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)

77 marrow biopsies of smouldering leukemia have been examined in triple blind fashion with the following results: the cellularity of the marrow is normal in three quarters of the cases. In one quarter the blast cells were homogenous, which confirms the diagnosis of leukemia. The frequences of the sheets of blast cells increase with the duration of the disease and reached 80% at the 20th month. In the other cases, blasts were seldom seen. Eosinophilia was frequent. Erythroblasts were always rare, in contrast to what is seen in sideroblastic anemias. The reticulin network was thickened in 25% of the cases. Thus, bone marrow biopsy may demonstrate many of the features supporting the diagnosis of smouldering leukemia.
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PMID:[Refractory anemia with partial myeloblastic medullary infiltration. Examination of marrow biopsies (author's transl)]. 106 64

Inversion of chromosome 16 was found in a 73-year-old female with acute myeloblastic leukemia (FAB:M2). Complete remission was achieved by combined chemotherapy (DNR, Ara-C, 6-MP, Prednisolone), but she relapsed 6 months later without CNS involvement and died of respiratory failure presumably due to cerebrovascular accident during remission reinduction chemotherapy. Biphenotypic surface markers (CD2+ and CD13+) were observed on relapse. Eosinophilia was not observed throughout. Our patient and the other reported case suggest that biphenotypism and the lack of eosinophilia and monocytosis in inv (16) leukemia may be correlated with a poor prognosis.
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PMID:[Inversion of chromosome 16 observed in acute myeloblastic leukemia (M2) with biphenotypic surface markers lacking monocytosis and eosinophilia]. 135 70

Eosinophilia may be associated with various pathologic states such as malignant disorders, atopic and parasitic diseases, certain infections, as well as drug reactions. We describe a case of a 48-year-old patient who was submitted to a single-course therapy with 2-chlorodeoxyadenosine because of hairy-cell leukaemia and previously did not respond to splenectomy. After the treatment marked transient eosinophilia appeared which preceded the achievement of complete remission. It is supposed that eosinophilia might have been caused by the release of cytokines from damaged leukaemic cells.
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PMID:Transient eosinophilia in a patient with hairy-cell leukaemia treated with 2-chlorodeoxyadenosine. 136 55

Acute lymphoblastic leukemia with eosinophilia is a rare but distinctive clinical entity. The eosinophilia in these patients can present before, concomitantly, or after the diagnosis of leukemia. Patients with this syndrome often suffer from the cardiovascular complications of severe eosinophilia, suffering excess morbidity and mortality as a result of their eosinophilia. Treatment of the eosinophilia in this syndrome consists of administration of induction chemotherapy, followed by prednisone and hydroxyurea if required for persistent eosinophilia. Eosinophilia often resolves with remission of leukemia, only to return at the time of relapse in a high percentage of cases. Patients with this syndrome characteristically have cytogenetic abnormalities involving the long arms of chromosomes 5 and 14. These cytogenetic abnormalities are not commonly seen in acute lymphoblastic leukemia and suggest that this syndrome may have a distinct pathophysiology and etiology. The affected region on chromosome 5 contains genes that control hematopoiesis, including eosinophilopoiesis. Further investigations into these cytogenetic abnormalities may provide insight into the etiology of the leukemia and eosinophilia characteristic of this syndrome.
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PMID:Acute lymphoblastic leukemia with eosinophilia. 237 8

