Twenty seven previously untreated patients of acute nonlymphocytic leukemia with age ranging from 30 to 77 years, received a 7-day remission induction regimen consisting of daunorubicin, cytosine arabinoside, 6-mercaptopurine and prednisolone (continuous-DCMP). Patients who achieved complete remission were given ten courses of consolidation therapy and followed without any maintenance therapy.
The complete remissions were obtained in 7 of 15 patients (46.6%) 60 years and older, and in 11 of 12 patients (91.7%) 30∼59, years of age.
Although a high mortality during periods of marrow hypoplasia after the intensive induction therapy, and early relapses in the 60 years and older patients remain major problems, our data suggest the elderly patients deserve a trial of intensive combination chemotherapy.

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Fifteen adult patients undergoing allogeneic bone marrow transplantation (BMT) received cyclosporine (CSP) as prophylaxis of graft versus host disease (GVHD). In our patients eleven were hematologic malignancies, and four were severe aplastic anemia. Twelve patients were HLA-matched, and three were one locus mismatched. Three patients received CSP only, twelve received CSP and short term methotrexate.
Seven patients had acute GVHD, but GVHD over Grade II were seen in only 3 patients who were transplanted from HLA-one locus mismathched donor. 7 patients had chronic GVHD.
CSP were given intravenously at 3∼5 mg/kg, starting 1 day before BMT. From about day 30, CSP was given orally. CSP concentrations when patients were given orally were lower in patients who had chronic GVHD. Although hypertension and water retention were seen in 8 patients, and renal dysfunction was seen in 3 patients, the side effects of CSP were mild and transient. There were no correlations between serum concentrations and the side effects of CSP. Three patients had the disturbance of hematopoiesis. Ten of fifteen patients are alive at median follow-up of 18.5 months (8∼41 months) after BMT.

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To investigate the role of erythropoietin in aplastic anemia, the effects of high titers of recombinant human erythropoietin (rh-Ep) on CFU-E and BFU-E in patients with aplastic anemia were studied in vitro. Colony assays were performed by methylcellulose culture methods added with 1 to 500 units of rh-Ep. In normal bone marrow, the maximum CFU-E colony formation was observed at 2 to 5 units of rh-Ep, and BFU-E at 2 to 10 units. Colonies did not increase by addition of higher titer of rh-Ep to the cultures. In aplastic anemia, the numbers of CFU-E and BFU-E were low at 2 units of rh-Ep in culture system. In most patients with aplastic anemia studied, erythroid colonies were increased in accordance with the increase of rh-Ep added to cultures.
These results suggest that the administration of high titers of rh-Ep in vivo may be useful for the improvement of anemia in aplastic anemia.

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We studied the expression of 2H4 and 4B4 on the surfaces of leukemia cells from 17 patients with adult T-cell leukemia (ATL) as well as of cells belonging to 2 T-cell lines derived from ATL patients. The effects of the supernatants obtained from culture fluids of the ATL cells and the T-cell lines on IgG production of a human B-cell line, CESS cells, were also examined.
On the surfaces of the ATL cells from 15 out of 17 cases and of the cells of 2 T-cell lines 4B4 obviously existed at higher percentage than 2H4 and more than 80% of ATL cells from 16 out of these 17 cases showed the expression of T4 (CD4). These findings revealed that the most of ATL cells had a helper-inducer phenotype.
Supernatants (Sups) of culture fluids of ATL cells from 4 patients and those of 2 T-cell lines were added at various concentrations to the CESS cells. In only 1 Sup from ATL patient enhanced the IgG production of the CESS cells at lower concentration. However, other 5 Sups suppressed the IgG production of the CESS cells in proportion to the increase of Sup added.
These results showed that phenotypical type of ATL cells does not always correspond to their functions, and the ATL cells may produce humoral factors that regulate B cell functions.

