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Acute myelocytic leukemia and human immunodeficiency virus infection
Letters to the Editor
V. Conesa, MD Department of Hematology General Universitary Hospital of Elche Alicante, Spain 1. Kiely PDW, Mcguckin CP, Collins DA, et al. Erythrocyte aplasia and systemic lupus erythematosus. Lupus. 1995;4:407– 411. 2. Linardaki GD, Boki KA, Fertakis A, Tzioufas AG. Pure red cell aplasia as presentation of systemic lupus erythematosus: antibodies to erythropoietin. Scand J Rheumatol. 1999;28:189 –191. 3. Orbach H, Ben-Yehuda A, Ben-Yehuda D, et al. Successful treatment of pure red cell aplasia in systemic lupus erythematosus with erythropoietin. J Rheumatol. 1995;22: 2166 –2169. 4. Chute JP, Hoffmeister K, Cotelingam J, et al. Aplastic anemia as the sole presentation of systemic lupus erythematosus. Am J Hematol. 1996;51:237–239. 5. Roffe C, Cahill MR, Sasmanta A, et al. Aplastic anaemia in systemic lupus erythematosus a cellular immune mechanism? Br J Rheumatol. 1991;30:301–304. 6. Marque´s JA, Rhim H, Distenfeld A. Inhibition of hematopoiesis by a plasma factor in a case of aplastic anemia associated with systemic lupus erytematosus. P R Health Sci J. 1995;14:293–296. 7. Tzioufas AG, Kokori SI, Petrovas CI, Moutsopoulos HM. Autoantibodies to human recombinant erythropoietin in patients with systemic lupus erytematosus. ArthritisRheum. 1997;40:2212–2216.
ACUTE MYELOCYTIC LEUKEMIA AND HUMAN IMMUNODEFICIENCY VIRUS INFECTION To the Editor: Infection due to the human immunodeficiency virus (HIV) is linked with hematologic malignancies (1– 6). We describe a case of acute myelocytic leukemia in a patient with HIV infection who was receiving high activity antiretroviral therapy. A 54-year-old man, known to be HIV antibody-positive since 1993, was diagnosed with Hodgkin’s disease in February 1999. He received chemotherapy and achieved a complete remission. A bone marrow biopsy was performed and showed an infiltrate of blasts (15%), which was
compatible with refractory anemia with excess blasts. Since June 1997, he had been receiving indinavir, lamivudine, and stavudine, and had an undetectable viral load and 224 CD4 lymphocytes/mm3 in August 1999. He was admitted to our hospital in February 2000 for fever without an apparent focus of infection. Laboratory tests revealed neutropenia (260 neutrophils/mm3), anemia (9 g/dL), and thrombocytopenia (80,000 platelets/mm3). Imipenem was administered. After 3 days of treatment, the fever persisted and vancomycin was added. At that time, chest radiographs showed an infiltrate in the left lung. On the sixth day of treatment, the fever resolved, although the patient remained neutropenic (⬍500/mm3). Another bone marrow biopsy was performed, revealing an infiltrate of blasts (80%); and a diagnosis of acute myelogenous leukemia of the M5 type was made. Induction chemotherapy with idarubicin and cytarabine was initiated. On day 9 after chemotherapy, the patient had a fever and began receiving antibiotic treatment. On day 30 after chemotherapy, a bone marrow biopsy showed hypercellularity with 90% blasts, indicating a lack of response. The patient’s clinical status progressively declined, and he died 34 days after chemotherapy had begun. Of the 23 cases of acute myelogenous leukemia reported in HIV-infected patients from 1985 to 2000, 62% were of the M4 or M5 type, compared with the 30% among non– HIV-infected patients (7). There is not enough evidence to firmly suggest that the degree of HIV-induced immunosupression may determine the presence of acute myelogenous leukemia, considering that almost the same number of cases have been reported among patients with CD4 lymphocytes counts ⬍200 and patients with ⬎500 (8). No death has been described during the induction phase of chemotherapy, and the initial response to chemotherapy is generally good, with a high rate of complete reJuly 2001
