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)

The Schleider and/or the Exner test have been found positive in twenty-one patients; five of these patients suffered of systemic lupus erythematosus (SLE). The Quick time and the activated partial thromboplastin time are normal in 52% of the cases. 40% have a minor haemorrhagic diathesis, without other significant clotting defect and 30% have thrombo-embolic complications. The Schleider index is more often strongly positive (greater than 2) in these two groups. 58% have an anemia, 25% a mild thrombocytopenia not deep enough to explain an haemorrhagic tendency (from 90.000 to 140.000/mm3). Several auto-immune tests are frequently positive even without SLE. The Schleider test is positive in 86% of the cases and appears a little more useful for the diagnosis than the Exner test, which has a 71% positivity.
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PMID:[Comparative study of 2 common tests for lupus anticoagulant determination: critical analysis of the results observed in 21 patients]. 251 2

Phenylhydrazine (PHZ) is a hemolytic agent which has been used in the treatment of polycythemia vera. Recent studies performed in our laboratory have indicated that the PHZ-induced anemia is immuno-hemolytic in etiology, and a prolonged bleeding time was present in some of the rats chronically treated with PHZ. The nature of this bleeding tendency was explored in the present experiment. PHZ was administered to rats once a week for a six week period. During this time, the animals were monitored for prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen concentration, and individual coagulation factor levels as well as routine plasma chemistries and blood cell counts. In addition, radioimmunoassays (RIA) for prostacyclin, a platelet aggregation inhibitor, and prostaglandin (PG) E2 were performed. PHZ-treated animals displayed a significant elevation in both PT and APTT when compared with saline injected controls, although plasma fibrinogen levels were not appreciably altered. Further tests revealed a PHZ-induced decrease in prothrombin and factor V levels. In addition, a significant increase in plasma serum glutamate oxaloacetate transaminase (SGOT), lactate dehydrogenase (LDH), and alkaline phosphatase levels was observed as well as a diminution in cholesterol and triglycerides following PHZ administration. PHZ treatment also induced an elevation in prostacyclin levels and transient thrombocytopenia. These findings indicate that several factors may contribute to the prolonged bleeding time in PHZ-treated rats including a drug induced thrombocytopenia possibly associated with enhanced synthesis of autologous immunoglobulin G (IgG) against the senescent red cell antigen, and diminished synthesis of vitamin K-dependent coagulation factors which may be mediated by reduced vitamin K uptake by the hypo-cholesterolemic subjects.
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PMID:Hemostatic alterations associated with phenylhydrazine-induced anemia in the rat. 262 15

A bleeding disorder (von Willebrand's disease) was diagnosed in a 9-year-old male Himalayan cat examined because of persistent oral bleeding after routine dental extraction. Bleeding subsided after empirical treatment, which included prednisolone, vitamin K1, and transfusion of fresh blood, but recurred spontaneously after 8 months of apparent good health. Pertinent results of routine laboratory testing included an inconstant prolongation of the activated partial thromboplastin time and recurring iron-deficiency anemia. Assays of specific coagulation factors revealed low factor VIII coagulant activity and undetectable factor VIII-related antigen, a pattern considered to be diagnostic of von Willebrand's disease. This condition, not previously reported in a cat, should be included in the differential diagnosis when cats are examined because of abnormal bleeding.
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PMID:A bleeding disorder (von Willebrand's disease) in a Himalayan cat. 310 51

An 18-year-old white woman admitted for an incomplete septic abortion was found to have thrombocytopenia, anemia, and increased activated partial thromboplastin time (PTT). Additionally, results of nontreponemal serologic tests for syphilis were positive, and the fluorescent antinuclear antibody was weakly positive. A mixture of the patient's plasma with normal control plasma showed that the elevation in activated PTT was the result of a circulating anticoagulant, not an inherent clotting defect. Sclerodermoid features were present and consisted of bound-down, hairless skin and scattered subcutaneous indurated plaques. A faint pattern consistent with livedo reticularis was recognized on all extremities. Biopsy specimens of sclerodermoid lesions showed increased and thickened dermal collagen consistent with morphea. We believe that this patient's condition represents an unusual connective tissue disease syndrome consisting of abortion, livedo reticularis, thrombocytopenia, circulating "anticoagulant," negative or slightly positive antinuclear antibodies, and false positive results on nontreponemal serologic tests for syphilis. Sclerodermoid lesions were also a unique feature in our patient.
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PMID:Connective tissue disease associated with sclerodermoid features, early abortion, and circulating anticoagulant. 314 41

Swiss albino mice were infected by the intraperitoneal route with P. berghei berghei malaria parasite, and platelets, white cell counts and some coagulation parameters were monitored in order to find out whether changes reported in man also occurred in the mice. Parasitaemia developed form the 2nd post-infection day and reached significant levels by the 4th-6th day. Reduced circulating platelets which reached severe thrombocytopenic levels were observed. parallel with the increasing degree of parasitaemia. Anaemia which progressed to severe degree was also observed as was a slight leucocytosis attributed to the presence of normal mouse erythrocytes in the peritoneal space. All untreated animals died by the 6th day of infection. Intramuscular chloroquine sulphate (20 micrograms/g body wt.) given for 7 days completely cured the malaria, and white cell and platelet counts were restored to preinfection levels in each animal about 2 weeks after treatment had ceased. Platelet hypersensitivity to exogenous ADP was observed within 48 hours of infection and persisted with the parasitaemia. Prothrombin time (PT) and activated partial thromboplastin time (APTT) were prolonged while clottable fibrinogen concentration was reduced.
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PMID:Platelet reactions in acute Plasmodium berghei infection in Swiss albino mice. 330 58

