A simple method was devised for determination of the storage iron decrease rate (SID) and the number of days to a recurrent state of iron deficiency. Several patients with iron deficiency anemia were given intravenous doses of iron, and their serum ferritin levels were periodically assayed. A serum ferritin decrease curve was plotted semi-logarithmically; back-extrapolation of that curve yielded the period of days (D) from the starting day of iron supplement therapy to the day by which serum ferritin had decreased to 12 ug/l. The amount of administered iron that was initially stored and eventually lost during period D was calculated by subtracting the amount of iron utilized for hemoglobin increase (R) from the total amount of iron administered (T) to each patient. R was calculated from values for patient body weight and change in hemoglobin concentration prior to and after therapy. SID values were obtained from the following formula: SID=(T-R)/D mg/day.
SID rates and the number of days to a state of recurrent iron deficincy were measured in 12 patients. SID rates ranged from 0.8 to 9.8 mg/day, and were larger in those patients who exhibited heavier blood loss. A correlation was observed between SID values and the half-times for serum ferritin decrease, as expressed by the equation, Y=248.5X^0.129 (r=0.129).
SID values reflected the negative iron balance of each patient. That observation suggested it should be possible to select a more appropriate intravenous iron dose for individual patients if their SID values are taken into full account.

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We report the first Japanese case of acute promyelocytic leukemia with t(11;17)(q23;q21) and CD56. A 41-year-old man with schizophrenia was hospitalized because of the appearance of blasts with Auer bodies in his peripheral blood. A bone marrow smear showed an abundance of abnormal cells with scanty azurophile granules in the cytoplasm and somewhat lobulated nuclei. Because the abnormal cells demonstrated strongly positive peroxidase reactivity with a few faggot bodies, the patient was given a diagnosis of acute promyelocytic leukemia (M3v according to the FAB classification). However, chromosome analysis revealed t(11;17)(23;q21). All-trans retinoic acid (ATRA) was not effective. Mitoxantrone was more effective than daunorubicin, and resulted in a complete remission with a normal karyotype. About 9 months later, the patient suffered a relapse. Surface marker analysis demonstrated blasts that were positive for CD56, CD13, and CD33. MEC (mitoxantrone, etoposide, cytarabine) therapy was ineffective. Although ATRA was administered at a dose of 80 mg/day for more than 2 months, the number of myelocytes and promyelocytes increased Finally CAG (cytarabine, aclarubicin, G-CSF) therapy was initiated, but the patient died due to intracranial invasion and hemorrhage accompanied by disseminated intravascular coagulation.

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A 44-year-old man was admitted because of persistent fever and pancytopenia. Because his bone marrow was hypoplastic and the karyotype of his marrow cells was normal, he was given a diagnosis of aplastic anemia, and treated with glucocorticoids and granulocyte colony-stimulating factor. Splenomegaly was later found and a splenectomy performed: pathological findings on resected tissue specimens disclosed non-Hodgkin's lymphoma, B-cell diffuse large. The patient was transferred to our hospital, where a bone marrow biopsy revealed lymphoma cells infiltrating his hypoplastic marrow. Complex chromosomal abnormalities were detected in marrow cells, but no lymphadenopathy was observed. A diagnosis of primary splenic lymphoma with infiltration of lymphoma cells into bone marrow was made, and chemotherapy was accordingly started. After multiple cycles of chemotherapy, the patient's marrow recovered to a normal state and his karyotype abnormalities disappeared. Six months later, pancytopenia reappeared and lymphoma cells were again detected in the patient's bone marrow. We reasoned that the hypoplastic state of his bone marrow was associated with the lymphoma, and that cytokines, including interferon-γ, may have been responsible for this association.

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A 78-year-old man was diagnosed as leukocytosis in February 1994. Physical examination revealed marked hepatosplenomegaly. A peripheral blood examination disclosed 95,090/μl leukocytes without hiatus leukemicus, 6.5 g/dl Hb, and 15.0×10⁴/μl platelets. The neutrophil alkaline phosphatase score was 27, and serum VB₁₂ was above 1,600 pg/ml. IgG was identified as monoclonal immunoglobulin of type λ. Bone marrow specimens demonotrated marked granulocytic hyperplasia. Neither the Philadelphia chromosome (Ph¹) nor BCR gene rearrangement was detected; hence, the diagnosis of Ph¹ (-) chronic myeloid leukemia (CML) was made. The patient was treated with hydroxyurea and low-dose VP-16 with no improvement, and died of pneumonia and sepsis in June 1995. This case was considered to be consistent with atypical CML (aCML) according to the FAB classification because monocytosis was not observed. It seems likely and interesting that the coexistent monoclonal gammopathy and aCML might have arisen from common abnormal hematopoietic stem cells.

