Bone marrow (BM) examination is the gold standard test in discriminating between hyperdestructive thrombocytopenia and hypoproductive thrombocytopenia. However, this procedure is invasive. Mean platelet volume (MPV) is simple and may be used as an alternative diagnostic test in distinguishing these two types of thrombocytopenia. All thrombocytopenic patients (platelet count: <150.0 x 10(9)/l), except those with congestive splenomegaly, thrombotic thrombocytopenic purpura, and disseminated intravascular coagulopathy, were enrolled into the study prospectively. The mean MPV of normal Thais (7.9 fl) was tested as a cutoff value. Any thrombocytopenic patient with MPV of >7.9 fl would be presumptively diagnosed as hyperdestructive thrombocytopenia, whereas one with MPV of 7.9 fl could predict hyperdestructive thrombocytopenia with a sensitivity of 82.3% (95% CI: 70.5-90.8), a specificity of 92.5% (95% CI: 79.6-98.4), a positive predictive value of 94.4% (95% CI: 84.6-98.8), a negative predictive value of 77.1% (95% CI: 62.7-88.0), and a likelihood ratio of 11.0. In conclusion, the mean MPV of normal Thais may be used as a cutoff value in distinguishing these two types of thrombocytopenia.

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Summary The bone marrows of 21 Thai adults infected with Plasmodium falciparum malaria were cultured for CFU‐E and BFU‐E by using AB serum, autologous serum (parasitaemia) and autologous serum (post‐parasitaemia). Six patients had no complication and 15 patients had pulmonary, renal or haematologic complications. In the non‐complicated cases, sera during parasitaemia did not suppress the post‐parasitaema CFU‐E and BFU‐E. Post parasitaemia, there was suppression of CFU‐E by parasitaemia sera. In the complicated cases, the autologous sera during parasitaemia suppressed the growth of both CFU‐E and BFU‐E both during and after parasitaemia (P <0.05). The post‐parasitaemia sera had neither a suppressive nor a stimulating effect. In the complicated cases, the progenitor cells cultured from the bone marrow post‐parasitaemia were fewer in number than those cultured from the bone marrow during parasitaemia using the same sera. Two possible mechanisms of suppression are postulated, namely the reduction of erythropoietin or the increased tumour necrosis factor during malarial infection. Further studies to clarify this are being carried out.

The objective of this study was to determine the hematopoietic effects and toxicity of low-dose granulocyte colony-stimulating factor (G-CSF) in myelodysplastic syndrome (MDS) patients with neutropenia. Recombinant human G-CSF (Lenograstim) was administered by daily subcutaneous injection with an initial dosage of 0.5 microg/kg per day for 2 weeks. Patients not responding to the initial dosage received the escalated dosage, 1 to 2 microg/kg per day for 2 weeks. Eligibility criteria were the following: French-American-British disease classification subtype refractory anemia (RA), refractory anemia with ringed sideroblasts (RARS), or refractory anemia with excess blasts (RAEB) with an absolute neutrophil count (ANC) of <1.5 x 10(9)/L. Criteria indicating response to treatment were ANC of >1.5 x 10(9)/L and doubling of ANC on at least 2 occasions. Thirty-two MDS patients were recruited from 6 university hospitals. Eighteen patients had RA, 4 had RARS, and 10 had RAEB. Median age was 56.4 years (range, 28-87 years). Twenty-six patients (81.2%) had an increase in ANC from a median of 0.94+/-0.35 x 10(9)/L to 4.24+/-3.78 x 10(9)/L. Three of 6 patients who did not respond to the initial dosage responded to the escalated dosage of 1 microg/kg per day. Eighteen (81.8%) of 22 patients with RA or RARS responded compared with 8 (80%) of 10 patients with RAEB. The response rates in patients with ANCs of <0.5 x 10(9)/L. 0.5 to <1.0 x 10(9)/L, and 1.0 to 1.5 x 10(9)/L were 80%, 70%, and 88.2%, respectively. The side effects were minimal. No significant changes in hemoglobin levels or platelet counts were observed. In conclusion, low-dose G-CSF administered by subcutaneous injection is well tolerated and effective in improving neutropenia in MDS patients.

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