Among 617 hospitalized patients who started long-term anticoagulant therapy, major bleeding developed before discharge in 28 (5 percent) and minor bleeding in another 38 (6 percent), with daily incidence rates of 0.4 and 0.5 percent, respectively. The most common site of bleeding was gastrointestinal, and one patient died from bleeding. Four independent risk factors for major in-hospital bleeding were identified and weighted using multivariate discriminant analysis in a randomly chosen group of 411 patients: co-morbid conditions other than the indication for anticoagulant therapy (specific signs of heart, liver, or kidney dysfunction, cancer, and severe anemia); the use of heparin to begin therapy in patients age 60 years or older; the intensity of therapy (measured by the maximal prothrombin time or partial thromboplastin time); and liver dysfunction that worsened during treatment. These findings were validated in an independent testing group of 206 patients; the risk factors identified 151 patients at low (1 percent) risk of major bleeding, 33 at moderate (6 percent) risk, and 22 at high (23 percent) risk. The accuracy and clinical impact of this prediction rule should be evaluated further in other hospitals.
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PMID:Identification and preliminary validation of predictors of major bleeding in hospitalized patients starting anticoagulant therapy. 349 97

(WB X C57BL/6)F1-W/WV mice possess a genetic defect in multipotential hematopoietic stem cells; the mice are anemic and lack mast cells. The authors injected diluted India ink intravenously into W/WV mice and congenic normal +/+ mice and searched for genetically determined differences in the development of complications of the injection. In both W/WV and +/+ mice, intravenous ink resulted in thrombocytopenia and markedly prolonged bleeding times, as well as prolonged partial thromboplastin and prothrombin times and reduced fibrinogen concentrations. These effects were similar in W/WV and +/+ mice, although the reduction in platelet counts was greater in W/WV mice. In addition, the mortality associated with ink injection was significantly higher in W/WV mice than in congenic +/+ mice. Most W/WV mice which died first exhibited paralysis, and examination under the dissection microscope revealed that ink injection resulted in significantly more cerebral thromboemboli in W/WV mice than in +/+ controls. Bone marrow transplantation from +/+ mice corrected both the mast cell deficiency and the anemia of W/WV mice and protected the W/WV recipients from the adverse consequences of ink injection. By contrast, +/+ mice rendered as anemic as W/WV mice by breeding did not exhibit increased morbidity and mortality after ink injection. (WC X C57BL/6)F1-Sl/Sld mice, which are anemic and lack mast cells because of a genetic defect different from that of W/WV mice, also exhibited increased morbidity and mortality after intravenous ink. Finally, mixture of ink with commercial heparin prior to intravenous injection markedly reduced the incidence of cerebral thromboembolism and death in W/WV mice. Taken together, these findings suggest that the increased morbidity and mortality exhibited by W/WV and Sl/Sld mice that received injected ink might be related to their mast cell deficiency rather than to their anemia. But measurement of the histamine content of the blood and various tissues of WBB6F1-+/+ mice injected with ink, and examination of their tissues in 1-mu sections, indicated that intravenous ink did not cause substantial mast cell degranulation. As a result, the possibility that mast cells protect +/+ mice from the adverse effects of intravenous ink by a mechanism other than degranulation and release of heparin, or that the differences in the response of W/WV or Sl/Sld mice and their +/+ littermates are due to defects other than their lack of mast cells, cannot be excluded.
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PMID:Higher susceptibility of mast-cell-deficient W/WV mutant mice to brain thromboembolism and mortality caused by intravenous injection of India ink. 351 1

A 16-year-old gelding was examined because of weight loss, inappetence, and intermittent fever of 2 months' duration. Preliminary laboratory findings revealed anemia, hypoproteinemia, thrombocytopenia, and prolongation of the activated partial thromboplastin time. A deficiency or inhibition of coagulation factor XI, factor XII, or high molecular weight kininogen was diagnosed. This defect was not associated with a bleeding diathesis, but should be considered as a cause of prolongation of the activated partial thromboplastin time.
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PMID:Deficiency of the contact phase of intrinsic coagulation in a horse. 383 95

Rats and mice were fed a diet containing aspirin at levels of 0, 0.3, 0.6 and 1.2% for 1 and 4 weeks. Haemorrhagic death and/or haemorrhagic anaemia occurred in rats in a dose-dependent manner. Prothrombin and kaolin-activated partial thromboplastin time indices were also decreased depending on the daily doses. However, no conspicuous haemorrhagic signs were found in mice given aspirin. These results suggest marked differences in haemorrhagic effects of aspirin between rats and mice. From results of supplementary experiments with two metabolites of aspirin, salicylic acid and gentisic acid, and from the fact of close relationship between hepatic concentration of salicylic acid and haemorrhagic effects of aspirin, it is inferred that salicylic acid may be a precursor for the active metabolite(s) to cause haemorrhage. The mechanism of species differences of aspirin is discussed.
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PMID:Differences in the haemorrhagic toxicity of aspirin between rats and mice. 387 9

Dural sinus thrombosis developed in a young man with paroxysmal nocturnal hemoglobinuria (PNH). His neurological disorder developed in the face of anemia and a urinary tract infection. Progressive neurological deterioration occurred in spite of anticoagulation, antibiotic and steroid therapy. The propensity to develop cerebral vein and sinus thrombosis in PNH may be due to release of thromboplastin material from hemolyzed red blood cells, the interaction of complement with red blood cells and platelets, or from increased sensitivity to platelet aggregation.
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PMID:Dural sinus thrombosis in paroxysmal nocturnal hemoglobinuria. 609 61


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