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Clinicopathologic analyses were done on 10 patients with follicular lymphoma including 8 patients with low grade malignancy. The complete response rate to chemo- and combined modality therapy was 80% with no deaths occurring in patients in complete remission with median follow-up of 73 months. The 5-years' survival for these 10 patients was 86%. There were two patients with second primary neoplasm, one with gastric cancer detected one year after initiation of chemotherapy, the other with leiomyosarcoma detected 3 years after cessation of chemotherapy. Histologic transformation from follicular medium sized cell to diffuse large cell was noted in one patient.

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Twenty two cases with Hodgkin's disease under 20 years of age who were diagnosed and treated in National Cancer Center during 1962∼1986 were studied retrospectively. The most common initial symptom was swelling of lymph nodes (86%) and only 5 cases (23%) showed “B” symptoms. Labolatory findings showed that there were some cases with increased WBC counts but only 2 cases with an elevated LDH value. In 2 out of 4 cases serum copper value correlated well with their clinical state. Histologically lymphocyte predominance type, mixed cellularity type and nodular sclerosis type almost equally occured in children younger than age 15 years. On the other hand nodular sclerosis type with mediastinal mass was predominantly encounterd in older patients (especially female). The ten years' survival rate in stage I and II patients was 59% compared with 21% in stage III and IV patients. As for the results of initial treatment, complete remission and 10 years' survival rate were 91% and 87% in recent 12 years (1975∼1986) compared with 55% and 36% in the preceding 13 years (1962∼1974) respectively. Autopsy findings revealed rare involvements of the central nervous system and kidneys. Various late effects which may be caused by escalating doses of radiotherapy occured in 6 out of 9 cases under the age of 15 years who survived. On the basis of these results lower-doses of radiotherapy combined with systemic chemotherapy appeared to be advisable for the treatment of childhood Hodgkin's disease.

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Six patients underwent allogeneic bone marrow transplantation (BMT) for treatment of acute non-lymphocytic leukemia. Hemopoietic reconstitution after BMT was monitored by peripheral blood counts, counts of bone marrow cellularity, bone marrow pictures, and clonal assays for myeloid progenitors (CFU-GM).
Although bone marrow samples were markedly hypocellular on day 7 posttransplant, myeloid and erythroid elements were seen in 5 of 6 patients. Peripheral blood recovery of these 5 patients was achieved by third weeks posttransplant. The values of (CFU-GM) per 1×10⁵ marrow mononuclear cells reached normal values on day 7 in two patients and significantly increased by day 28 in a patient. After day 84 the values of (CFU-GM) were remained almost normal and they had no relation to the occurence of chronic graft-versus-host disease (GVHD). But in patients with chronic GVHD, marrow (CFU-GM) values were significantly increased on day 7 and day 14. These results suggest that marrow (CFU-GM) values by day 28 may predict the occurence of chronic GVHD.

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An 8 year-old girl with paroxsmal cold hemoglogunuria (PCH) is reported. She was referred to our clinic because of acute anemia, and found to have PCH after clinical and laboratory examination. Anti-P₁ antibody and Donath-Landsteiner (D-L) antibody were detected. In Coombs' test with variable incubation temperatures, positive IgG on her erythrocytes changed to negative as temperature of incubation was elevated. Also activation of complement was detected on the surface of her erythrocytes. Clinical improvement was obtained by blood transfusion, and positive Coomb's test and D-L test turned to negative.

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A 64-year-old woman with a monoclonal gammopathy was admitted to Nagoya National Hospital with the complaint of occasional hemoptysis. On examination, there was no hepatosplenomegaly or no lymphadenopathy. The hemoglobin was 10.1 g/dl; platelets 22.5×10⁴/μl; white blood cells 4.9×10³/μl, with 4% of atypical lymphocytes. Immunoglobulin analysis of the serum by immunodiffusion revealed an IgG of 1,459 mg/dl, an IgA of 219 mg/dl, and an IgM of 5,091 mg/dl. Serum viscosity was 4.9. Serum immunoelectrophoresis demonstrated atypical precipitant arcs reacting with mu and kappa antisera. Urine immunoelectrophoresis showed a positive reaction against kappa antiserum. Radiologic studies of the bones revealed generalized osteoporosis with multiple punched out lesions of the skull. Thirty percent of bone marrow nucleated cells was atypical plasma cells, the presence of which was verified by electron microscopy. Although they were positive mainly for cytoplasmic mu and kappa chains by immunoperoxydase studies, cells positive for gamma, alpha, or lamda chains were occasionally found, indicating that normal immunoglobulin synthesis was not suppressed in this case of IgM myeloma.