Ten characteristics of bone marrow (BM) biopsies in paraffin sections, obtained at diagnosis from patients with myelodysplastic syndromes (MDS) classified according to the FAB criteria, were analysed to identify both the most relevant morphologic data and any possible influence on survival. Agreement between two observers was obtained for 94% of the data. BM cellularity was increased in 63% of the cases and was higher in refractory anaemia with excess of blasts (RAEB). RAEB in transformation (RAEB-t) and chronic myelomonocytic leukaemia (CMML) (P = 0.001). Dysmegakaryopoiesis and dyserythropoiesis were present respectively in 83% and 72% of the cases, with slight differences among the FAB subtypes. Abnormal localization of immature precursors (ALIP) was found in more than half of the cases and somewhat more frequently seen in the RAEB + RAEB-t + CMML group (P = 0.07). Eosinophilia, plasmacytosis and reticulin fibrosis were evident in 26%, 18% and 47% of the cases respectively. Cellularity (P = 0.006), eosinophilia (P = 0.009) and, to some extent, dysmegakaryopoiesis (P = 0.07) bore a certain relationship with survival on univariate analysis. The presence of ALIP was not seen to affect the outcome. Multivariate analysis showed that the cellularity and presence of dysmegakaryopoiesis, in BM biopsy, added significant independent prognostic information to that achieved with age, platelet count and proportion of blast cells in BM aspirate, three variables with proven prognostic value in MDS patients. Using a regression model including these five characteristics we have stratified the patients into low, intermediate and high-risk groups with different survivals (P = 0.00001). The present findings show that BM biopsy is able to provide both morphological characteristics and information about the prognosis of survival, and should thus be included in the initial evaluation of MDS.
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PMID:Bone marrow biopsy in myelodysplastic syndromes: morphological characteristics and contribution to the study of prognostic factors. 237 20

Abnormalities of chromosome 16 in AML include del(16q), inv(16) and t(16;16). These three groups have been categorized together and have been associated with high complete remission (CR) and survival rates following Ara-C-based chemotherapy. We have reviewed the 63 AML or MDS patients with an abnormality of chromosome 16 treated at MD Anderson Cancer Center (MDACC) over the past 18 years. Marked differences in survival and remission duration (RD) were noted between the inv(16) or t(16;16) patients and those with del(16q), whose outcome was no better than other M4 AML or MDS patients treated during the same period. Other differences characterizing del(16q) included a lack of CNS relapses, lower incidences of eosinophilia and M4 FAB subtype. Half the inv(16) patients had additional karyotypic abnormalities. The overall survival and remission duration for those patients were no different from those for patients with inv(16) alone, although the probability of remaining in first CR at 2 years was higher in the inv(16) alone group. There was no difference in overall survival for the 45 patients who received HDAC vs those who did not. The incidence of CNS relapse was, however, markedly reduced for the HDAC patients. Eosinophilia did not correlate with improved survival. We conclude that del(16q) confers a different prognosis from inv(16) and t(16;16) and for the purposes of prognostication or treatment recommendations should no longer be categorized with them. Additional karyotypic changes however, which accompany inv(16) in 50% of cases do not influence the overall outcome compared to patients with inv(16) alone.
Leukemia 1995 Jun
PMID:Cytogenetic and clinical correlates in AML patients with abnormalities of chromosome 16. 759 86

Eosinophilia may complicate allogeneic bone marrow transplantation (BMT) after treatment with preparative regimens that include total body irradiation (TBI). This complication is of uncertain significance and has not been reported after treatment protocols which do not contain TBI. We reviewed our experience using busulfan and cyclophosphamide (CY), instead of TBI, as the preparative regimen for allogeneic BMT to study the incidence and relationship to graft-versus-host disease (GVHD) of post-treatment eosinophilia. Fifty-five consecutive patients receiving busulfan 16 mg/kg and CY 120 mg/kg for the treatment of leukemia were reviewed. All patients received non-T cell-depleted, HLA-matched sibling or unrelated donor marrow 2 days after chemotherapy was complete. Cyclosporine (CYA) and methylprednisolone were given to prevent GVHD. Thirty-nine patients surviving 100 days post-transplant were evaluated; 11 (28%) patients developed eosinophilia (defined as an absolute eosinophil count of > 500 x 10(6)) after transplant. Only 2 patients were still taking methylprednisolone at the onset of eosinophilia. At the onset of eosinophilia 5 of these 11 patients (45%) and GVHD that worsened within 2 months. In the other 6 patients (55%), GVHD was not present initially but developed in all 6 patients at a median of 4 months after the onset of eosinophilia. We conclude that eosinophilia can complicate allogeneic BMT not preceded by TBI and that it often heralds the onset of worsening of, or de novo, GVHD.
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PMID:Eosinophilia after allogeneic bone marrow transplantation using the busulfan and cyclophosphamide preparative regimen. 883 34

