Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet functions and blood coagulation have been regularly investigated in 31 patients undergoing maintenance haemodialysis for 5 months to 6 years. Fifteen of them suffered from at least two arteriovenous fistula thrombosis during the year prior the first examination. Eleven patients, including eight with recurrent thrombosis, received 300-400 mg per day dipyridamole during 1 month to 2 years. Some abnormalities are commonly observed in the whole studied population: lowering of platelet adhesiveness, defective aggregation in the presence of both collagen and ADP 5. 10-5 M; increased level of factor V and mainly factor VIII. Mean platelet factor 3 activity was in the normal range with variations from one case to another. The only unusual feature observed in patients with recurrent thrombosis was an increase of platelet aggregation induced by ADP 0.5. 10-6 M. Neither spontaneous aggregation nor significant abnormality of plasminogen level and plasma antithrombin activity were observed. Under dipyridamole therapy, correction of platelet hyperaggregability was observed in all patients and improvement of platelet adhesiveness in half the studied cases (despite the unchanged anaemia). The treatment significantly decreased the frequency of arteriovnous fistule thrombosis in the six patients observed during two consecutive years, the first one without and the second under treatment: the total number of thrombosis was 18 during the first and 3 in the second period.
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PMID:[Disorders of haemostasis in patients undergoing maintenance haemodialysis, with special reference to recurrent arteriovenous fistula thrombosis. Effects of dipyridamole (author's transl)]. 82 31

Several different preparations of cross-linked hemoglobin (CLHb) are being evaluated for their efficacy and safety as red cell substitutes in a variety of preclinical and clinical settings. Because CLHb is known to sequester nitric oxide (NO) and inhibit NO-mediated processes, we hypothesized that CLHb would have a hemostatic effect by enhancing platelet reactivity, inducing vasoconstriction, or both. Infusion of o-raffinose CLHb shortened the prolonged microvascular bleeding time and decreased blood loss from ear incisions in rabbits rendered anemic and thrombocytopenic. Moreover, this hemostatic effect persisted for at least 24 hours after infusion. Phenylephrine induced a degree of vasoconstriction similar to that induced by CLHb but did not shorten the bleeding time or decrease blood loss, suggesting that vasoconstriction alone cannot account for the hemostatic effect of CLHb. There was no evidence of CLHb-induced activation of coagulation in vivo, since infusion of CLHb did not increase circulating levels of thrombin-antithrombin complex. In vitro, CLHb abolished the inhibitory effect of the NO donor 3-morpholinosydnonimine on platelet aggregation and enhanced the aggregation of stimulated but not resting platelets. This potentiating effect was not attenuated by the addition of superoxide dismutase or catalase. To evaluate the potential arterial thrombogenicity of CLHb, a model of carotid artery thrombosis was developed in rabbits without thrombocytopenia or anemia. Compared with albumin infusion, CLHb infusion shortened the time to complete carotid occlusion. These data suggest that CLHb may shift the thromboregulatory balance toward clot formation, resulting in decreased bleeding in anemic and thrombocytopenic rabbits and possibly increasing arterial thrombogenicity in normal rabbits.
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PMID:o-raffinose cross-linked hemoglobin improves the hemostatic defect associated with anemia and thrombocytopenia in rabbits. 1107 64

A 13-year-old neutered male Jack Russell Terrier (Parson Russell Terrier) was presented to the Texas Veterinary Medical Center with a history of lethargy, depression, vomiting, and fever. The dog had mildly regenerative anemia, severe thrombocytopenia and low antithrombin activity. Marked splenomegaly was found on physical examination and imaging studies, and malignant round cell neoplasia and marked extramedullary hematopoiesis were diagnosed on aspirates of the spleen. The dog underwent exploratory laporatomy and splenectomy. Because of a rapid decline in clinical condition postsurgery, the dog was euthanized. Splenic and hepatic biopsies were submitted for histopathologic evaluation. A neoplastic population of round cells was found throughout the splenic parenchyma and within hepatic sinusoids. The neoplastic cells stained strongly positive for CD3 (T-cell marker) and were negative for CD79a (B-cell marker) and lysozyme (histiocytic marker). A diagnosis of T-cell lymphoma was confirmed by assessment of T-cell clonality using canine-specific polymerase chain reaction-based techniques. Although expression of the gammadelta T-cell receptor was not evaluated, this case shares many similarities with a rare syndrome in humans known as hepatosplenic gammadelta T-cell lymphoma.
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PMID:Morphologic, immunohistochemical, and molecular characterization of hepatosplenic T-cell lymphoma in a dog. 1519 70

