Flow cytometry was used to detect platelet-associated fibrinogen (PA-Fbg), platelet-associated fibronectin (PA-FN) and platelet-associated thrombospondin (PA-TSP) on the surface membrane of platelets and plasma (P)-TSP in 30 patients with lung cancer (16 case of adenocarcinoma and 14 of squamous cell carcinoma). ELISA was used to analyze β-TG and PF4. In the lung cancer group, β-TG and PF4 were higher than those of a normal control group. PA-Fbg values were correlated with β-TG and PF4 values. Each adhesive protein had a higher value in the patient than in the normal control group, and the degree of the increase was related to the progression of clinical disease stage. In the squamous cell carcinoma group, the P-TSP value was significantly elevated. Platelet size increased as the clinical stage of the disease progressed.
These results suggest the following:
1. An increase in PA-Fbg can indicate the presence of activated platelets.
2. In patients with lung cancer, activated platelets appear in the blood, and their numbers increase as the clinical stage of the disease progresses.
3. Differences in histologic type led to differences in binding adhesive protein.

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Renal and electrolyte disturbances in 91 patients with chronic myelogenous leukemia (CML) were analyzed over a period of these twenty years. At diagnosis, renal and electerolytes were studied in 72 patients including 65 in chronic cases, 5 in accelerated phase and 2 in blastic crisis. There were 8 cases of hypocalcemia among 62 patients and 5 cases of hyperphosphatemia among 48 patients. The cases of hyperphosphatemia and renal dysfunction had short median survival. There were no significant differences of renal and electrolyte disturbances between before and after chemotherapy. Various electrolyte dysturbances, that is, hyponatremia, hypo-, hyperkalemia, hypocalemia, hypo-, hyperphosphatemia, were found in the blastic crisis of CML. In the last admission, renal dysfunction and various electrolyte disturbances were present in almost half of the cases. Pathological studies were performed in 18 autopsy cases. Acute tubular insufficiency or necrosis, hypercalcemic nephropathy, and renal infiltration of leukemic cells were recognized in patients who had renal dysfunction.

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Myeloperoxidase (MPO)-and Sudan Black B-not more than 3%-positive, esterase staining-negative, lymphoid, megakaryocyte lineage and erythriod surface marker-negative and electron microscopic platelet peroxidase-negative acute leukemia (AL) was diagnosed as acute undifferentiated leukemia (AUL), and myeloid marker (CD13, CD33), electron microscopic MPO (EMMPO), and DNA analysis of immunoglobulin heavy chain and T cell receptor as well as chemotherapy and its reactivity were examined. Of 239 cases of AL, 10 (4.2%) were AUL, and of these 10 cases, 9 were CD13 or CD33-positive AML-MO (MO) cases. Of 9 cases examined for EMMPO, 4 (44%) were positive, and of 3 cases of MO subjected to DNA analysis, 1 and 1 showed rearrangements of immunoglobulin heavy chain and T cell receptor β chain, respectively. Of 6 cases of MO on myeloid induction therapy, 1 and 1 showed complete remission (CR) and partial remission (PR), respectively, each having lymphoid genotype, and 4 showed no remission (NR), being 3 of them EMMPO-positive. Of 2 cases on lymphoid induction therapy, 1 and 1 showed CR and NR, respectively, the former being EMMPO-positive MO. BHAC-EM therapy with behenoyl cytosine arabinoside, VP-16 and mitoxantrone performed on 2 cases refractory to any one of both these myeloid and lymphoid induction therapies led to CR in all these 2 cases.

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The effects of antimetabolites on the growing dynamics of human bone marrow stromal cells and their support of hemopoietic cells were tested by using a modified version of Dexter's culture system. Cytosine arabinoside (ara-C) was found to suppress neither the growing dynamics nor the supportability. On the other hand, methotrexate (MTX) suppressed the supportiveness, even though it hardly suppressed the growing dynamics. The recognition of injury to marrow cells could be of potential importance in cancer chemotherapy. Our in vitro evidence may provide clinical insights for cancer chemotherapy including prolonged marrow suppression or pretreatment of bone marrow transplantation.

