| Objective: The primary goal of this study was to summarize the clinical manifestations as well as characteristic, treatment and clinical turnover of chronic myelogenous leukemia, in order to provide valuable reference for clinical work.Methods: The clinical data of 38 CML patients, 21 male and the others female was analyzed retrospectively. Out of the 38 patients, 6 were in accelerated phase and 32 in blastic phase. There were 16 cases (50.0%) of acute granulocytic transformation, 1 case (3.125%) of acute myelomonocytic transformation, 4 (12.5%) acute monocytic transformation, 1 (3.125%) acute megakaryocytic transformation, 7 cases (21.875%) of acute lymphocytic transformation, as 2cases (6.25%) of extramedullary acute transformation as well as 1 (3.125%) acute basophilic transformation.Results:1 The period from morbidity to AP/BP ranged from about 3 months to 144 months, with an average of 47.5 months.2 The period between AP/BP and death ranged from 1 day to 14 months, with an average of about 4 months.3 Major causes of death was infection and multiple organ failure.4 Among the 38 paitents during their treatment of CP, 4 was medicated with simply gleevec, 10 with hydroxyl urea, 3 with hydroxyl urea and gleevec, and 21with hydroxyl urea and interferon. During BP, the major treatment is combination chemotherapy. We chose VCDP in acute lymphocytic transformation while HA in acute granulocytic transformation. 4 cases gave up further treatment; 19 discharged from hospital voluntarily after improvement or deterioration after 1 to 4 courses of treatment; 14 cases insisted on the treatment, 10 died while the other 4 were still alive. Conclusions: The incidence of CML is low, with no significance between genders. CML may occur at any age with an average age of 40.5, showing the rejuvenation of the afflicted group. Causes of CML is complex with regard to heredity, physics, chemistry, biology and social psychology. The clinical manifestation of AP/BP is various but with no specifics. The most common symptoms are the progressive intumesce of the spleen as well as fever. In BP, there are different degree of rising ofβ2-microglobin, blood uric acid and BUN, which is an implication for the progression of the disease. The extent of myelofibrosis may be related to the stages and prognosis of CML. The influence of gender, age and the bulk of spleen on treatment are of no statistical significance, while the hemogram possesses makes obvious difference. Prognosis of CML-BP is pessimistic. The HU and IFN cannot prevent the progress of CML, while gleevec could return the tide of AP back to CP, in other words, turn BCR/ABL + back to BCR/ABL -. We have to choose different combination chemotherapy schemes according to different patients. The main objective of treatment of CML is to postpone the advent of AP/BP and prolong the survival time. Gleevec and allo-HSCT are the best way to cure. The administration of HU and IFN regularly is effective for those who cannot afford the previous two treatment. Sokal/Hasford integrated system is useful. Haemogram and blood biochemisty should be observed and detected. Bone marrow pathology ,immunohistochemisty and chromosome examination are of high importance in term of observation and prognosis of CML. |
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