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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In cold autoimmune hemolytic anemia, the causative autoantibodies (cold agglutinins) are most reactive at low temperatures. The anti-I type of cold agglutinin is found in cold hemagglutination disease and in hemolytic anemia secondary to malignant lymphoma, leukemia, or atypical pneumonia. The anti-I type of cold agglutinin is found in many patients with infectious mononucleosis and in an occasional patient with other lymphoproliferative disorders. Paroxysmal cold hemoglobinuria, a disorder in which exposure to cold temperatures triggers massive hemolysis, is characterized by a unique biphasic cold autoantibody called the Donath-Landsteiner antibody. By way of summary and review of this and the two previous articles in this series, table 4 presents a practical approach to diagnosis of the autoimmune hemolytic anemias.
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PMID:Autoimmune hemolytic anemia. 3. Cold antibody type. 48 74

Autoimmune hemolytic anemia often develops in patients with chronic lymphocytic leukemia, particularly elderly women. It is heralded by a drop in the hematocrit, elevation of reticulocytes, development of jaundice, or a rise in the indirect fraction of serum bilirubin. Evidence of hemolysis supports the diagnosis, and a positive result of the Coombs test confirms it. Survival time is considerably shorter in patients who have both diseases than in those with chronic lymphocytic leukemia alone. Presenting symptoms in patients with the two diseases may include weakness, dizziness, fever, or hemorrhagic phenomena. If the anemia is severe, palpitations, otic pulsations, and cardiac decompensation are common. Physical examination may show enlargement of reticuloendothelial structures. On the other hand, some patients may be essentially asymptomatic. The hemolytic process must be treated as a separate entity, as even vigorous treatment of the leukemia often does not control it. Corticosteroid therapy is preferred, with splenectomy as a second line of defense. If the patient is not a good surgical risk, chemotherapy should be considered. Transfusions are usually incompatible but should be risked if progressive congestive failure, neurologic disturbance, angina, or signs of an impending infarct are present.
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PMID:When autoimmune hemolytic anemia complicates chronic lymphocytic leukemia. 63 66

A case of hairy cell leukemia (HCL) presenting as autoimmune hemolytic anemia (AHA) is described. A 40-year-old woman presented with severe hemolytic anemia. The morphological and immunological studies of bone marrow and spleen revealed a hairy cell leukemia. Although autoimmune diseases are a well known complication of HCL this is the first description of AHA as a complication of HCL.
Leukemia 1992 Jun
PMID:Hairy cell leukemia and autoimmune hemolytic anemia. 153 59

A 78-year-old woman, who had axillary lymphadenopathy but no hepatosplenomegaly, was admitted because of lymphocytosis. The leukocyte count was 18.1 x 10(9)/l with 72% abnormal cells. Neither anemia nor thrombocytopenia was present. Many abnormal cells and erythroblasts were seen in the bone marrow. These abnormal cells had irregular nuclei but no granules in the cytoplasm. The surface markers of these cells were positive for E-rosette, CD 2, CD 3, and Leu 7 but negative for CD 4, CD 8, CD 11 (OKM 1), CD 16 (Leu 11), and HLA-DR. The DNA analysis revealed the rearrangement of T-cell receptor beta-chain genes. Direct Coombs test was positive and red-cell life-span (51Cr) was T 1/2 = 19.5 days. The patient was diagnosed as having T-CLL with mild autoimmune hemolysis and was followed without treatment. Seven months later, the leukemia cells of peripheral blood increased to 62.6 X 10(9)/l and the frank autoimmune hemolytic anemia developed. After prednisolone, vincristine and cyclophosphamide were administered, leukemia cells of blood decreased. Anemia with reticulocytopenia, however, persisted and direct Coombs test became negative. In the bone marrow at that time, many neutrophils and megakaryocytes besides leukemia cells were preserved, but erythroblasts were hardly seen, namely a pattern of red cell hypoplasia was observed. The patient deteriorated rapidly and died 26 months after initial recognition of lymphocytosis. When complement was added, the patient's serum obtained during red cell hypoplasia but not during autoimmune hemolysis inhibited BFU-E and CFU-GM in in vitro colony assays. This case indicates that not only B-CLL but also T-CLL is accompanied by immune hematocytopenia.
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PMID:[Red cell hypoplasia following autoimmune hemolytic anemia associated with T-CLL: report of a case and review of the literature]. 250 1

