Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0022116 (ischemia)
91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most commonly recognized cause of mesenteric venous thrombosis following splenectomy is hypercoagulation secondary to reactive thrombocytosis. A case is reviewed in which hypercoagulation followed splenectomy for idiopathic thrombocytopenic purpura (ITP) in spite of persistent thrombocytopenia. Episodic mesenteric venous occlusion occurred due to antithrombin III deficiency. This hypercoagulable state may be the cause of primary acute mesenteric venous occlusive disease. Symptoms and signs suggesting thrombosis in the portal circulation demand immediate coagulation studies since even in the thrombocytopenic patient thrombotic proglems can occur. Surgical intervention is the treatment of choice for segmental small bowel ischemia; warfarin therapy is indicated when there is evidence of antithrombin III deficiency.
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PMID:Antithrombin III deficiency causing postsplenectomy mesenteric venous thrombosis coincident with thrombocytopenia. 6 57

A common although infrequently recognized complication associated with the use of a pneumatic tourniquet is profuse bleeding from the wound after deflation of the tourniquet. The purpose of this study was to determine whether intravascular coagulation and fibrinolysis could be induced in subhuman primates by tourniquet ischemia, and whether this phenomenon could be altered by pretreatment of the animal with heparin. It was shown that, after 2(1/2) hours of tourniquet ischemia, (400 mmHg) to one lower limb, fibrinogen levels were significantly lower (p < .005), antithrombin III levels were significantly lower (p < .05), plasminogen levels were significantly lower (p < .05), fibrin split products significantly higher (p < .025) and fibrinopeptide A levels were significantly higher (p < .02) than values measured simultaneously in the control limbs. After pre-treatment with sodium heparin, 30 units/kg, there was no change in antithrombin III levels or fibrinogen levels, but fibrin split products in the experimental limbs were significantly elevated (p < .05) when compared to control limbs. In both groups the abnormal levels returned to control levels 5-30 minutes after tourniquet deflation. We conclude that intravascular coagulation and fibrinolysis develop within ischemic subhuman primate limbs during tourniquet ischemia. Pretreatment with heparin prevents the consumption of fibrinogen and antithrombin III but does not prevent the increase in fibrin split products which was observed. It is possible that intravascular coagulation and fibrinolysis contribute to post tourniquet bleeding.
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PMID:Intravascular coagulation and fibrinolysis within primate extremities during tourniquet ischemia. 11 39

In this paper the authors try to specify the leg ulcers physiopathology. They have first studied the vascular deficits, and they are able to conclude that this deficit is not the only factor responsible for the thrombosis. They try to rediscover the factors which could lead to the thrombosis, on the created local conditions (circulatory slackening, cooling, ischemia), by using clinical and biological "check-ups" as well as an exploration of the clotting. In many patients we find an anomaly such as: clotting "check-ups" disturbance, thrombocyte hyperaggregability, fibrinolysis deficit, antithrombin III deficit, cryoprecipitate, circulating immune complexes, hepatic "check-up" alteration. It is difficult to establish an accurate relation between these anomalies and a thrombosis but the frequent existence of such anomalies makes us think that they play a part in the ulcerations coming-up.
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PMID:[Leg ulcer. Vascular and thrombosis factors. Each responsibility of those factors? (author's transl)]. 50 59

Following liver transplantation, the decision to retransplant in cases in which graft function is marginal must be taken early. Plasma coagulation factor monitoring was evaluated as an early predictor of graft failure requiring retransplantation in the first posttransplant week. Plasma levels of fibrinogen, factors V, VII, VIII, IX, antithrombin III, protein C, and plasminogen were measured in all patients at 0, 12, 24, 48, 72, 96, and 120 hours posttransplant in 46 patients who received 56 grafts and results were compared between livers that failed early (group 1) and those that functioned adequately (group 2). Six grafts were included in group 1: one patient died before retransplantation, four were retransplanted once, and one patient was retransplanted twice. Three grafts had primary nonfunction (PNF), 2 had obstructed portal veins, and 1 had a long period of warm ischemia during the initial transplant. In group 1, plasma levels of factor V were significantly lower than in group 2 at 24, 48, and 72 hours posttransplant (21.2% +/- 14.2%, 12.4% +/- 4.5%, and 13.0% +/- 5.0% v 39.1% +/- 23.9%, 48.8% +/- 31.9%, and 60.9% +/- 25.9%; P less than .05, P less than .01, and P less than .005, respectively). Similarly, plasma levels of factor VII were significantly lower in group 1 over the same period of time (7.3% +/- 2.7%, 4.2% +/- 1.8%, and 4.7% +/- 2.5% v 27.4% +/- 17.1%, 34.1% +/- 21.6%, and 34.8% +/- 18.6%, respectively; P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coagulation plasma factor levels are early indicators of graft nonfunction following liver transplantation in children. 150 Oct 1

The influence of a disturbed hemostasis as one of the causes of retinal vein occlusions is still controversial. We investigated the functional state of the coagulation system in 16 patients, 7 with a nonischemic and 9 with an ischemic retinal vein occlusion, with an enzyme-linked immunosorbent assay for the determination of thrombin-antithrombin III complex (TAT). Patients with a history of thromboembolic disease, raised blood pressure and/or badly managed diabetes mellitus were excluded from the investigations. In healthy individuals the plasma concentration is 1.45 ng/ml +/- 0.4 (mean value +/- SD), ranging from 1.0 to 4.1 ng/ml. In our patients we measured TAT concentrations ranging from 2.0 to 48.0 ng/ml. In 2 of 7 plasma samples from patients with nonischemic retinal vein occlusion (2.1-6.3 ng/ml, mean = 3.3, SE +/- 0.6) and in 6 of 9 in ischemic retinal vein occlusion (2.0-48.0, mean = 13.2, SE +/- 5.1) TAT concentrations were found to be increased. These data indicate that disturbed hemostasis may be involved in retinal vein occlusion, especially that caused by ischemia. Furthermore, TAT may be useful in differentiating ischemic from nonischemic retinal vein occlusion.
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PMID:[Thrombin-antithrombin III complex. Cause of venous vascular occlusion of the retina]. 158 96