mission obtained, which suggests that chemotherapy is a good treatment option. Our patient had no response to chemotherapy, although he was older than 50 and his was a secondary disease— both bad prognostic factors. Survival among patients infected with HIV has clearly improved without a decrease in the incidence of non-Hodgkins’ lymphoma (2). That means the frequency of secondary acute myelogenous leukemia is likely to increase in coming years (9). Julia´n Olalla, MD Jose´ R. Costa, MD Rafael Rubio, MD Eugenio Jime´nez, MD Rosa Toscano, MD Federico Pulido, MD Internal Medicine Department Universitary Hospital “12 de Octubre” Madrid, Spain 1. Center for Diseases Control Task Force on Kaposi Sarcoma and Opportunistic Infections. Epidemiological aspects of the current outbreak of Kaposi sarcoma and opportunistic infections. N Engl J Med. 1982; 306:248 –252. 2. Rubio Garcı´a R. Impact of HAART in natural history of AIDS related non-Hodgkin lymphomas. AIDS Cyber J. 2000;3:1–10. Available at: Http.www.prous.com/ttmsida. 3. Mansberg R, Rowlings PA, Yip MY, Rozenberg MC. First and second remissions in a HIV positive patient following remission induction therapy for acute non-lymphoblastic leukaemia. Aust NZ J Med. 1991;21: 55–57. 4. Rubio R, Pulido F, Pintado V, et al. NonHodgkin’s lymphomas associated with the acquired immunodeficiency syndrome. A multicenter clinical study of 77 cases. Med Clin (Barcelona). 1995;104:481– 486. 5. Gaidano G, Carbone A. AIDS-related lymphomas: from pathogenesis to pathology. Br J Haematol. 1995;90:235–243. 6. Monfardini S, Vaccher E, Pizzocaro G, et al. Unusual malignant tumours in 49 patients with HIV infection. AIDS. 1989;3:449 – 452. 7. Lo¨wenberg B, Downing JR, Burnett A. Acute myeloid leukemia. N Engl J Med. 1999;341:1051–1062. 8. Hentrich M, Rockstroh J, Sandner R, et al. Acute myelogenous leukaemia and myelomonocytic blast crisis following polycytemia vera in HIV positive patients: report of cases and review of the literature. Ann Oncol. 2000,11:195–200. 9. Leone G, Mele L, Pulsoni A, et al. The incidence of secondary leukemias. Haematologica. 1999;84:937–945.
THE AMERICAN JOURNAL OF MEDICINE威
Volume 111 79
V. Conesa, MD Department of Hematology General Universitary Hospital of Elche Alicante, Spain 1. Kiely PDW, Mcguckin CP, Collins DA, et al. Erythrocyte aplasia and systemic lupus erythematosus. Lupus. 1995;4:407– 411. 2. Linardaki GD, Boki KA, Fertakis A, Tzioufas AG. Pure red cell aplasia as presentation of systemic lupus erythematosus: antibodies to erythropoietin. Scand J Rheumatol. 1999;28:189 –191. 3. Orbach H, Ben-Yehuda A, Ben-Yehuda D, et al. Successful treatment of pure red cell aplasia in systemic lupus erythematosus with erythropoietin. J Rheumatol. 1995;22: 2166 –2169. 4. Chute JP, Hoffmeister K, Cotelingam J, et al. Aplastic anemia as the sole presentation of systemic lupus erythematosus. Am J Hematol. 1996;51:237–239. 5. Roffe C, Cahill MR, Sasmanta A, et al. Aplastic anaemia in systemic lupus erythematosus a cellular immune mechanism? Br J Rheumatol. 1991;30:301–304. 6. Marque´s JA, Rhim H, Distenfeld A. Inhibition of hematopoiesis by a plasma factor in a case of aplastic anemia associated with systemic lupus erytematosus. P R Health Sci J. 1995;14:293–296. 7. Tzioufas AG, Kokori SI, Petrovas CI, Moutsopoulos HM. Autoantibodies to human recombinant erythropoietin in patients with systemic lupus erytematosus. ArthritisRheum. 1997;40:2212–2216.
