The clinical studies about the electrolyte abnormality (EA) in patients with malignant lymphoma (ML) are rarely reported. We analized the EA and renal insufficiency in 123 patients with ML between Jun. 1976 and Jan. 1989; 8 patients with Hodgkin's disease, and 115 patients with non-Hodgkin's lymphoma (NHL). Before treatment, the incidence of the EA was 24.2% and hypercalcemia, hypocalcemia, and hyperkalemia were predominant. After treatment it became to 74.7% and the number of hyponatremia and hypokalemia increased. The incidence of proteinuria and renal insufficiency (serum creatinine above 1.5 mg/dl), were 7.3% and 2.4% before treatment, and became to 26.8% and 26.8% after treatement, respectively. There was a significant difference between two groups with and without the EA before treatment as for serum lactate dehydrogenase (LDH) levels (p<0.01), clinical stages (p<0.05) and the incidence of bone marrow involvement (p<0.01). In 34 autopsied cases, 3 cases showed massive renal involvement and about a half of cases showed various renal changes. The EA before treatment was caused by extrarenal factors, because the incidence of proteinuria and renal insuffiency were almost same to healthy controls. And renal factors play an important role on the E.A after treatment. Above results suggest that the EA befor treatment indicates the progress of malignant lymphoma and the EA after treatment measns not only the progress of the disease but also thrapyrelated renal damages.

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In order to evaluate precisely the fibrinolytic states in clinical disorders, plasma levels of D dimer (cross-linked fibrin degradation products) were measured by a newly developed, rapid quantitative method based on the latex photometric immunoassay in patients with hematological malignancies, diabetes mellitus, collagen disease, liver disease, thrombotic disease and disseminated intravascular coagulation (DIC). Plasma levels of D dimer were elevated in a variety of diseases, especially in DIC. Patients with hematological malignancies, liver disease and thrombotic disease also had relatively high levels of D dimer. On the whole, D dimer values were positively correlated with plasmin-α₂-plasmin inhibitor complex and thrombin-antithrombin III complex. In addition, plasma D dimer was measured during fibrinolytic therapy with urokinase or tissue-type plasminogen activator; its elevation was detected in some patients. These findings indicate that accelerated fibrinolysis is frequently observed in a variety of diseases, and that a rapid quantitative measurement of D dimer would be valuable for the precise assessment of fibrinolysis in these disease states.

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One hundred hemophilia A and 30 hemophilia B patients who had been treated with non-heated and heated factor VIII or prothrombin complex concentrates were examined by immunological tests including Clq-bearing immune complexes assay. Antibodies to human immunodeficiency virus type 1 (HIV-1), hepatitis B virus (HBV), hepatitis C virus (HCV) and human parvovirus B19 (B19) were analyzed by Western blotting, enzyme immunoassay, passive hemagglutination or radio-immunoassay. Clq-bearing immune complexes were assayed by a monoclonal anti-Clq ELISA system (Immunomedics). Seropositivity to HIV-1, HBV, HCV, and B19 was 56.9%, 87.7%, 79.2% and 100% respectively. Clq-bearing immune complexes were positive in 109 of the 130 patients (83.8%). The positivity and the levels were extremely higher than those in normal individuals. Clq-bearing immune complex levels in patient positive for HIV-1, HCV, or HBV were higher than those in the negative group (HIV: P<0.001, HCV: P<0.005, HBV: P<0.05). When the patients were divided into four groups according to seropositivity to HIV-1 and/or HCV, Clq-bearing immune complex levels were the highest in the group positive for both antibodies, and the lowest in the group negative for both antibodies. These results suggested that each viral infection influences the formation of immune complexes and repeated viral infection increased the level of Clq-bearing immune complexes in these patients.

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An autopsy case of polycythemia vera with der (15) and der (20) associated with remarkable neutrophilia was reported. A 87-year-old man was diagonosed as polycythemia vera in August 1987. The red blood cell count was 621×10⁴/μl, Ht 58.5% and the white blood cell count 45,400/μl with 92% neutrophils. The splenomegaly, increased red bood cell volume and the low erythropoietin level were present. The arterial SaO₂ value was above 92%. The chromosome analysis of bone marrow cells revealed 46, XY, -15, -20, +der (15) t(15;?)(q13-15;?), +der (20) t(20;?)(q11;?). The breakpoint in No. 20 was in q11. The remarkable leukocytosis with relative and absolute neutrophilia were observed. Particularly late in the clinical course the white blood cell count was 92,900/μl with 99% neutrophils. The Ph¹ chromosome was negative and the bcr rearrangement was not detected. He died of bronchopneumonia in January 1989. At the autopsy findings neither the marrow fibrosis nor the extramedullary leukemic cell infiltration was noticed.

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A 52-year-old male was addmitted to the hospital because of abdominal mass. Bone marrow examination revealed 26% blasts, which morphology was L3 in FAB criteria. Abdominal tumor was resected and histologic feature of the tumor was malignant lymphoma, small non-cleaved cell, Burkitt's. Lymphoma cells from the resected tumor were cultured and a cell line was established. Cytological studies of the original tumor cells and the cell line revealed that the lymphoma was negative both for EBNA and EBV DNA, and possessed t(8;14)(q24;q32) in chromosome analysis. Surface antigens were positive for HLA-DR, CD19 and CD20, but negative for CD10. The lymphoma also expressed a monoclonal pattern (IgG, κ type) both of surface immunoglobulin and cytoplasmic immunoglobulin. Thus, the lymphoma was originated from mature B-lymphocyte. We analysed clinicopathological findings of 216 patients who were reported as Burkitt's lymphoma in Japan. Of 35 cases examined for cell EBNA, 7 (20%) were positive for EBNA. Of 86 cases tested for surface immunoglobulin of tumor cells, 67 expressed IgM alone and 10 IgG alone on tumor cells. Cytoplasmic immunoglobulin of tumor cells was positive in 61% of patients. Of 11 cases positive for cytoplasmic immunoglobulin, IgM was detected in 8 patients and IgG only in our patient.