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Serum erythropoietin (Epo) levels were measured in 53 patients with multiple myeloma (MM), 49 normal subjects and 53 patients with some hematological diseases including aplastic anemia (AA), iron deficiency anemia, etc. to study the significance of erythropoietin in anemia of MM. The serum Epo level was 72.0±94.4 mIU/ml (mean±SD) in MM patients, which was significantly higher than in normal subjects (24.1±6.1 mIU/ml), but lower than in AA patients (7069.9±9406 mIU/ml). A significant inverse correlation was found between the hemoglobin (Hb) levels and the logarithmic values of serum Epo levels (r=-0.543, p<0.05) in MM patients. This inverse correlation was stronger (r=-0.636, p<0.05) in MM patients without renal dysfunction than in whole MM patients, while no correlation was observed in MM patients with renal dysfunction. These results indicate that MM patients with renal dysfunction have a low ability to synthesize Epo and that the supplemental therapy of recombinant Epo is effective to improve their anemia. In addition, the circadian rhythm of serum Epo level was lower in the morning than in the afternoon in both MM patients and normal controls. Serum Epo levels after chemotherapy in MM patients were elevated temporarily and then decreased in spite of no change of blood Hb level.

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Urinary excretion of parathyroid hormone-related protein (PTH-rP) was measured by radioimmunoassay in 25 patients with adult T-cell leukemia (ATL), in 68 patients with other hematologic disorders and in 13 asymptomatic individuals seropositive for human T-cell leukemia virus type I (HTLV-I). The mean levels of urinary PTH-rP in ATL patients with hypercalcemia (11.01 μg/g·Cr) were higher than in ATL patients with normocalcemia (5.16 μg/g·Cr). The mean levels in patients with acute type (8.84 μg/g·Cr), lymphoma type (4.18 μg/g·Cr) and crisis ATL (18.20 μg/g·Cr) were significantly higher than in urine of healthy controls. However, all asymptomatic carriers of HTLV-I and patients with chronic and smoldering ATL had normal urinay PTH-rP levels. In 7 patients with acute myelogenous leukemia, 1 patient with blastic crisis of chronic myelogenous leukemia and 3 patients with malignant lymphoma, the urinary levels of PTH-rP were above the normal range. Urinary levels of PTH-rP of the ATL patients with hypercalcemia correlated with the serum calcium levels. Urinary levels of PTH-rP of the all ATL correlated with serum lactic dehydrogenase level. These findings suggest that the measurement of urinary levels of PTH-rP is useful for evaluation of ATL and that some tumor cells of other hematologic diseases may produce PTH-rP.

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A pregnant woman with congenital antithrombin III (AT III) deficiency was given AT III concentrate and warfarin at the first and after 36th week of gestation periods and at the other gestation period, respectively. The patient developed thrombosis in the left leg, but fibrinopeptide A (FPA) and thrombin-AT III complex (TAT) had already shown high values one week before, suggesting the possibility of their being forecast markers of thrombosis. The administration of AT III concentrate caused an improvement in thrombosis. Therefore, in case of high FPA and TAT values as determined one or two times a week, the administration of AT III concentrate was thought necessary. In case of warfarin, however, non-administration during the 6th∼9th weeks of gestation for the purpose of avoiding teratogenicity and frequent blood coagulation tests taking heed of overdosage for the purpose of avoiding fetal central nervous system abnormalities were suggested necessary.
Delivery was eventless, both mother and child being doing very well; umbilical blood AT III activity was 18%. It is generally difficult for us to form the diagnosis as AT III deficiency only from AT III activity at neonatal stage, but in the present study, we analyzed the restriction fragment length polymorphism of the AT III gene using umbilical blood, and succeeded in diagnosing the neonatal child as AT III deficiency.

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Subcutaneous administration of recombinant human Interleukin-1β (IL-1β) in a dose of 1-3×10⁴ U/day for 14 to 72 days resulted in an increase in circulating granulocytes and bone marrow monocytes in all the 4 patients examined. Circulating platelet count was also increased in two of four patients with myelodysplastic syndrome (MDS) and aplastic anemia (AA). Bone marrow examination revealed an increase in megakaryocyte count in these patients, whereas the percentage of blast was not changed. An increase in blood platelet count was accompanied by an increase in serum GM-CSF in a patient with AA, whereas serum IL-6 level was not changed throughout the treatment with IL-1β. These findings suggest that IL-1β may be useful for the treatment of a proportion of patients with MDS and AA who are associated with thrombocytopenia.