T-cell chronic lymphocytic leukemia: clinical aspects and laboratory findings of five patients. This study illustrates the main clinical aspects and laboratory findings for five patients suffering from T-cell chronic lymphocytic leukemia. They make up 5% of our observations in the Department of Oncology-Hematology at the Busto Arsizio Hospital. Three patients with phenotype CD3+/CD4+ showed a fast course with skin involvement and poor response to chemotherapy (mean survival: 12 months). The course of a patient with unusual phenotype CD3-/CD4+ associated with autoimmune hemolytic anemia and end-stage prolymphocytic transformation was better (survival: 58 months). For 12 years we have been observing a woman suffering from the recently defined CD3+/CD8+/HNK1+ large granular lymphocytes chronic lymphocytosis with associated neutropenia. The disease has good prognosis, with poor symptomatology even without therapy. This study supports the immunological classification of the chronic lymphoproliferative diseases of leukemia and lymphoma with different clinical aspects and prognoses. This method of classification may be important in the consideration of some therapeutical approaches.
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PMID:[Chronic T-cell lymphocytic leukemia: clinical and laboratory aspects of 5 patients]. 278 7

An indirect platelet radioactive antiglobulin test (PRAT) was used to evaluate serum antiplatelet antibody and complement activation in 114 patients with lymphoproliferative disease. Overall, 60% of serum samples gave a positive indirect PRAT. Positive PRAT was observed in 85% of patients with chronic lymphocytic leukemia (CLL) and megakaryocytic thrombocytopenia, as well as in about half the patients with CLL and a normal platelet count or amegakaryocytic thrombocytopenia. In contrast to findings in patients with idiopathic autoimmune thrombocytopenic purpura or in those with leukemia who were alloimmunized, positive PRAT in patients with lymphoproliferative disease was predominantly caused by C3-only sensitization of platelets. Results were analyzed in relation to other clinical and laboratory findings. There was no significant difference in antiglobulin sensitization pattern between CLL and other lymphomas, different cell type, stage of disease, presence or absence of splenomegaly, recent or distant chemotherapy, sex, or history of pregnancy. Previous transfusion did affect antiglobulin sensitization patterns, as did presence of autoimmune hemolytic anemia. A high frequency of low serum complements (CH50, C3, C4, and factor B) and increased circulating immune complexes was observed; these did not correlate with frequency or sensitization pattern of positive PRAT. Amounts of bound anti-C3 and anti-IgG were significantly higher in patients with lymphoproliferative disease and positive antiglobulin test than in normal individuals; there was, however, no correlation between amount of antiglobulin serum bound and platelet counts. There was an 87% correlation in direct and indirect PRAT in 24 patients tested.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Indirect platelet radioactive antiglobulin test in patients with lymphoproliferative disease. 394 93

The preparation of a feline Coombs serum (rabbit antifeline gamma globulin) is described. The direct antiglobulin test using this serum was performed on 20 anemic and 20 healthy control cats. Red cell membrane antibodies were detected in cats with feline leukemia virus infection and in others with inflammatory and neoplastic diseases. A low titre of cold agglutinating antibody was present in a high proportion of the control cats. Positive direct antiglobulin tests were noted in cats without overt hemolytic disease. It was concluded that the direct antiglobulin test in anemic cats has certain diagnostic limitations. A positive reaction should be interpreted cautiously especially when there is no clinical or laboratory evidence to support a diagnosis of autoimmune hemolytic anemia.
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PMID:The diagnostic significance of a positive direct antiglobulin test in anemic cats. 609 76