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Although recently the occurence of a malignant neoplasma as a complication of uremia is becoming more frequently, pharmacokinetics of antitumor agents are not precisely studied in patients with impaired renal function. In this report we investigated pharmacokinetics of enositabine (BHAC), arabinosylcytosine (Ara-C) and etoposide (VP-16) in a patient on maintenance hemodialysis who suffered from acute myelomonocytic leukemia and treated by BHAC-EV regimen. Pharmacokinetic parameters of BHAC in uremia were not different from that in patients with normal renal function, and hemodialysis did not affect on the plasma level of BHAC. No significant accumulation of Ara-C was seen in uremia, but there remained the possibility that Ara-C could be removed by hemodialysis. So BHAC was able to be used in uremic patients safely. Since VP-16 was proved to be not a hemodialyzable but an accumulative substance and prolongation of plasma half life was prompt in uremia, VP-16 should be administered to uremic patients very cautiously. From these results BHAC-EV regimen was presumed to be a safely, well tolerated and beneficial regimen in uremic patients.

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A 60-year-old man was admitted to our hospital because of fever, hemorrhagic tendency, anemia and neulological abnormality. A blood count revealed that the hemoglobin was 6.8 g/dl, the reticulocyte was 17.3 percent with 2 erythroblasts per 100 white cells, the white cell count was 7,100/μl and the platelet count was 0.8×10⁴/μl. Peripheral blood smear demonstrated marked fragmentation of red cells. Bone marrow examination disclosed the marked erythroid hyperplasia. Althoug the bleeing time was prolonged (14 minites 30 seconds), the other hemostatic data were within normal limits. The serum bilirubin level was 1.57 mg/dl; LDH level, 1,437 U/l; creatinine level, 0.92 mg/dl; BUN level 14.7 mg/dl. Haptoglobin was below 10 mg/dl. Results of immunological tests were all negative except the result of PAIgG (576.6 ng/10⁷ cells). The urinalysis showed proteinuria, microhematuria and trace granular and hyaline casts. A diagnosis of thrombotic thrombocytopenic purpura was made. The patient was initially treated with prednisolone (60 mg), aspirin (1,000 mg), dipyridamole (150 mg), gabexate mesilate (1.5 g), sodium oxagrel (80 mg) daily with little response. The thirty days after admission, infusion of γ globulin (20 g, daily) was given for 3 days. The clinical state and laboratory findings became dramatically improved shortly after the administration of γ globulin and the labortory data came to be normalized after 1 month. After ten months of this treatment, the patient is remained asymptomatic and the hematological data are within normal range without using any drug. A trial seems justified to confirm the value of this mode of therapy.

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Two patients with orthostatic purpura were reported. Case 1: A 47-year-old man was admitted to our institution because of multiple purpuric eruptions over the legs after the long periods of sitting or standing. Bleeding time was 4.0 min. Platelet aggregation induced by ADP was disaggregated and no aggregation was observed when induced by collagen and epinephrine. He was diagnosed as having release abnormality of the platelets caused by glutathion administered for treatment of liver damage for several years. Purpura, however, appeared even though platelet function became normal after discontinuing glutathion. Purpura proved to be induced by the long periods of sitting or standing. Case 2: A 37-year-old woman was admitted to our hospital because of purpuric eruptions over the legs for three years. Bleeding time was 2.0 min. Platelet aggregation induced by ADP, epinephrine, collagen and ristocetin was normal. Purpura was caused by long periods of standing without movement. Wearing elastic panty horse showed reduced appearance of the purpura. Biopsy specimens from both patients revealed no abnormal findings. Both patients had no abnormal results in coagulation studies. Purpura seemed to be caused by the increased capillary pressure after the prolonged periods of standing. No case report concerning orthostatic purpura or mechanical purpura has been published.

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Platelet funcions and morphological changes of megakaryocytes were investigated in three cases with chronic neutrophilic leukemia (CNL). The bleeding time was prolonged, the ADP, collagen, epinephrine-induced aggregation of platelets decreased in one case. The adhesiveness, epinephrine-induced aggregation and adenine nucleotide content of platelets decreased in one other case. Magakaryocyte size in CNL was larger than in CML and this difference of the megakaryocyte sizes was related to DNA content distribution of the megakaryocytes. Atypical megakaryocytes were apparently found in one case. The present study suggests that CNL is a stem cell disorder.

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A 60-year-old woman was admitted to our hospital because of gastric ulcer, anemia and leukocytosis in November 1984. Blood cell counts on admission were as follows: RBC 407×10⁴/μl, Hb 9.8g/dl, WBC 33,000/μl (baso 8%, eo 7%, myelo 11%, meta 2%, stab 4%, seg 54%), Plt 93.7×10⁴/μl. Bone marrow showed hypercellular and myeloid hyperplasia. She was diagnosed as Ph¹-chromosome positive chronic myelogenous leukemia. She received natural interferon-alpha at the dosage of 600×10⁴ IU daily for 22 days from January 14, 1985. After March 1985, she has been given intermittent administration of interferon once in 10 to 20 days, and maintained normal blood cell counts. Cytogenetic improvement was seen on 35 months after the start of IFN and complete suppression of Ph¹ chromosome was observed at July 1990 (66 months after).

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