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The clinical significance of antinuclear antibodies (ANA) in patients with chronic idiopathic thrombocytopenic purpura (ITP) was evaluated. Serum samples of 55 patients with ITP without clinical features of systemic lupus erythematosus (SLE) were examined. The average follow-up period was 5.5 years. Positive ANA was found in 23 of the 55 patients. Twelve of these 23 showed a high-titer of ANA. There was no difference in platelet counts between ANA positive patients and negative patients, and there was no correlation between platelet counts and antibody titers. Ten of the 23 positive sera had precipitating antibodies to nuclear antigens; 7 SS-A and 3 RNP antibodies. The platelet counts of the 7 cases with anti-SS-A antibody positive were slightly low compared with those of the anti-SS-A antibody negative patients. None of the 10 patients developed SLE during the average follow-up period of 8.1 years. These results suggest that ITP patients who have a high-titer of ANA or antibody against SS-A do not allways develop SLE. It was concluded that ANA with a high titer or precipitin to nuclear antigens, particularly SS-A, dose not predict a high risk of developing SLE in the future.

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We investigated 9 cases of Ki-1 lymphomas morphologically and immunohistochemically. The lymphoma cells infiltrated in the lymph nodes in 7 cases, in the skin in 6 cases, in both in 4 cases and in the bone marrow in 2 cases. In lymph nodes, the giant tumor cells infiltrated paracortical areas, showing a sheet-like appearance or free cell growth pattern and in the marginal and medullary sinuses as well. In the skin, they formed subcutaneous tumor and infiltrated diffusely also in dermis. All cases were positive for Ber-H2, Ki-1 and HLA-DR and 8 cases revealed some of the T cell phenotypes. But Leu-4 and βF1 for which all 11 peripheral T cell lymphomas were positive, were only positive in 2 cases, respectively. In the present study, the tumor cells were positive for a few antibodies for T lymphocytes and there were few cases showed positivity for Leu-4 and βF1. The results suggest that it was questionable whether the tumor cells were derived from T lymphocytes. There may be few cases of Ki-1 lymphomas of distinct T cell lineage.

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Serum aldolase A (ALD-A) levels were determined in patients with leukemia using a radioimmunoassay method. The method is a double antibody radioimmunoassay consisting of purified ALD-A as ligand, chicken antisera to ALD-A and rabbit antibodies to chicken IgG. Serum ALD-A levels of 41 normal healthy subjects ranged from 130 to 210 ng/ml (mean±2SD; 171±39 ng/ml). Serum ALD-A levels ranged from 90 to 200 ng/ml in patients with 42 non-neoplastic hematological diseases with the exception of hemolytic anemia. In contrast, 61 patients with acute leukemia before treatment exhibited increased serum ALD-A levels ranging from 125 to 1,550 ng/ml, with a mean value of 480 ng/ml. Serum ALD-A levels in 24 patients with chronic myelocytic leukemia (CML) during the chronic phase also exhibited high mean values of 481 ng/ml in a range of 270 to 1,100 ng/ml. Serum ALD-A levels were higher than 210 ng/ml in 85.2% of the patients with acute leukemia and in all patients with CML. Serum ALD-A levels tended to be decreased within the normal range, if those patients could achieve complete remission. In contast, serum ALD-A levels showed a tendency to increase if those patients experienced a relapse of leukemia. These results suggest that the measurement of serum ALD-A levels by radioimmunoassay is useful for diagnosis and prediction of relapse in patients with leukemia.

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The measurement of erythrocyte zinc protoporphyrin (ZPP) with a hematofluorometer is known to be a simple and cost-effective method to screen iron deficiency and lead poisoning. We measured ZPP on blood samples from 201 children suffering from various diseases, which revealed that ZPP has better sensitivity and specificity for identifying iron deficiency than serum ferritin and percent transferrin saturation. ZPP levels in various anemias were also measured. ZPP rose markedly (>200μmol/mol heme) in untreated iron deficiency anemia and returned to normal in 3∼4 months since the initiation of iron therapy. Moderate elevation of ZPP was observed in acute leukemia (at onset and during induction therapy), MDS, aplastic anemia and some other anemic conditions. These findings suggest that erythrocyte ferrochelatase may be unexpectedly affected in anemias even except lead poisoning.

