Multicenter randomized control trial on safety of domestic idarubicin for acute leukemia / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To evaluate the safety of domestically produced idarubicin in the treatment of acute leukemia by a multicenter randomized control trial.</p><p><b>METHODS</b>This trial was carried out in the hemotologica department of five hospitals throughout China, with hospitalized patients who suffered from acute myelogenous leukemia ( AML except M3 type) , acute lymphocytic leukemia ( ALL) , chronic myelogenous leukemia-blast (CML-blast) , totally 155 patients. Those with severely cardial, hepatic or renal disfunction or those who had ever treated with > or = 200 mg/m(2) idarubicin were excluded from the trial. All patients signed the letter of consent as required by the Ethics Committee of our government. In this study, 155 leukemia patients were randomly grouped into: 1. test group treated using domestic idarubicin, 2. control group using imported idarubicin. The acute myelogenous leukemia regimen included idarubicin 8 mg/m(2), dl -3 plus cytosine arabinoside 100 mg/m(2), dl - 7 for 1-2 cycles. The regimen for acute lymphocytic leukemia was idarubicin 8 mg/m2, dl - 3; vincristine 2 mg/mr, dl; cyclophosphamide 750 mg/m2, dl ; plus prednisone 60 mg/m(2),dl - 14 for 1-2 cycles.</p><p><b>RESULTS</b>Clinical response rate of the tested group treated with domestic idarubicin and control group treated with imported idarubicin was 78. 1% (50/64) vs. 76.9% (50/65) without any statistically significant difference between the two groups(P >0. 05). Grade Ill - IV hematological toxicity rate of the domestic idarubicin group and imported idarubicin group was 74. 0% vs. 73. 1% , respectively (P = 0. 73). Drug-related death was observed in 3 of 77 patients in the domestic idarubicin group (3.9%) due to cerebral hemorrage or septic infection. The incidence of non-hematological toxicities in domestic idarubicin group and imported idarubicin group was 84. 4% vs. 79. 5% for nausea or vomiting, 70. 1% vs. 71. 8% for infection, 42. 9% vs. 41. 0% for mucositis, 33. 8% vs. 33. 3% for alopecia, 28.6% vs. 28. 2% for serum glutamicoxalacetic transaminase abnormalitis, 16. 9% vs. 10. 3% for cardiac toxicity, all without statistically significant differences between these two groups (P > 0. 05). Discontinuation of treatment due to non-hematological toxicity was not neccessary.</p><p><b>CONCLUSION</b>Domestic idarubicin is comparable to imported counterpart in efficiency and safety for the treatment of acute leukemia. The most severe side effects of domestic idarubicin is hematological toxicity, which should be closely observed and treated in time, while its non-hematological toxicity is tolerable.</p>

Multi-institutional randomized controlled clinical trial on China made 4-demethoxydaunokrubicin (IDA) in the treatment of acute leukemia / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To evaluate the efficacy and safety of IDA (Haizheng Parmacy, China) in the treatment of acute leukemia.</p><p><b>METHODS</b>A multi-institutional single-blind randomized controlled clinical trial was carried out. A total of 155 newly diagnosed patients with AML and ALL were enrolled. The patients were randomly divided into two groups, one was given IDA (n = 77) and the other given zevodas (Pharnacia & Upjohn, n = 78) for comparison.</p><p><b>RESULTS</b>All the patients enrolled in this trial were eligible for assessment of side effects, and 129 patients for evaluation of overall response rate. In patients treated with IDA vs zevodas, the overall response rate (OR) was 78.1% vs 76.9%, CR was 68.8% vs 67.7%; in AML patients, OR was 82.4% vs 71.8%, and CR was 76.5% vs 64.1%; in ALL patients, OR was 80.0% vs 81.8%, and CR was 68.0% vs 68.2%. There was no sitatistically significant difference in hematologic and non-hematologic toxicities between the two groups.</p><p><b>CONCLUSION</b>The efficacy of IDA in the treatment of acute leukemia is comparable to that of zevodas. Both have similar toxic side effects.</p>

Clinical and molecular-biological study of a May-Hegglin anomaly family / 中华血液学杂志

<p><b>OBJECTIVE</b>To study the changes of platelet in May-Hegglin anomaly (MHA) and the molecular pathogenesis mechanism.</p><p><b>METHODS</b>Peripheral blood was drawn from the MHA proband, her father and her uncle. Platelet count and morphology were examined by automatic blood cell counter and microscopy, respectively. The platelet membrane protein was examined by flow cytometry. Membrane antibodies were determined by ELISA. PCR was used to amplify the exons 25, 31 approximately 32, 38 and 40 of the MYH 9 gene in the MHA patient and her diseased father. Furthermore, PCR products were sequenced, a specific point mutation was identified and inclusions (Dohle's body) in the neutrophil was detected by indirect immunofluorescence technique.</p><p><b>RESULTS</b>It was proved that in MHA patients, platelet count was higher by cell counter than by microscope (P < 0.01). Giant platelet was 94% but platelet membrane proteins (CD41, CD61, CD42A, CD42b) were in normal range. Membrane antibodies was undetectable. An A5521G mutation (GAG-->AAG) in the exon 38 was found in the proband and her diseased father, resulting in a characteristic change of NMMHC-A1841 (Glutamic acid-->Arginine), which was not found in other members of the family and in normal controls. Spindle-like inclusions with fluorescence were clearly displayed in neutrophil cytoplasm.</p><p><b>CONCLUSION</b>The molecular pathogenesis mechanism of May-Hegglin anomaly is the mutation in MYH 9 gene.</p>