1,721,241 research outputs found
Cost-effectiveness of screening and extended anticoagulation for carriers of both factor V Leiden and prothrombin G20210A
No full textLife expectancy and prognostic factors in the classic BCR/ABL-negative myeloproliferative disorders
No full textAmong the 'classic' BCR/ABL-negative chronic myeloproliferative disorders, primary myelofibrosis (PMF) is associated with a substantial life-expectancy reduction. In this disease, initial haemoglobin level is the most important prognostic factor, whereas age, constitutional symptoms, low or high leukocyte counts, blood blast cells and cytogenetic abnormalities are also of value. Several prognostic systems have been proposed to identify subgroups of patients with a different risk, which is especially important in younger individuals, who may benefit from therapies with curative potential. Essential thrombocythaemia (ET) affects the patients' quality of life more than the survival, due to the high occurrence of thrombosis, whereas polycythaemia vera (PV) has a substantial morbidity derived from thrombosis but also a certain reduction in life expectancy. Therefore, in the latter disorders, prognostic studies have focused primarily on prediction of the thrombosis, with age and a previous history of thrombosis being the main prognostic factors of such complication. The importance of higher leukocyte counts in thrombosis development has been recently pointed out in ET and PV, where a role for mutated JAK2 allele burden has also been noted. With regard to PMF, the possible association of the mutation with shorter survival and higher acute transformation rate is currently being evaluated
Medical diagnostic reasoning. Epistemological modeling as a strategy for design of computer-based consultation programs
No full text
Cold haemagglutinin disease with severe anaemia, reticulocytopenia and erythroid bone marrow.
No full textA quantitative assessment of total, effective and ineffective erythropoiesis, and mean red cell life-span was performed in 2 patients with idiopathic cold-haemagglutinin disease (CHAD) who had severe anaemia, reticulocytopenia and erythroid bone marrow. In both cases, ineffective erythropoiesis represented the major factor in the pathogenesis of the anaemia. The most likely explanation of this was that cold antibodies had some effect on the maturing red-cell precursors. Ineffective erythropoiesis has already been shown in patients affected by auto-immune haemolytic anaemia due to warm antibodies with reticulocytopenia and erythroid bone marrow. Therefore, it is apparent that both warm and cold antibodies may cause not only peripheral destruction of mature red cells but also intramedullary death of red-cell precursors
An improved method for liquid scintillation counting of 59Fe in ferrokinetic studies.
No full textA new method for liquid scintillation counting of 59Fe in plasma and whole blood is described. This method allows a better analysis of iron kinetics in man
Iron kinetics.
No full textChater on iron kinetics in man and the use of mathematic models for its analysis
In vitro platelet aggregation defects in patients with myeloproliferative disorders and high platelet counts: are they laboratory artefacts?
No full textAbstract
It has been recently shown that in vitro platelet aggregation is inhibited when platelet concentration in platelet-rich plasma (PRP) is "normalized" by the addition of platelet-poor plasma (PPP). In this study we tested the hypothesis that the large amount of PPP required to "normalize" PRP in patients with thrombocytosis may result in falsely defective platelet function. To this end, we evaluated platelet aggregation in PRP samples "normalized" with either PPP or buffer in 16 patients with high platelet counts induced by myeloproliferative disorders. Comparison with the results obtained in healthy subjects demonstrated that patients had reduced platelet responses to ADP or collagen in PRP/PPP samples, but normal responses in PRP/buffer. By contrast, the majority of patients had severely defective platelet response to epinephrine independently from the methodological approach. We suggest that the reduced in vitro platelet aggregation previously described in patients with myeloproliferative disorders and thrombocytosis partially derived from a laboratory artefact
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