Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023473 (chronic myeloid leukemia)
 18,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

At the Clinic for Hematology of the Military Medical Academy in Belgrade two patients had been treated from November, 1983 to July, 1986, in whom the existence of chronic myelogenous leukemia (CML) was established with negative Ph'-chromosome, as well as the existence of acquired partial erythrocyte aplasia (APEA). In the male patient of 58 years of age and the female patient of 71, APEA was established at the same time as CML. The maladies showed to be refractory to antileukemia (busulfan, hydroxyurea) and immunosuppressive (corticosteroid, androgen) therapy in both of the patients, while in the first patient splenectomy was also without effect on the course of the disease. Serumal inhibitors of erythropoiesis were not registered. After 18 months of disease duration one patient had a blastic transformation of CML into acute myeloblastic leukemia (AML) of the M1 form, and death appeared under the clinical manifestation of sepsis during iatrogenic aplasia of the bone marrow. The other patient died 32 months after start of illness because of intracranial hemorrhage, without signs of HML metamorphosis. In the discussion, previous illnesses are considered--kidney tuberculosis and polyarthralgias--as well as the applied treatment of these illnesses (antituberculotics and nonsteroid antirheumatics) as possible etiological factors in the appearance of APEA. The mutual link between APEA and CML, though exceptionally rare, is possible, and erythroblastopenia can precede or occur simultaneously with CML or during its treatment. APEA is usually the sign of CML terminal metamorphosis into acute leukemia, though it sometimes coexists with CML as an independent malady.
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PMID:[Erythrocyte cell aplasia in chronic myeloid leukemia--coincidence or pathogenic link]. 212 May 56

We report a single center experience of 222 patients (pts) less than 18 years old transplanted from 1973 to 1987. The median age was 11 years (1-18). The donor was a monozygotic twin (9 pts), an HLA-id sibling (193 pts), an HLA-id, parent (9 pts), a mismatched related donor (9 pts) and a matched unrelated donor (1 pt). Ninety-six pts were transplanted for SAA. Conditioning varied with time but the majority (59 pts) received CY 150 mg/kg and 6 Gy TAI. The long term actuarial survival is 66% with a median follow-up of 3 years. The group who received CY 200 mg/kg and MTX had a 33% long term survival (LTS). GVH was the main complication with 40% acute and 37% chronic GVHD. Chronic GVHD tended to improve with time after 2 to 4 years of evolution. Ninety pts were transplanted for leukemia (35 AML, 45 ALL and 11 CGL), 20 pts were in relapse. Pts in CR had a LTS of 40%, in pts in relapse, it was 12%. The main causes of death were: interstitial pneumonitis (30%), relapse (27%), GVH (15%). Thirty-five pts were transplanted for constitutional disease: Fanconi anemia (FA) (26 pts), Dyskeratosis congenita (2 pts), Blackfan-Diamond erythroblastopenia (2 pts), Glanzmann thrombasthenia (1 pt), osteopetrosis (1 pt) and Gaucher's disease (1 pt). In FA, the LTS is 70% with a CY 20 mg/kg, 5 Gy TAI regimen. In all disease categories, we did not find any influence of donor's sex on GVH and survival.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pediatric bone marrow transplantation for leukemia and aplastic anemia. Report of 222 cases transplanted in a single center. 267 24

A variety of immunohematological complications may occur after ABO-incompatible BMT. We report a CML patient (blood group O) who received a BMT from an HLA-identical sibling (blood group AB). The transplant was followed by normal myeloid and megakaryocytic engraftment, but erythroblastopenia persisted for more than 200 days after BMT. By bone marrow culture studies, a complement-dependent serum inhibitor of hemopoiesis was detected, suggesting immunological inhibition of erythropoiesis. The patient was resistant to a number of treatments such as intravenous gamma-globulins, prednisolone and high-dose erythropoietin. Full engraftment with normal blood counts and marrow cellularity was achieved after two dose-escalating CD34+-enriched donor lymphocyte infusions (DLI). This experience suggests that CD34+-enriched DLI may be an effective treatment for patients with delayed engraftment or late graft failure due to major ABO-incompatibility.
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PMID:CD34+-enriched donor lymphocyte infusions in a case of pure red cell aplasia and late graft failure after major ABO-incompatible bone marrow transplantation. 975 54