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Thirty-two patients with leukemia or non-Hodgkin's lymphoma (NHL) who underwent high-dose chemotherapy without total body irradiation (TBI) and peripheral blood stem cell autografts (PBSCT) were evaluated for the occurrence of clinically manifested varicella-zoster virus infection (VZV). In a minimum follow-up of 3 mo, there were 14 cases with VZV; 12 patients were treated with intravenous acyclovir and 2 patients received additional intravenous VZV hyperimmune immunoglobulin preparations. History of previous varicella-zoster at some time before PBSCT was the only significant risk factor for the development of VZV. Furthermore, a significant association between VZV and higher disease-free survival rate after PBSCT was proved. Development of minor and reversible VZV is rather common event after high-dose chemotherapy without TBI and PBSCT. VZV appears to be one of the factors which reflects basic physiologic mechanism preventing relapse of leukemias or NHL after PBSCT.

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We examined 14 patients (18 cases) with idiopathic thrombocytopenic purpura (ITP) during pregnancy at our department. ITP, which had improved, recurred during pregnancy in 4 cases while it developed for the first time during pregnancy in 10 cases. In the other 4 cases, pregnancy occurred in the course of ITP. Although a normal infant was born in 14 cases, 3 stillbirth and a premature infant was observed in 4 cases. Six deliveries had some toxemia of pregnancy. A transient decrease in neonatal platelets was observed in 4 of 14 cases and mother's platelets count was less than 40×10³/ul in the 4 cases. Although antinuclear antibody, Coomb's test and antiphospholipid antibody were positive in some cases, these were not markedly related to clinical course or neonatal pletelets count. Eleven cases were treated with glucocorticoids, high dose gamma globulin or platelets transfusion, but 11 cases were not treated. Since ITP is frequently observed during pregnancy and may be some risk factor for pregnancy, treatment of ITP is important during pregnancy.

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A 58-year-old man with cyclic thrombocytopenia who was initially diagnosed as idiopathic thrombocytopenic purpura (ITP), concomitant with chronic thyroiditis and ankylosing spondylitis, was reported. Serum level of T 3 (0.48 ng/ml) and T 4 (2.1 μg/ml) were both subnormal and that of TSH (257.1 μU/ml) was markedly elevated. Thyroid test (6400×) and microsome test (6400×) was both positive, but anti-nuclear antibodies were negative. Radiographic findings of lumbar spine showed the typical “bamboo spine” and HLA B 27 was positive. Therapies for ITP, such as adrenocorticosteroids including steroid pulse therapy, high-dose intravenous gamma-globulin, danazol, slow infusion of vinca alkaloids and splenectomy, were only effective transiently. After these therapies platelet counts began to fluctuate from 0.4×10¹⁰/L to 34.4×10¹⁰/L, therefore the diagnosis of cyclic thrombocytopenia was done. Interestingly low-dose methotrexate (MTX) was effective, and the cyclic fluctuation of platelet counts disappeared. These observations in this case were very suggestive of the pathogenesis of cyclic thrombocytopenia and mechanisms of cyclic change of platelet counts.

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In this report, we described a case of acute lymphoblastic leukemia with leukoencephalopathy that responded to oxygenation under hyperbaric pressure (OHP) therapy. The patient was 6 year-old female who was diagnosed as acute lymphoblastic leukemia (ALL) one year and 9 months earlier. After the first relapse of the central nervous system (CNS) leukemia, intrathecal administration of methotrexate (MTX) and skull irradiation induced CNS remission. The patient was readmitted because of second CNS relapse. After the third administration of weekly intrathecal MTX injection, apathy and finger tremor were observed. Her conscious disturbance continued for two weeks and magnetic resonance imaging (MRI) revealed abnormal findings in the white matter of her brain. Subsequently OHP therapy was commened, and the conscious disturbance was improved gradually. One month later, neurodisturbance resolved completely and the findings of MRI were improved. We could not find any case of leukoencephalopathy which was treated with OHP in the literature. But our case suggested that OHP therapy is valuable in patient with leukoencephalopathy in the early stage.