Cadmium, a highly toxic heavy metal, is distributed widely in the general environment. The characteristic clinical manifestations of chronic cadmium intoxication include renal proximal tubular dysfunction, osteomalacia and anemia. Accumulating evidence suggests that cadmium toxicity may also affect various organs such as the liver, lung, testis and hematopoietic system. The aim of this study was to determine the effect of chronic cadmium exposure on the anticoagulant system in rats. Fourty-five adult Wistar albino rats were randomly allocated into 2 groups. While the control group was given tap water, the animals in the cadmium group were treated with 15 ppm CdCl(2) for 4 weeks. Blood cadmium concentration, prothrombin time, activated partial thromboplastin time, plasma protein C and antithrombin activity, and platelet count were determined in the rats. Blood cadmium concentrations increased in the experiment group compared to the control group (p < 0.001). Results also show that cadmium exposure shortened prothrombin time (p < 0.05) and activated partial thromboplastin time (p < 0.01) in rats. Protein C (p < 0.001) and antithrombin (p < 0.001) decreased to statistically significantly lower levels in rat plasma after cadmium exposure when compared to the control group. When the number of thrombocytes was compared between 2 groups, a decrease was observed in the group treated with CdCl(2), which was, however, not statistically significant (p > 0.05). In conclusion, when the parameters of the hemolytic system are considered, the decrease in protein C and antithrombin activities and the shortening of prothrombin time and activated partial thromboplastin time suggests the presence of a hypercoagulable state during chronic cadmium intoxication. Therefore, it may be stated that chronic cadmium toxicity sets the stage for hypercoagulation and hence increases the risk of thrombosis.
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PMID:The effects of chronic cadmium toxicity on the hemostatic system. 1756 33

During the period January 2002-December 2004, we assessed 30 sickle-cell anaemia patients admitted to hospital in Al Khobar with vaso-occlusive crisis for levels of antithrombin (AT) III, protein C (PC) and protein S (PS). We also did platelet aggregation studies. Steady state levels were assessed during follow-up and compared with 36 adult controls. Levels of PC, PS and AT III in the control group were significantly higher than in those in vaso-occlusive crisis and those in steady state (P < 0.001). There was a statistically significant difference between controls and patients for all platelet aggregation factors except adrenaline. There was no significant difference between the levels of PC, PS, AT III and platelet aggregation variables in patients in the steady state and in vaso-occlusive crisis.
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PMID:Platelet aggregation and physiological anticoagulants in sickle-cell disease. 1768 47

In clinical trials up to 30% of patients with acute coronary syndromes (ACS) or undergoing percutaneous coronary intervention (PCI) experience bleeding complications, and even higher rates have been reported in contemporary practice. A growing body of data suggests a strong correlation between bleeding and both short- and long-term adverse outcomes, including mortality, which is independent of baseline characteristics and remains evident in most trials, despite variations in the definition of major bleeding. Although the value of antithrombin and antiplatelet therapy in reducing the risk of ischemic events is well established, the mechanisms of action that confer the benefits of these therapies have an inherent tendency to increase the risk of bleeding complications. As a result, characterization of baseline hemorrhagic risk is critical and must be accomplished before selecting an antithrombotic therapy. Risk factors for bleeding may be divided into two categories: nonmodifiable (including age, gender, race, weight, renal insufficiency, anemia, and acuity of presentation) and modifiable (including choice of antithrombotic therapy and PCI procedural characteristics). Of these predictive factors, the choice, dosage, and duration of the antithrombin and/or antiplatelet regimen are perhaps the most readily modifiable, especially in patients with an increased risk of bleeding. This review explores the nature of the association between bleeding and adverse outcomes, including mortality; evaluates risk factors for bleeding; and examines mechanisms for reducing bleeding complications through the selection of appropriate antithrombotic therapy.
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PMID:Bleeding complications in acute coronary syndromes and percutaneous coronary intervention: predictors, prognostic significance, and paradigms for reducing risk. 1822 49

Although the use of oral and intravenous antiplatelet and antithrombin therapy in the acute and chronic settings of percutaneous coronary intervention (PCI), acute coronary syndromes (ACS), and ST-segment elevation myocardial infarction (STEMI) effectively reduce ischemic event rates, they are mechanistically and inextricably linked to an increased risk of bleeding. As longer courses of more complex, potent regimens are used, increased efficacy may be offset by increases in major, minor, and nuisance bleeding, both in the inpatient and outpatient setting. Consequently, more frequent challenges with cessation of and compliance with antithrombotic therapy are to be expected. Extensive data indicate that bleeding complications (1) occur with relative frequency; (2) independently affect adverse outcomes, such as mortality; (3) carry similar importance in adversely influencing mortality as ischemic events; (4) can be predicted by recognizing patient, presentation, treatment, and procedural risk factors for bleeding; and (5) can be modified by pharmacologic and nonpharmacologic means. Factors associated with increased bleeding risk include: (1) patient characteristics (including advanced age, female sex, hypertension, renal disease, anemia, previous history of bleeding, and perhaps diabetes mellitus), (2) clinical presentation (bleeding rates appears lowest for PCI, higher for ACS, and highest for STEMI), (3) abnormalities of cardiac biomarkers and/or electrocardiography, (4) invasive procedures (such as cardiac catheterization and PCI), and (5) the choice of antiplatelet and antithrombin therapy. In the context of a bleeding assessment, evidence-based decision making should always result in the selection of appropriate pharmacologic and nonpharmacologic strategies, invasive or conservative management plans, and stent types (bare metal vs drug-eluting) that will offer the best balance of benefit and risk with the goal of optimizing outcomes.
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PMID:Predictors and impact of bleeding complications in percutaneous coronary intervention, acute coronary syndromes, and ST-segment elevation myocardial infarction. 1969 55

