are important precautions to prevent fatal pulmonary embolism developing in such patients.
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PMID:[Acute fatal pulmonary embolism: its prevention, diagnosis and treatment]. 236 72

The rate of glucose-stimulated insulin release was found to be increased but that of proinsulin conversion decreased in islets removed from diazoxide-treated rats. This coincided with an elevated islet proinsulin/insulin ratio. The defect in proinsulin conversion was not corrected by preincubating the islets, at high glucose concentration, in the presence of either urokinase or rat serum. Likewise, the administration of kallikrein inhibitor in vivo did not affect the rate of proinsulin conversion as measured in vitro. Since these results fail to document a role for exocytosis-coupled endocytotic uptake of circulating factors in the efficiency of proinsulin conversion, it is speculated that the slackening of the latter process in islets removed from diazoxide-treated rats could be somehow linked to sustained inhibition of insulin release.
Diabetes Res 1989 Feb
PMID:Diazoxide-induced long-term hyperglycemia. II. Slackening of proinsulin conversion. 266 20

232 consecutive patients with acute myocardial infarction were treated either with 2 x 10(6) IU urokinase as an intravenous bolus injection, or 250,000 IU streptokinase intracoronary, or 60 mg recombinant tissue-type plasminogen activator (rt-PA) over 90 min. All patients enrolled had chest pain for more than 30 min and less than 3 h before admission and a typical electrocardiogram. Contra-indications to thrombolytic treatment were absent. All bleeding complications occurring within 24 h after admission were assumed to be due to thrombolytic therapy. Bleeding complications occurred in 14 patients (6.5%). Only seven patients received a blood transfusion (3%). No correlation was evident between previous hypertension, diabetes mellitus, smoking, sex, age, fibrinogen level before and 24 h after thrombolytic therapy and bleeding complications. The risk of bleeding was not significantly different between the different thrombolytic regimens despite marked differences in the fall of the fibrinogen level. The decrease of fibrinogen following thrombolytic therapy did not influence the patency rate of the infarct vessel. Thrombolytic therapy in acute myocardial infarction is a safe treatment even among patients advanced in years and with medically controlled hypertension and diabetes mellitus, irrespective of the kind of thrombolytic treatment.
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PMID:Bleeding after thrombolysis in acute myocardial infarction. 270 62

Plasminogen Activator Inhibitors (PA Inhibitor) have recently been identified in plasma. They are directed against t-PA and Urokinase. Two PA Inhibitors have been described: PA Inhibitor 1 from endothelial cells, hepatocytes and platelets and PA Inhibitor 2 from placenta. Enzymatic assays have been developed. They show that plasma levels of PA Inhibitor are very low under normal conditions, but a considerable increase (X10 or 20) is found in several pathological conditions (thrombo embolic disease, atherosclerosis, thrombotic risk factors (obesity, hypertriglyceridemia, diabetes) inflammatory syndrome, post operative period for PA Inhibitor 1, and in some physiological conditions (pregnancy for PA Inhibitor 2). These results plead for a pathogenic role of PA Inhibitor 1 in the development of thrombosis. Pharmacological products able to decrease the plasma level of PA Inhibitor are as yet scarce. Stanozolol, an anabolic steroid, some biguanides such as Metformin possess this property.
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PMID:[Anti-activator inhibitors of plasminogen]. 311 99

Rat islets of Langerhans produce plasminogen activators (PA). The islet level of PA and the enzyme secreted in the islet incubation medium, are regulated by agents which modulate insulin synthesis and release. The cellular PA activity is due to 2 molecular forms of the enzyme, a Mr 72,000 and a Mr 48,000 species found in almost equal proportions. But the enzyme activity in the medium is due to only the lower molecular weight form. It is shown that this enzyme activity in the medium is due to immunologically identifiable urokinase type PA (uPA) and the cellular enzyme activity is due to both, uPA and tissue-type PA (tPA).
Diabetes Res 1987 Sep
PMID:Selective secretion of only the urokinase plasminogen activator from rat islets of Langerhans. 312 Dec 32

The effects of sulfonylureas on the production of plasminogen activator (PA) and antiactivator (PAI) were investigated using bovine aortic endothelial cells. All compounds studied stimulated PA release (1.3- to 5.2-fold), with glipizide being the most potent, followed by tolazamide, chlorpropamide, and tolbutamide, in that order, while glyburide was the least effective. Both tissue-type and urokinase-type PA production was enhanced. Studies using metabolic inhibitors indicated that both RNA and protein syntheses are required for the sulfonylurea-mediated stimulation of PA release. In addition to continuous release of the two PAs, there was also a continuous release of a single PAI, which did not show an increase after the sulfonylureas. These results suggest that, in addition to their beneficial effects in the treatment of diabetes mellitus, some sulfonylurea compounds may also have significant thrombolytic effects. These results also suggest that pharmacological enhancement of PA production by vascular endothelial cells may be a promising antithrombotic mechanism.
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PMID:Effects of sulfonylureas on the synthesis and secretion of plasminogen activator from bovine aortic endothelial cells. 312 27


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