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The authors report a rare case of chronic myelogenous leukemia (CML) in which the Ph¹ clone disapeared after remission induction of lymphoid crisis. A 58-year-old man was admitted to our hospital because of fever in July 1988. The white cell count was elevated. Bone marrow aspirate showed hypercellularity with myeloid hyperplasia. In the chromosomal analysis, Ph¹ chromosomes were detected in 100% of bone marrow cells analysed. Diagnosis of CML was made and treatment was initiated with recombinant interferon-α 2a. Hemotological remission without cytogenetic improvement was achieved. In March 1990 he developed lymphoid crisis with proliferation of CD10-positive cells. The chromosomal analysis revealed additional abnormalities including, 45, X, -Y, t(9;22)(q34;q11), +1, -8. With vincristine 0.6 mg×4, pirarubicin 15 mg×4, dexamethasone 40 mg×4 therapy complete remisson was obtained. In December 1990 the Ph¹ positive clone completely disappeared judging from normal karyotypes in the chromosomal analysis and the disapearance of M-bcr gene rearrangement.

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A 53-year-old male was diagnosed as having ataxic polyneuropathy associated with IgM-κ monoclonal gammopathy in January 1988. Plasmapheresis and chemotherapy with chlorambucil and Melphalan-Prednisolone were effective for his neuropathy, but hemolytic anemia appeared in February 1989. The diagnosis of low-titer cold agglutinin disease (IgM-κ) with anti-Pr₂ specificity was made. Hemolytic anemia became refractory to high-dose corticosteroids, and fever, hepatosplenomegaly and severe pancytopenia appeared in January 1990. Bone marrow involvement of malignant lymphoma (μ, κ) was found, and he died of pneumonia and gastrointestinal bleeding after the start of chemotherapy. Postmortem examination revealed a widespread infiltration of malignant lymphoma, diffuse, large cell (B-cell) type. Erythrophagocytic histiocytes also increased in bone marrow, liver, spleen and lymph nodes, as if there were hemophagocytic syndrome associated with lymphoma present. In addition to the high thermal amplitude of cold agglutinin in this case, the systemic activation of histiocytes induced by the development of malignant lymphoma may be responsible for progressive hemolysis and severe pancytopenia.

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A 32 year-old female admitted to our hospital with pancytepenia. The hematological data on admission were: RBC: 247×10⁴/μl, Hb: 8.8g/dl, Plts: 13,000/μl, WBC: 2,500/μl. Bone marrow aspirate and biopsied speciemen showed marked hypocellularity without infiltration of abnormal cells. A diagnosis of aplsatic anemia was made. Neither high-dose methyl-prednisolone pulse therapy nor anti-lymphocyte globulin were effective. With combination of oxymetholone (30 mg/day), recombinant erythropoietin (rHuEpo; 12,000 U/day, three times a week) and recombinant granulocyte-colony simulating factor (rHuG-CSF; 33 μg/day) for 3 months, remarkable improvements of hematological data were obtained. Her hemoglobin level reached 11.4 g/dl, and platelets count 49,000/μl. However, 4 weeks after the withdrawal of erythropoietin and G-CSF administrations, her platelet count fell to 12,000/μl. It was suggested that combination therapy with erythropoietin and G-CSF were effective for aplastic anemia.

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A 21-year-old woman was admitted to our hospital because of high fever, cough, and headache. Other clinical manifestations included hepatosplenomegaly, anemia, leukopenia, and mild liver dysfunction. As she had been diagnosed to have systemic lupus erythematoses (SLE) previously, we first suspected that this disease had become exacerbated. However, the titers of anti-EB virus (VCA-IgG) and some other viruses were high on admission, and hemophagocytosis by macrophages was observed on bone marrow examination. Therefore, she was diagnosed to have virus-associated hemophagocytic syndrome (VAHS). Predonisolone therapy was then initiated, but the patient responsed poorly. We next tried gamma globulin, and the clinical findings and laboratory data were improved. Our patient showed a very favourable clinical course following gamma globulin therapy, suggesting that steroid and gamma globulin should be considered as a treatment even in the early stages of this syndrome in adults.

