Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tn polyagglutination (persistent mixed-field polyagglutination) was detected in the blood of a 66-yr-old male laborer at the time of a splenectomy for life-threatening thrombocytopenia. Confirmation that the polyagglutination was caused by Tn activation was established by the use of lectins, by failure of the patient's red cells to react with sera from other patients with Tn polyagglutination, by weak aggregation with polybrene, by low red cell sialic acid levels, and by the persistence of polyagglutination over several years of testing. Two years after the discovery of the Tn polyagglutination, the patient developed acute myelomonocytic leukemia. Vigorous chemotherapy regimens resulted in clinical remission of the leukemia and the Tn polyagglutination. This report describes the first known case of Tn polyagglutination preceding the development of acute myelogenous leukemia.
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PMID:Tn polyagglutination preceding acute leukemia. 28 7

This report discusses the case of a 60-year-old man who presented in 1969 with thrombocytopenia and mild marrow hypoplasia. A diagnosis of paroxysmal nocturnal haemoglobinuria (PNH), was established. The subsequent course included episodes of overt intravascular haemolysis. Thrombocytopenia reverted on several occasions during Oxymetholone therapy. The terminal phase of the illness was marked by the development of a leukocytosis and densely hypercellular bone marrow with splenomegaly. The features were those of a myeloproliferative disorder, although frank leukaemia did not develop.
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PMID:A case of paroxysmal nocturnal haemoglobinuria terminating in a myeloproliferative syndrome. 28 62

On the basis of five observations of adult patients with the clinical feature of mature cellular leukaemia which proved to be therapy-refractory and which was characterized by a rapid course is referred to the necessity of the differentiation of such cases from the classical myeloic leukaemia. The cardinal symptoms of this type of disease, which probably is identified with the cases described in literature as atypical chronic myelosis, as paraneutrophil leukaemia or as acute myelofibrosis, and also shows common features with the juvenile chronic myelosis, are, apart from the mature cellular differential blood picture a short life expectancy (less than 1 year), an initial thrombocytopenia, a normal or increased activity of the alkaline granulocyte phosphatase, the lack of Ph1-chromosome as well as the bad therapeutic reaction to busulfan. The observation of the simultaneously existing fibroses of the bone marrow as well as of the final increase of immature blasts induced the classification of the clinical picture as a special form of the myeloproliferative syndrome.
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PMID:[Acute mature myelocytic leukemia as a form of the myeloproliferative syndrome]. 29 99

Esophageal hematoma secondary to thrombocytopenia has only recently been described in the literature in a single case report. This article presents the clinical manifestations and radiographic findings of 4 additional cases of esophageal hematoma secondary to thrombocytopenia. Three patients were receiving treatment for leukemia, and the other patient had aplastic anemia. Previously reported cases of esophageal hematomas from other causes are reviewed.
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PMID:Esophageal hematoma associated with thrombocytopenia. 30 10

The increased incidence of leukemia in patients with trisomy 21 is well established. A blood disorder which may be mistaken for acute leukemia may occur in infants with trisomy 21. The authors report a newborn with trisomy 21 and hematologic findings suggesting acute leukemia (hyperleukocytosis, anemia, thrombocytopenia; replacement of bone marrow by blast-like cells). Without treatment spontaneous and complete recovery occurred. Cytochemistry and therapy are discussed in this paper.
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PMID:["Pseudoleukemia" in a newborn infant with trisomy 21]. 32 1

In a phase II trial, prednimustine was often efficient in treating chronic lymphoid leukaemia (CLL) patients and was also active in some patients with lymphosarcoma, melanoma and bronchus carcinoma. Tolerance was generally excellent, the most critical side effect being thrombocytopenia in the case of CLL.
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PMID:A phase II clinical trial of prednimustine. Clinical screening cooperative group of E.O.R.T.C. 32 10

