Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026986 (myelodysplastic syndrome)
 14,926 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effects of heparin, dextran sulphate (MDS), gabexate mesilate (FOY), nafamostat mesilate (FUT-175) and argipidine (MD-805) on APTT, PT, thrombin time (TT) and kaolin-activated PTT (KPTT) with various concentrations of phospholipid for screening of lupus anticoagulants (LA). Heparin, MDS and FUT-175 had a greater effect on APTT than PT. On the contrary, MD-805 had a similar effect on both APTT and PT, which suggests that MD-805 inhibits thrombin generation equally on intrinsic and extrinsic coagulation pathways. Heparin and MD-805 were more effective on TT than MDS, FUT-175 and FOY at high concentrations significantly prolonged TT. But, at even higher concentrations of FUT-175, prolongation of TT was reduced contrary to our expectation. With FOY TT became less prolonged with a passage of time, suggesting time-dependent reduction of its anticoagulant activity. Heparin (0.1-0.2 U/ml) and MDS (0.1-0.3 mg/ml) did not have any effect on KPTT with high concentration of phospholipid, but did FUT-175. It suggests that phospholipid inhibits anticoagulant activity of heparin and MDS. Anti-phospholipid activity of heparin and MDS is similar to that of LA. We concluded that the differentiation of LA from heparin-like inhibitors is needed.
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PMID:[The effects of various anticoagulants on blood coagulation: with special reference to false positive lupus anticoagulants]. 251 25

A case of 68 years old women suffering from chronic anemia, myelodysplastic syndrome and treated with progestogen due to endometrial hypertrophy is presented. Initially she was admitted to a regional hospital because of progressive weakness and exertional dyspnea. Three months earlier she reported an episode of acute dyspnea and chest pain. On the basis of clinical symptoms and perfusion lung scintigraphy pulmonary embolism (PE) was diagnosed. Patient received i.v. heparin which was changed to s.c. nadroparine subcutaneously. Platelet count dropped to 55,000'/ml on fifth day of treatment from initial level of about 200,000'/ml. Heparin induced thrombocytopenia was diagnosed, heparin was stopped and ticlopidine was recommended. After 3 weeks symptoms suggesting recurrent PE were observed. The patient was transferred to National Tuberculosis and Lung Diseases Research Institute. Recombinant hirudine (Refludan) was administrated (bolus 0.4 mg/kg and initial dose of infusion 0.1 mg/kg/h) overlapping with acenocoumarol from second day. Dose of r-hirudine was adjusted to achieve APTT prolongation 1.5 to 2.5 times of mid-normal range. During treatment with r-hirudine no bleeding and new thromboembolic complications occurred. Platelets count remained within normal range. After 14 days clinical improvement was observed, though symptoms of right ventricular overload and hypoxemia were still present after 6 months of treatment with oral anticoagulants suggesting chronic thromboembolic pulmonary hypertension.
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PMID:[Recombinant hirudine in suspected heparin induced thrombocytopenia--case report of pulmonary embolism]. 1143 91