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A 66-year-old female was admitted with high fever and loss of consciousness. For the past one year, she has experienced recurrent febrile episodes. On admission, the presence of monocytosis, thromobocytopenia of the peripheral blood and dysplastic findings of the bone marrow cells indicated chronic myelomonocytic leukemia (CMMoL). The high fever persisted in spite of treatment with antibiotics. Although she was treated by pulse therapy with methyl-prednisolone, her clinical symptoms did not improve. Pleural effusion and ascites were also noted. Treatment with F-COP (epirubicine, cyclophosphamide, vincristine, prednisolone) therapy, resulted in a dramatic improvement of her condition. The F-COP therapy was given monthly for the next 7 months. This case suggests that F-COP therapy may be effective for some patients with CMMoL.

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A 73-year-old man was admitted to our hospital on April 30, 1990, because of fever persisting for 18 months. Bone marrow puncture and biopsy were performed, because examination on admission revealed an elevated leukocyte count and anemia while his superficial lymph nodes, liver and spleen were not palpable. The results of the bone marrow biopsy revealed evidence of granuloma. Around May 10, the patient developed hepatosplenomegaly and enlargement of left cervical lymph nodes. Based on the results lymph node biopsy, a diagnosis of Hodgkin's disease was made, and CHOP therapy was instituted on May 20. However, the patient developed interstitial pneumonia and died on July 3. This patient's disease was manifested by fever of unknown origin. Bone marrow biopsy revealed granuloma with histiocytes predominating, and the patient subsequently developed lymph node enlargement. His disease was then diagnosed as Hodgkin's disease on the basis of a biopsy. Malignant lymphomas associated with granulomas in the bone marrow, liver or spleen are for the most part found in the advanced stage of the disease. It should be borne in mind, however, that some patients may exhibit granuloma formation in their bone marrow prior to lymph node enlargement or hepatosplenomegaly, as in the present case.

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A 42-year-old male was diagnosed as having Ph-positive chronic myelogenous leukemia (CML) in 1988. He had been treated with ranimustine and interferon α. In April 1990, he was admitted to our hospital because of hemorrhagic diathesis. Blood counts revealed a white blood cell count of 319,200/μl with 12 per cent blasts, a hemoglobin level of 9.2 g/dl, and a platelet count of 48,000/μl. The bone marrow aspiration revealed hypercellularity with 68. 2 per cent blasts, and chromosomal analysis showed 48, XY, +8, double Ph. A combination chemotherapy containing vindesine, cytarabine and prednisolone was administered. Four days later, he suddenly complained of headache and vertigo. CT scan of the brain showed a high density area at the cerebellar vermis. He was then treated with intensive combination chemotherapy including enocitabine, daunomycin, 6-mercaptopurine and prednisolone. He attained a hematological response and clinical improvement temporarily, as the cerebellar tumor regressed. In September he had headache and vertigo again, and CT scan revealed a rapid increase in size of the cerebellar tumor. Local irradiation with total doses of 19 Gy brought about a partial resolution of the lesion, and relief from the symptoms. In November, his hematological conditions deteriorated gradually and he died of brain hemorrhage on November 22, 1990. Post-mortem examination disclosed a 1×1cm sized mass in the cerebellar vermis which showed a fibrous change surrounded with hemosiderin-laden macrophages microscopically. We reviewed the eight reported cases of CML with intracranial tumors, and discussed the factors which had contributed to the prolongation of suvival in our patient.

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Fourtythree-year-old man with schizophrenia, who had been diagnosed as chronic myelogenous leukemia (CML) and had been treated with hydroxyurea for 3 months, developed blastic crisis. The cytochemical study of the blastic cells showed POX (+), SBB (+) and TdT (+). The surface marker analysis revealed that the blastic cells expressed both myeloid (CD13, 33) and lymphoid (CD10, 19) markers. In the chromosomal analysis, additional chromosomal abnormality (11q+) was detected in all cells analysed (20/20) in addition to the standard type Ph¹ chromosome. He was diagnosed as biphenotypic blastic crisis, and vincristine-prednisolone therapy was started. Initially, he responded to VP therapy well, but gradually became refractory to the therapy after 5 courses of VP. As many myeloblasts containing azurophilic granules were seen in the bone marrow after VP therapy, low dose Ara-C therapy was combined to VP. After 21 days of low dose Ara-C and VP, the percentage of the blast in the BM was significantly decreased and normal myeloid diferentiation was observed after transient BM suppression. The chromosomal analysis showed the partial reappearance of standard Ph¹ chromosome in 55% of the cells analyzed (11/20). Taken together, our data suggested that the combination of VP and low-dose Ara-C therapy might have some therapeutic benefit for the treatment of the CML with blastic crisis.