Hematological malignancies accompanied by eosinophilia are reviewed in relation to chromosomal changes and cytokine production. Eosinophilia accompanied by hematological malignancies can be divided into two groups. In some myelogenous leukemias, including acute myelomonocytic leukemia with eosinophilia (FAB M4Eo), acute myeloblastic leukemia (FAB M2 t(8;21)) and chronic myelogenous leukemia, neoplastic cells themselves appear to differentiate into eosinophils. On the other hand, transformed tumor cells secrete some eosinophil-stimulating cytokines, including interleukin-3, interleukin-5 and granulocyte-macrophage colony-stimulating factor and these cytokines stimulate the proliferation of normal eosinophil precursors in some lymphoid malignancies, including some types acute lymphoblastic leukemia (especially with t(5;14)) or malignant lymphoma, including Hodgkin's lymphoma and adult T cell lymphoma/leukemia.
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PMID:[Hematological malignancies with eosinophilia]. 849 61

A 43-year-old male with newly diagnosed hairy cell leukaemia underwent a single course of 2-chlorodeoxyadenosine (2-CdA). Skin rash, facial swelling and marked eosinophilia developed 20 d after treatment and were resolved by 7 d of steroid therapy. Eosinophil peak in peripheral of the eosinophil population showed a high expression of the IL-2 receptor alpha-chain (CD25), representing up to 94% of gated cells. HLA-DR and CD4 antigens were constantly negative; eosinophils strongly reacted with the secretory form of the eosinophil cationic protein (ECP), recognized by EG2 monoclonal antibody. IL-5 serum levels were markedly elevated at the onset of eosinophilia, returned to normal levels after its disappearance and positively correlated with eosinophil count (r = 0.94, P = 0.016). Eosinophilia is an uncommon finding after treatment with 2-CdA. It is unclear whether these phenomena represented a true allergic reaction to the drug or the effect of massive tumour cell lysis and haemopoietic pancytopenia with immunosuppression, which induced the release of IL-5 and possibly other cytokines.
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PMID:Hypereosinophilia during 2-chlorodeoxyadenosine treatment for hairy cell leukaemia. 860 11

Eosinophilia and allergic skin reactions are uncommon events after 2-chlorodoxyadenosine (2-CdA, cladribine) administration. A multicentre retrospective analysis of eosinophilia in 360 patients treated with 2-CdA for lymphoid malignancies has been made. B-cell chronic lymphocytic leukaemia (B-CLL) was diagnosed in 153, hairy cell leukaemia (HCL) in 68, low-grade non-Hodgkin's lymphoma (LGNHL) in 119, high-grade NHL in 2 and Waldenstrom's macroglobulinaemia (WM) in 18 patients. 2-CdA was administered at a dose 0.12 mg/kg/d in 2-h intravenous infusion for 5 consecutive d. The courses were repeated monthly. Patients with HCL received 1 cycle of 2-CdA, with NHL 2-6 (mean 3.5) cycles and with B-CLL 3-6 (mean 5) cycles. Twenty patients (5.5%), including 5 with HCL, 6 with LGNHL, 7 with B-CLL and 2 with WM, developed peripheral blood eosinophilia. The mean values of absolute eosinophil count were 0.78x10(9)/l (0.58-1.06x10(9)/l), 0.71x10(9)/l (0.52-1.3x10(9)/l), 85 (0.56-1.82x10(9)/l) and 0.75 (0.74-0.76x10(9)/l), respectively. Eosinophilia occurred in 13 patients after 1 course, in 4 after 2 courses, and in 5 after > or =3 courses of the therapy. In 17 cases it resolved spontaneously. Allergic skin lesions with pruritus were noticed in 3 patients simultaneously with an increase in eosinophil count. All of them required antihistaminic drugs and/or corticosteroids. One patient with B-CLL experienced repeated episodes of eosinophilia. The highest incidence of 2-CdA-induced eosinophilia was noticed in patients with MW (11.1%) and HCL (7.4%) who received only 1 cycle of this drug and entered a complete remission. This side effect was less frequently observed in LGNHL and B-CLL, i.e. in 5.0% and 4.6% of cases, respectively. The mechanism of 2-CdA-induced eosinophilia is not clear. It has been postulated that massive tumour cell lysis may trigger a release of IL-5 and probably other cytokines. The allergic mechanism of 2-CdA-induced eosinophilia is also possible, especially in patients with simultaneous skin reactions.
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PMID:2-Chlorodeoxyadenosine (cladribine)-related eosinophilia in patients with lymphoproliferative diseases. 933 19


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