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A case of large granular lymphocyte (LGL) leukemia with ascites and CNS involvement was reported.
A 39-year-old Japanese female was admitted to our hospital in March, 1987 because of high fever. Her clinical and hematological features were characterized by generalized lymphadenopathy, marked hepatosplenomegaly, high serum LDH level (3,257 mU/ml), marked leukocytosis (71,000/ul) with 74% LGLs and bone marrow infiltration with 57% LGLs. Despite of chemotherapy, ascites, retroperitoneal mass and CNS involvement developed and she died of sepsis after three months. LGLs from the patient's blood, marrow and ascites, stained positively for acid phosphatase. These LGLs were E rossete+ and Fc (IgG) receptor+ and were positive for CD2, OKM1, HLA-DR and Leu 11, but were negative for CD1, CD3, CD4, CD8 and Leu 7 as well as for terminal deoxynucleotidyl transferase activity. The natural killer activity against K562 target cells was high and was significantly augmented after stimulation by recombinant human interleukin 2. These LGLs also demonstrated normal antibody-dependent cytotoxicity activity. Cytogenetic study on bone marrow cells and ascitic cells revealed clonal chromosomal abnormalities. These clinical, hematological, immunological and cytogenetic findings suggest that this patient had a neoplastic proliferation of natural killer cells.

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A case of Waldenström's macroglobulinemia (WMG) with principally pulmonary manifestation is presented.
A 47-year-old man was admitted to our hospital with complaints of shortness of breath and an increasingly enlarged right pulmonary nodule, which had first been discovered about 2 years prior to admission. The liver, spleen and lymph nodes were not enlarged. Hematological examination revealed Hb 12.8 g/dl, platelet 28.2×10⁴/μl and WBC 7,400/μl without pathological cells. A bone marrow aspirate showed no remarkable abnormalities. A quantitative measurement of serum immunoglobulin gave values for IgG of 2,264 mg/dl, IgA of 393 mg/dl and IgM of 1,332 mg/dl, and M-protein of IgM, K type was observed on serum immunoelectrophoresis. Chest X-ray film showed a 5×4 cm poorly defined mass in the right middle lobe. Histological examination of a mass obtained by an open lung biopsy revealed diffuse proliferation of lymphoplasmacytoid cells. Monoclonal IgM, K was demonstrated in the cytoplasma of these cells by the PAP method. These data established the diagnosis of pulmonary WMG. He received VEPA therapy, and pulmonary mass lesion gradually decreased and his serum IgM level had decreased to 465 mg/dl 2 months after the initiation the chemotherapy.

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A 73-year-old man was admitted into the hospital because of lumbago in October, 1986. Laboratory examination on admission showed anemia, an IgA-κ Bence Jones proteinemia. The bone marrow picture disclosed a marked involvement by the neoplastic cells, followed by leukemic conversion 2 weeks later. The leukemic cells displayed a lymphoblastoid appearance on light microscopy, but rather compatible with plasma cells on electron microscopy, showing some strands of rough endoplasmic reticulum and a prominent Golgi apparatus in the cytoplasm. The cells expressed a wide spectrum of surface markers, including those of plasma cell (PCA-1, OKT10), B cell (B1, sIg) and CALLA. Reverse hemolytic plaque assay disclosed the immunoglobulin production of monoclonal κ chain, but a heavy chain production was recognized only in a small proportion of the cells. Under the diagnosis of multiple myeloma, he was treated with vincristine, cyclophosphamide, and prednisolone. But he died of renal failure complicating hypercalcemia after only three months of the admission in accordance with previous reports that CALLA-positive myeloma was associated with poor prognosis. This case may also represent the clinical, morphological and phenotypic diversity in multiple myeloma.