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In a 47-year-old male patient a tonsillar swelling was pointed out in May, 1991. Lymph node biopsy revealed that he had malignant lymphoma (diffuse large cell type). He had no hepatic dysfunction on admission, but because of positive hepatitis B (HB) antigen and negative HB antibody, he was diagnosed as an asymptomatic HB carrier. The staging examination showed that he had stage IIA lymphoma. Treatment with the COP-BLAM regimen was initiated on June 8. But the level of serum GOT and GPT increased to 286 IU/l and 392 IU/l, respectively. Serum DNA polymerase also increased to 9492 cpm. Interferon-α (3×10⁶ units daily) was administered intramuscularly from June 8. Serum DNA polymerase decreased to zero on September 2, and his HBe antibody became positive indicating seroconversion. COP-BLAM chemotherapy without prednisolone was initiated from September 9 and complete remission was achieved. He was discharged from our hospital on September 25. It has been frequently reported that asymptomatic HB antigen carriers developed fulminant hepatitis during the course of chemotherapy. Our case suggests that it is necessary to continue chemotherapy in order to attain seroconversion by early use of interferon-α, when lymphoma patients display aggravated hepatic dysfunction and increased DNA polymerase levels.

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Pneumocystis carinii pneumonia (PCP) is a major opportunistic infection in acquired immunodeficiency syndrome (AIDS) and is treated with co-trimoxazole, pentamidine and others. The severe adverse reactions, including bone marrow suppression, by these therapeutic agents often preclude their continued use. A 14-year-old male HIV-positive hemophilia A patient, who was complicated by disseminated intravascular coagulation syndrome (DIC) following acute pancreatitis during treatment for PCP, was treated with proteinase inhibitors and anticoagulant agents. He was improved and discharged. As pentamidine may cause pancreatitis and develop DIC, it is important that pancreatic enzymes should be carefully followed when this agent administrated. In this case, granulocyte colony-stimulating factor and erythropoietin were effective for the bone marrow suppression, suggesting that importance of these agents for the prophylaxis of other secondary infections during the treatment.

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The patient was a 76-year-old female who had been referred to our hospital because of fever of unknown origin on October 15, 1987. On admission, the body temperature was 38.6°C and atonic palsy of the left upper limb was noted. Abnormal laboratory findings included CRP5+, an increase in LDH, Hb 7.9g/dl. The cause of the fever could not be identified. The fever did not respond to various treatment. The patient developed DIC in late October and died on November 5. In autopsy histological examination revealed tumor cells in the vessels of the generalized organs. A diagnosis of neoplastic angioendotheliosis (NAE) and immunohistologically B lymphoma was made. We reviewed the literature on 37 Japanese cases of NAE. The cases, consisting of 19 males and 18 females, were aged 37∼87 years with a median value of 60 years. The symptoms observed during the course were most frequently mental or neurological symptoms and fever, and rash was uncommon. Laboratory findings were non-specific and biopsy was needed for definitive diagnosis. By autopsy, lesions were noted more frequently in the brain, kidneys, and lungs, and the findings in the skin were indeterminate. These observations suggest that when NAE should be considered, kidney, lung or skin biopsy should be performed for definitive diagnosis.

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A 73-year-old male had severe lumbago and right inguinal lymphadenopathy. A CT scanning of his abdomen showed marked enlargement of right psoas and erector spinae muscles. The biopsies of the lymph node and the muscles revealed non-Hodgkin's lymphoma of follicular mixed type with muscle invasion. THP-COPE therapy was begun. The swelling of the muscles diminished and the lumbago resolved rapidly. It was reported that clinically prominent infiltration of lymphoma in skeletal muscle was rarely and psoas muscle was for the most part. We have to consider that psoas muscle invasion of lymphoma cause hard to cure lumbago.

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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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