ACUTE MYELOCYTIC LEUKEMIA AND HUMAN IMMUNODEFICIENCY VIRUS INFECTION To the Editor: Infection due to the human immunodeficiency virus (HIV) is linked with hematologic malignancies (1– 6). We describe a case of acute myelocytic leukemia in a patient with HIV infection who was receiving high activity antiretroviral therapy. A 54-year-old man, known to be HIV antibody-positive since 1993, was diagnosed with Hodgkin’s disease in February 1999. He received chemotherapy and achieved a complete remission. A bone marrow biopsy was performed and showed an infiltrate of blasts (15%), which was
compatible with refractory anemia with excess blasts. Since June 1997, he had been receiving indinavir, lamivudine, and stavudine, and had an undetectable viral load and 224 CD4 lymphocytes/mm3 in August 1999. He was admitted to our hospital in February 2000 for fever without an apparent focus of infection. Laboratory tests revealed neutropenia (260 neutrophils/mm3), anemia (9 g/dL), and thrombocytopenia (80,000 platelets/mm3). Imipenem was administered. After 3 days of treatment, the fever persisted and vancomycin was added. At that time, chest radiographs showed an infiltrate in the left lung. On the sixth day of treatment, the fever resolved, although the patient remained neutropenic (⬍500/mm3). Another bone marrow biopsy was performed, revealing an infiltrate of blasts (80%); and a diagnosis of acute myelogenous leukemia of the M5 type was made. Induction chemotherapy with idarubicin and cytarabine was initiated. On day 9 after chemotherapy, the patient had a fever and began receiving antibiotic treatment. On day 30 after chemotherapy, a bone marrow biopsy showed hypercellularity with 90% blasts, indicating a lack of response. The patient’s clinical status progressively declined, and he died 34 days after chemotherapy had begun. Of the 23 cases of acute myelogenous leukemia reported in HIV-infected patients from 1985 to 2000, 62% were of the M4 or M5 type, compared with the 30% among non– HIV-infected patients (7). There is not enough evidence to firmly suggest that the degree of HIV-induced immunosupression may determine the presence of acute myelogenous leukemia, considering that almost the same number of cases have been reported among patients with CD4 lymphocytes counts ⬍200 and patients with ⬎500 (8). No death has been described during the induction phase of chemotherapy, and the initial response to chemotherapy is generally good, with a high rate of complete reJuly 2001
mission obtained, which suggests that chemotherapy is a good treatment option. Our patient had no response to chemotherapy, although he was older than 50 and his was a secondary disease— both bad prognostic factors. Survival among patients infected with HIV has clearly improved without a decrease in the incidence of non-Hodgkins’ lymphoma (2). That means the frequency of secondary acute myelogenous leukemia is likely to increase in coming years (9). Julia´n Olalla, MD Jose´ R. Costa, MD Rafael Rubio, MD Eugenio Jime´nez, MD Rosa Toscano, MD Federico Pulido, MD Internal Medicine Department Universitary Hospital “12 de Octubre” Madrid, Spain 1. Center for Diseases Control Task Force on Kaposi Sarcoma and Opportunistic Infections. Epidemiological aspects of the current outbreak of Kaposi sarcoma and opportunistic infections. N Engl J Med. 1982; 306:248 –252. 2. Rubio Garcı´a R. Impact of HAART in natural history of AIDS related non-Hodgkin lymphomas. AIDS Cyber J. 2000;3:1–10. Available at: Http.www.prous.com/ttmsida. 3. Mansberg R, Rowlings PA, Yip MY, Rozenberg MC. First and second remissions in a HIV positive patient following remission induction therapy for acute non-lymphoblastic leukaemia. Aust NZ J Med. 1991;21: 55–57. 4. Rubio R, Pulido F, Pintado V, et al. NonHodgkin’s lymphomas associated with the acquired immunodeficiency syndrome. A multicenter clinical study of 77 cases. Med Clin (Barcelona). 1995;104:481– 486. 5. Gaidano G, Carbone A. AIDS-related lymphomas: from pathogenesis to pathology. Br J Haematol. 1995;90:235–243. 6. Monfardini S, Vaccher E, Pizzocaro G, et al. Unusual malignant tumours in 49 patients with HIV infection. AIDS. 1989;3:449 – 452. 7. Lo¨wenberg B, Downing JR, Burnett A. Acute myeloid leukemia. N Engl J Med. 1999;341:1051–1062. 8. Hentrich M, Rockstroh J, Sandner R, et al. Acute myelogenous leukaemia and myelomonocytic blast crisis following polycytemia vera in HIV positive patients: report of cases and review of the literature. Ann Oncol. 2000,11:195–200. 9. Leone G, Mele L, Pulsoni A, et al. The incidence of secondary leukemias. Haematologica. 1999;84:937–945.
THE AMERICAN JOURNAL OF MEDICINE威
Volume 111 79