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A case of primary myelofibrosis complicated with pericardial effusion and proteinuria is described.
A 66-year-old female was admitted to our hospital because of abdominal fullness and shortness of breath. On admission, hepatosplenomegaly and pericardial effusion were observed. Blood examination revealed leukoerythroblastic anemia and thrombocytosis with tear drop cells and giant platelets. Bone marrow aspiration was dry tap and its biopsy showed remarkable myelofibrosis. Urinalysis indicated severe proteinuria. Although neutrophilic alkaline phosphatase score was low, no signs of acute blastic crisis of chronic myelogenous leukemia was found. The diagnosis of an atypical type of primary myelofibrosis was obtained. Administration of MCNU was started in August 1987. Hepatosplenomegaly, pericardial effusion and proteinuria were gradually improved after the administration.
The etiology of the pericardial effusion and proteinuria were not obvious, however, these facts suggest that these abnormal findings might be related to PMF itself and MCNU was effective to PNF.

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A near-tetraploid clone was observed at the 5th relapse in a 34 year-old female with acute granulocytic leukemia. She was referred to Hiroshima University Hospital presenting with palpitation in May 1978. On admission she had a WBC count of 2,900/μl with 31.5% blasts, platelet count of 2.4×10⁴/μl and hemoglobin of 2.8 g/dl. A bone marrow aspirate showed hypercellular with 88.5% blasts. Most of them were weakly positive for peroxidase reaction. Occasional Auer rod and/or fine azurophilic granules were observed. DCMP therapy (daunorubicine, cytosine arabinoside, 6-mercaptopurine, and prednisone) was started and the first complete remission was achieved in August 1978.
Afterward, the 5th relapse occurred in August 1986 and several kinds of drugs were given without effects. She died 8 years and 9 months after the diagnosis.
Karyotype prior to treatment showed a normal diploidy without tetraploid mitoses. However, cells with near-tetraploid (mode: 91) were observed predominantly on the 5th relapse sample and almost all mitoses were occupied with near-tetraploidy at the terminal stage.
Results of serial cytogenetic and hematologic study showed a close correlation between the incidence of near-terraploid mitsses and that of very large blast cells. The significance of tetraploidy in previously reported 44 cases including our case was discussed.

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Two cases of Ph¹-negative chronic myelogenous leukemia (CML) are described, they were 66-year-old female and 73-year-old male. Both patients shared all of the following features: presence of anemia, thrombocytopenia and leukocytosis with every stage of neutrophilic differentiation, hypercellular bone marrow with hyperplasia of the degranulated neutrophilic series, diminished neutrophilic alkaline phosphatase, elevated serum lysozyme and vitamin B₁₂ level, mosaic pattern of trisomy 8 and normal karyotypes in chromosome analysis, and markedly increased number of CFU-GM. In addition, bcr rearrangement by Southern blot hybridization was not demonstrated in these patients. The diagnosis of chronic myelomonocytic leukemia was not verified, however, because of the absence of monocytosis in peripheral blood. The existence of so-called Ph¹-negative CML like these two cases as a diagnostic entity must be further studied.

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A 84-year-old man was admitted with palpitation, edema of legs and anemia during a long course of diabetes mellitus, prostatic hypertrophy and prostatic cancer. He revealed purpura on the hands and massive microhematuria.
He had received antibiotic therapy for a urinary tract infection for a period of time, but he had no history of hemorrhagic tendency or blood transfusion.
Coagulation studies showed the prolongation of whole blood clotting time and PT (prothrombin time). Activity of factor V was 14% of that of normal control plasma. The titer of factor V inhibitor was 4.9 Bethesda units/ml.
The inhibitor of the patient was supposed to belong to IgA and IgG judging from inhibitor neutralization test. PT was improved after discontinuance of administration of antibiotics and administration of azathioprine. Moreover, even after administration of prednisolone with antibiotics, PT and activity of factor V recovered to normal range.
He died from respiratory failure. Autopsy revealed double cancer of prostate and descending colon.
The appearance of factor V inhibitor was likely caused by antibiotics, double cancer, and age-related immune disorders.