The adenosine deaminase-resistant purine deoxynucleoside 2-chloro-2'-deoxyadenosine (CdA) is markedly toxic in vitro to nondividing and proliferating normal human lymphocytes and to many leukemia cell specimens. The CdA is also effective against mouse L1210 leukemia in vivo. The present investigations have examined the pharmacology, chemotherapeutic activity, and toxicity of CdA in nine patients with advanced hematologic malignancies refractory to conventional therapy. When administered by continuous intravenous infusion, the deoxyadenosine analog was well tolerated. As monitored by radioimmunoassay, plasma CdA levels rose gradually during the infusions. The CdA was not deaminated significantly. In all patients with leukemia, the CdA lowered the blast count by at least 50%. In one patient with a T-cell leukemia-lymphoma, and in another patient with chronic myelogenous leukemia in blast crisis, the CdA infusion eliminated all detectable blasts from the blood and bone marrow. In a patient with a diffuse lymphoma complicated by severe autoimmune hemolytic anemia, CdA treatment quickly terminated the hemolytic process. Bone marrow suppression represented the dose-limiting toxicity, and was related to plasma CdA levels, cumulative drug dosage, and the rapid release of CdA that accompanied tumor cell lysis.
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PMID:Antileukemic and immunosuppressive activity of 2-chloro-2'-deoxyadenosine. 658 95

In a retrospective study of 39 splenectomies, patients with increased blood cell breakdown (13 cases of idiopathic thrombocytopenic purpura (ITP), 5 cases of hereditary spherocytosis, 2 of Felty's syndrome and 2 of autoimmune hemolytic anemia) were compared with those patients also presenting decreased blood cell production [14 cases of myelofibrosis (MF) with splenomegaly and 3 cases of advanced chronic myelogeneous leukemia (CML)]. Platelet regeneration post-operatively was significantly (p less than 0.01) more rapid in the ITP than in the MF group. Only 1/22 patients in the ITP group had major post-operative complications as compared to 10/17 in the MF group. None of the patients in the ITP group died within 25 days of operation as compared to 5/17 in the MF group. Only 3/22 patients in the ITP group lost more than 800 ml of blood during the operation as compared to 8/17 with MF. No statistically significant higher blood loss was found in patients with less than 30 x 10(9) platelets/l preoperatively, compared to those with higher platelet counts. However, correlation between the splenic weights and amount of blood loss was statistically significant (p less than 0.01). Thus, splenectomy seems much better tolerated in patients with ITP, even if platelets are low, than in patients with myelofibrosis.
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PMID:[Splenectomy in idiopathic thrombopenic purpura and in myelofibrosis. A retrospective study of platelet increase, hemorrhagic complications and mortality]. 719 36

Recently there have been increasing reports of HIV infection acquired through transfusion of HIV seronegative blood in Thailand due to high incidence of HIV new infection in blood donors. Blood or blood components (BC) prepared from HIV seronegative blood donation pose significant hazards to recipients because of the risk of viremia during the "window period" of HIV infection. This paper presents the HIV seroprevalence in hematologic patients other than hemophiliacs who received multiple blood transfusion at Ramathibodi Hospital. The retrospective analysis was done on 167 patients: 132 thalassemia, 19 leukemia, 5 aplastic anemia, 5 ITP, 2 pure red cell aplasia, 2 congenital non spherocytic hemolytic anemia, 1 hereditary spherocytosis and 1 autoimmune hemolytic anemia patients, who received blood transfusion during January 1, 1987 till February 29, 1992 at the Department of Pediatrics, Ramathibodi Hospital. The number of blood or BC transfused in each patient was 1-154 units with the average of 23 units per patient per 5 years with a total 4,000 units. All were HIV sero-negative. Anti-HIV screening was performed periodically in these patients about 1-2 times per year or as necessary. The results were HIV seronegative in all cases. The reason for negative results cannot be explained clearly. It should be noted that our thalassemic patients receive leukocyte poor blood and avoid a hypertransfusion program. Patients with other blood diseases received both whole blood and BC. The HIV contaminated blood in the window period was estimated to be 1:10,000 in Thailand which showed HIV antigen positive but antibody negative. These patients may be fortunately received HIV non contaminated blood.
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PMID:HIV seroprevalence in hematologic patients other than hemophiliacs at Ramathibodi Hospital. 788 70


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