We report a case of unstable angina in an active phase of polymyositis. A 51 year-old man was admitted with a diagnosis of polymyositis and unstable angina with ST elevation on prolonged rest chest pain. Rest anginal attack which had been refractory to conventional antianginal medications was controlled by high dose of glucocorticosteroid. Electrocardiography revealed multifocal premature ventricular contraction. Since silent ischemia on exercise persisted, percutaneous transluminal coronary angioplasty (PTCA) was performed on a stenotic lesion in the left anterior descending artery. Since there was recurrent anginal attack, re-PTCA was carried out at the same site. He was discharged in a good condition. This case is considered to be associated with cardiac involvement of polymyositis because of ventricular arrhythmia, persistent increased serum levels of CPK-MB, and the marked benefits of corticosteroid against unstable angina. In addition, clinical manifestations, coronary arteriographic findings, and increased plasma levels of thrombin-antithrombin III complex suggest that cardiac involvement in polymyositis accelerates intracoronary thrombus formation and/or coronary spasm.
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PMID:[A case of unstable angina pectoris associated with an active phase of polymyositis]. 158 49

It has been suggested that unstable angina at rest, like acute myocardial infarction, might be associated with a thrombotic process. In order to study the hypothesis that myocardial ischemia during exercise could also be associated with an activation of blood coagulation and/or fibrinolysis, we investigated the presence of plasma markers of a prethrombotic or thrombotic state (thrombin-antithrombin III complexes TAT, prothrombin fragment F1 + 2, and D-dimers DD) in 100 consecutive patients with confirmed or suspected coronary artery disease during ergometric test with myocardial thallium-201 scintigraphy. Symptoms and scintigrams allowed to define three groups of patients: those showing no ischemia (n = 79) and those with symptomatic (n = 8) or silent myocardial ischemia (n = 13). Before exercise, DD and TAT levels were not significantly different among the three groups. On the other hand, the F1 + 2 levels were slightly albeit significantly higher in the patients without ischemia than in the patients with symptomatic or silent ischemia. After exercise, no significant difference was found between the three groups. Exercise induced a significant and parallel increase in both the TAT and the F1 + 2 levels (but not of the DD levels) in the three groups. Thus, our study does not support the hypothesis that myocardial ischemia, silent or symptomatic, is associated with an activation of plasma coagulation and fibrinolysis that can be distinguished from the exercise-induced thrombin generation.
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PMID:Effects of exercise test on plasma markers of an activation of coagulation and/or fibrinolysis in patients with symptomatic or silent myocardial ischemia. 160 40

More than a dozen primary hematologic disorders have been associated with ischemic stroke. Inherited deficiencies of antithrombin III, protein C, and protein S have been linked with stroke in case reports; optimal screening requires functional as well as antigenic assays. Antiphospholipid antibodies and lupus anticoagulants are the most frequently identified acquired states associated with ischemic stroke. Polycythemia vera, sickle cell anemia, sickle-C disease, and essential thrombocythemia are the major disorders of formed blood elements causing stroke. Special, step-wise screening for occult prothrombotic entities in stroke patients is recommended for young persons with stroke of uncertain cause, for those with prior venous thrombosis, for those with a family history of unusual thrombosis, and for those with no other explanation for recurrent stroke. Acquired, perhaps transient, abnormalities of platelets, coagulation inhibition, and fibrinolysis may contribute importantly to brain ischemia in synergy with other mechanisms, but at present these remain ill-defined. The contribution of prothrombotic diatheses to stroke is probably underrecognized and warrants further investigation.
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PMID:Hematologic disorders and ischemic stroke. A selective review. 186 63

A patient with congenital protein-C deficiency was treated with stanozolol for 8 weeks to increase circulating levels of protein C. A rise in protein C was achieved, accompanied by an increase in factor II, factor X, antithrombin III, and protein S; but at the 8th week the patient suffered a transient ischemia attack.
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PMID:Transient ischemic attack in a patient with congenital protein-C deficiency during treatment with stanozolol. 318

Clinical pathology is a valuable adjunct to physical examination of cases of colic. The present review considers evaluation of cases of colic for three main purposes: (1) making a prognosis, (2) deciding whether to operate, and (3) making a diagnosis. Blood tests noted to be useful for prognostication were hematocrit, lactate and urea nitrogen concentrations, pH, anion gap, fibrin/fibrinogen degradation products, antithrombin III activity, prothrombin time, and thrombin time. Horses with a poor prognosis often have relative polycythemia, marked lactic acidosis, high anion gap, azotemia, and coagulation abnormalities evidenced by increased fibrin/fibrinogen degradation products, decreased antithrombin III activity, and prolonged prothrombin and thrombin times. The decision to operate is usually a clinical one, supported by relative polycythemia, hyperglycemia, and, possibly, abnormal peritoneal fluid analysis. Diagnosis of the primary problem (causing the colicky signs) is also often based largely on physical examination. However, peritoneal fluid analysis provides worthwhile data, especially in cases of peritonitis or intestinal ischemia and infarction.
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PMID:Use of clinical pathology in evaluation of horses with colic. 332 25


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