In May 1972, the Cancer and Leukemia Group B initiated a randomized study comparing the effectiveness of CCNU and methyl-CCNU in patients with advanced malignant lymphomas, including Hodgkin's disease (HD), lymphosarcoma (LYS) and reticulum cell sarcoma (RCS). A single dose of 100 mg/m2 of CCNU or 150 mg/m2 of methyl-CCNU was given orally every 6 weeks. In patients with leukopenia or thrombocytopenia, due to prior treatment, this dose was reduced to 70 mg/m2 of CCNU and 100 gm/m2 of methyl-CCNU. Of 109 evaluable patients, 60 received CCNU and 49 received methyl-CCNU. Response rates (complete and partial) to CCNU and methyl-CCNU were respectively 42% (14/33) and 15% (3/20) in HD, 21% (3/14) and 21% (3/14) in LYS, 15% (2/13) and 27% (4/15) in RCS. Responses to methyl-CCNU, but not to CCNU, were seen only in patients who developed significant hematologic toxicity. Responses to both drugs were generally of short duration due to the advanced stage of the disease. Renal, hepatic or neurological toxicity was not observed. In conclusion, CCNU proved to be superior to methyl-CCNU for the treatment of advanced HD. CCNU was also observed to be of higher activity in Hodgkin's than in non-Hodgkin's lymphomas.
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PMID:Comparison of methyl-CCNU and CCNU in patients with advanced forms of Hodgkin's disease, lymphosarcoma nad reticulum cell sarcoma. 34 94

The efficacy of trofosfamide (Ixoten; Noristan), a derivative of cyclophosphamide, was investigated in 76 patients. Those with solid tumours were given 50 mg/kg in 6 divided doses in 48 hours; those with chronic lymphatic leukaemia were treated with 100 mg orally 3 times a day for up to 10 weeks. Side-effects of treatment included leucopenia, thrombocytopenia, a fall in the haemoglobin level, haematuria and occasional alopecia. Nausea was never severe, and occurred in only half of the patients on a high dose and in none of the patients on a low dose. A therapeutic effect was observed in patients with breast cancer, cancer of unknown origin and pancreatic cancer. Twenty-one of 24 patients with chronic lymphatic leukaemia (all of whom had aggressive disease) responded to treatment, and complete remission (including normal bone marrow), was achieved in 5 of these patients.
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PMID:Trofosfamide in the treatment of patients with cancer. A pilot trial. 35 87

B- and T-cell surface markers were determined in 26 adult patients with lymphoproliferative malignancies who had bone marrow and blood involvement. The patients in whom more than 60% of the abnormal cells were immunoglobulin-bearing cells were considered to have B-cell lymphoproliferative malignancy. The diagnosis of a T-cell disorder was made in those patients in whom more than 70% of the cells formed E rosettes (T cells). Those patients in whom 30% and more of the abnormal cells did not show B- and T-cell surface markers were regarded as suffering from "null" cell disorder. The B-cell type of lymphoproliferative malignancy was the most commonly encountered (63%) with an equal male to female ratio. In addition, 4 male patients with "hairy-cell" leukaemia were shown to have a B-cell disorder. T-cell disorders were found in 3 male patients; 1 patient had acute lymphoblastic leukaemia and in the other 2 the histopathological diagnosis was well-differentiated lymphoma and Sternberg sarcoma. Four patients with "null" cell lymphoma were found, the histopathological diagnoses in all were poorly-differentiated lymphocytic lymphoma, and 3 of the 4 patients were males. Further haematological investigations of the B-cell and the non-B-cell disorders showed that although the bone marrow was equally extensively infiltrated in both groups, the non-B-cell disroders were more commonly associated with complications of anemia and thrombocytopenia. It is therefore postulated that the abnormal lymphoid cell involved in B-cell disorders is an end-stage cell and not the haemopoietic stem cell.
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PMID:B- and T-cell markers in lymphoproliferative disorders with blood and bone marrow involvement. 35 21

Diminished survival of transfused platelets occurred in two patients given co-trimoxazole, and a third patient taking this drug developed thrombocytopenia. By means of an indirect immunofluorescence assay antibodies against donor platelets coated with co-trimoxazole were found in the sera in all cases. These antibodies were directed against the trimethoprim component of co-trimoxazole and not against sulphamethoxazole. Co-trimoxazole is a potent antimicrobial agent and is advocated for treatment and prophylaxis in leukaemia. Hence its adverse effect on platelets is of great importance.
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PMID:Immunological effect of co-trimoxazole on platelets. 39 22


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