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We encountered 2 patients with multiple myeloma in a family with 11 siblings, suggesting that the occurrence of the disease may be associated with genetic factors. Patient 1: The second daugher (age 79) was given a diagnosis of multiple myeloma and admitted to our hospital in December 1997 for treatment. IgG-λ type M protein was detected by serum immunoelectrophoresis, punched out lesions (+) by X ray examination, and atypical plasma cells (14% of total) by bone marrow examination. Patient 2: The fifth daughter (age 68) received a diagnosis of multiple myeloma and was admitted to our hospital in May 1997 for treatment. Bence Jones-κ type and IgA-κ type M protein were detected by serum immunoelectrophoresis, punched out lesions (+) by X ray examination, and atypical plasma cells (90% of total) by bone marrow examination. It was noted that the sixth daugther had leukemia; hence, 3 of the 11 siblings had blood disorders. For this reason, HLA studies were performed and detected A31, B39, B51, and Cw7 in patient 1 and A31, B51, B62, and Cw4 in patient 2. Further case studies will hopefully reveal more details concerning the relationship between myeloma and HLA.

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We report a case of Burkitt's lymphoma originating in gluteal muscle tissue. A 61--year-old Japanese man was admitted to our hospital due to painful swelling of the left femur and gluteal region in October 1996. A laboratory examination disclosed elevated levels of serum lactate dehydrogenase and soluble interleukin 2 receptor. Gallium scintigraphy demonstrated accumulations in the left femur and gluteal region. Magnetic resonance imaging yielded intense signals and disclosed swelling of muscle tissue in the same region. Pathological examination of biopsy specimens from the left femur revealed a starry-sky pattern, and a chromosomal analysis revealed t(2;8)(p11;q24). Heightened concentrations of antibody for Epstein-Barr virus were not detected. Non-African type Burkitt's lymphoma was diagnosed on the basis of these findings. CHOP therapy and irradiation of the affected region were initially effective, but the disease eventually became resistant to treatment. The patient died of cerebral hemorrhage. As far as we know, this is the first report in Japan of Burkitt's lymphoma originating in muscle tissue.

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A 42-year-old woman underwent a myomectomy on March 31, 1998. On the 10th postoperative day, leukopenia and reticulocytopenia were observed. Bone marrow aspiration revealed severe erythroblastopenia with giant proerythroblasts, suggesting a recent parvovirus infection. Both anti-parvovirus B19 IgM antibody and IgG antibody seroconversion was observod, and human parvovirus B19 DNA was detected by polymerase chain reaction (PCR) methods. The hematologic data on the patient rapidly improved thereafter. It was determined that acute-phase serum had inhibited CFU-E and BFU-E derived colony formation. Based on these findings, parvovirus B19-induced aplastic crisis was diagnosed. Fibrin sealant, which is a typical hemostatic agent produced from blood, had been during the operation. Human parvovirus B19 DNA was detected in the fibrin sealant by PCR. Our case report documents the transmission of human parvovirus B19 by fibrin sealant.

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A 37-year-old woman was given a diagnosis of cervical cancer in August 1994. Because of severe thrombocytopenia, she was given radiation therapy at 50 Gy with great effectiveness. The thrombocytopenia was diagnosed as idiopathic thrombocytopenic purpura. Because the patient refused to undergo a splenectomy operation, she was treated with prednisolone, γ-globulin, and danazol with no effect. In January 1995 she began receiving azathioprine and her platelet count gradually increased. In March, she complained of severe left abdominal pain but abdominal computed tomography (CT) scans showed no abnormal findings. Nonetheless, the patient's lumbago persisted and her liver dysfunction was progressive. Abdominal CT scans performed on April 18 disclosed multiple liver tumors. The patient died on April 28. Autopsy revealed that the cervical cancer was the primary origin of the liver tumors. We concluded that extra precautions should be taken when administering immunosuppressive therapy to patients with a history of malignant diseases.

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