Abnormality in hematological condition including hemolytic disorders has been suggested one of the risk factor of pulmonary thrombosis. We previously reported that phenylhydrazine (PHZ) could induce acute thrombosis in the rat lung. In this study, time-related hematological and histopathological changes were evaluated in PHZ-treated rats to reveal the pathogenesis of pulmonary thrombosis in hemolytic condition. Male Sprague-Dawley rats were administered PHZ at 40 mg/kg/day daily for up to 4 days (n=6). At 24 h after the last administration (i.e. on days 1, 2, 3, or 4), animals were euthanized and samples were subjected to hematology, light microscopy, and electron microscopy. PHZ-treated rats developed severe anemia on day 1 or later. On day 2 and after, congestion in the alveolar septa corresponding to accumulation of deformed/ghost erythrocytes in the alveolar capillaries was observed, which was the earliest change that preceded thrombus formation. Focal fibrin deposition in the alveolar septa was noted on day 3 and it expanded widely by day 4, while endothelial injury were minimally noted just on day 4. These congestive/thrombotic changes were predominant in the pulmonary capillaries. Changes in hemostatic parameters were noted only on day 4; which were prolonged prothrombin time and activated partial thromboplastin time, greatly increased plasma thrombin-antithrombin complex levels with statistical significance, and slightly decreased fibrinogen levels. In conclusion, the trigger of acute pulmonary thrombosis in PHZ-treated rats was considered to be regional stasis resulting from blockage caused by the deformed erythrocytes, and subsequent systemic hemostatic disruption.
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PMID:Hematological and morphological investigation of thrombogenic mechanisms in the lungs of phenylhydrazine-treated rats. 2240 72

Hepcidin controls systemic iron availability, and its excess contributes to the anemia of chronic diseases, the most prevalent anemia in hospitalized patients. We previously reported that heparins are efficient hepcidin inhibitors both in vitro and in vivo, but their anticoagulant activity limits therapeutic use. We studied nonanticoagulant heparins produced by N-acetylation and oxidation/reduction (glycol-split) that lost antithrombin-binding affinity. Four nonanticoagulant heparins inhibited hepcidin expression in hepatic HepG2 cells and primary hepatocytes. The 2 most potent ones used in mice suppressed liver hepcidin expression and serum hepcidin in 6 hours, with a significant decrease of spleen iron. This occurred also in lipopolysaccharide (LPS)-treated animals that mimic inflammation, as well as after chronic 1-week treatments, without evident adverse effects on coagulation. Heparin injections increased iron mobilization and facilitated the recovery from the anemia induced by heat-killed Brucella abortus, a model of inflammatory anemia. The heparins were used also in Bmp6(-/-) mice. A single dose of heparin reduced the already low level of hepcidin of these mice and prevented its induction by LPS. These nonanticoagulant compounds impair bone morphogenetic protein /sons of mothers against decapentaplegic signaling with no evident adverse effect in vivo, even when administered chronically. They may offer a strategy for the treatment of diseases with high hepcidin levels.
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PMID:Glycol-split nonanticoagulant heparins are inhibitors of hepcidin expression in vitro and in vivo. 2462 50

The clinical symptoms, causative factors, and prognosis in Japanese patients with cerebral venous thrombosis have not been adequately characterized. The present study describes these features in patients in Japan. Twenty-two patients with cerebral venous thrombosis were retrospectively identified. Diagnosis was confirmed by either digital subtraction angiography, magnetic resonance venography, or contrast-enhanced computed tomography. Demographic data and clinical and radiological features were recorded and analyzed for each patient. Prognosis was evaluated by the modified Rankin scale (mRS) at the time of hospital discharge. The most frequent symptom of cerebral venous thrombosis was headache (59.1 %). Causative factors included congenital thrombophilia (31.8 %), acquired thrombophilia (27.3 %), and iron-deficiency anemia (13.6 %). Of seven patients with congenital thrombophilia, four had mutations in the protein S gene, two had mutations in the protein C gene, and one had mutations in the antithrombin gene. All patients were alive at discharge from hospital. Nineteen of the 22 patients (86.4 %) recovered completely or exhibited only mild residual symptoms (mRS 0-2). However, three patients (13.6 %) had a poor prognosis (mRS 3-5). Cerebral venous thrombosis in Japanese patients is frequently associated with congenital thrombophilia and protein S gene mutation.
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PMID:Clinical features and underlying causes of cerebral venous thrombosis in Japanese patients. 2459 15


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