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A 61-years old woman who had been healthy without history of abnormal bleeding, developed widely spreaded ecchymosis and intramusclar bleeding in March, 1987
She was hospitalized for this hemorrhagic diathesis in May, 1987 and the following laboratory data were revealed: activated partial thromboplastin time (APTT), 76.7 seconds; factor VIII procoaglant activity, 2%; factor VIII inhibitor, 27 Bethesda units/ml. The inhibitor was an immunoglobulin of IgG type. Her clinical data of the blood were normal, and tests for antibodies, such as RA test, LE test and thyroid test were negative.
Pysical examination revealed ecchymosis over her right arm and swelling and pain in the right arm.
She was first treated with a large dose of factor VIII concentrates, but the effect was insufficient. Then predonisolone was given, which resulted in decreasing of the inhibitor and improvement of the coagulation profiles.
This treatment appeared to offer effective control on severe hemorrhage in patients with factor VIII inhibitors.

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Two cases of consumption coagulopathy found in the patients having mitral stenosis with atrial thrombus were reported. In case 1, although anticoagulant (Warfarin) administration did not correct the hemostatic abnormality, combination of tranexamic acid with anticoagulant was effective.
In case 2, atrial thrombus found in the echocardiography prior to the onset of thromboembolism in the lower limbs has been disappeared after embolism. Anticoagulant was effective for the improvement of hemostatic abnormality. We considered mitral stenosis with atrial thrombus as one of causes of the consumption coagulopathy.

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Three cases of refractory anemia (RA) are presented. They developed a complete, an intestinal, and an incomplete type of Behçet's disease after 13 years, 6 months, and 4 years of illness, respectively. They showed normal or only slightly reduced neutrophil counts in spite of anemia and thrombocytopenia.
Although the precise etiology of Behçet's disease is still obscure, it is suggested that immunological reactions against Streptococcus viridans in chronic infection, and auto-oxidative damage induced by oxygen intermediates derived from stimulated neutrophils may play an important role in causing endothelial injury in the disease. Therefore, it is possible to speculate in our cases that the known susceptibility to bacterial infections in myelodysplastic syndromes, and the absence of neutropenia may have been responsible for the association of RA with Behçet's disease. It is also suggested that neutrophils are necessary for endothelial cell damage.

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Hairy cell leukemia (HCL) is characterized by slow proliferation of special mononuclear cells. Although splenectomy has been evaluated to be the most effective traditional treatment for HCL, the response of patients to splenectomy is not necessarily satisfactory. Recently, the treatment of HCL with Interferon-α has been reported to be effective, and we report a female case of HCL who showed marked improvement in her hematological findings with this therapy.

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A 55-year-old woman developed a secondary leukemia following 1-year treatment of Hodgkin's disease. She was admitted to our hospital because of the celiac lymphadenopathy. Open laparotomy was performed. Biopsy specimens of the lymphnode demonstrated Reed Sternberg cells with mature lymphocytes. She was diagnosed as having Hodgkin's disease (lymphocyte predominant type). She was treated by the combination chemotherapy consisting of mitoxantrone, cyclophosphamide, vincristine and prednisolone for Hodgkin's disease in November 1986.
Hodgkin's disease achieved complete remission and she was regularly followed. No abnormal findings were observed in the peripheral blood and bone marrow. But thrombocytopenia and the blastoid cells appered in the peripheral blood in February 1988. The bone marrow specimen was hypercellular and occupied by 90% of blastoid cells that were positive for peroxidase staining.
She was diagnosed as having AML from the bone marrow aspiration and biopsy specimens. She did not respond to several chemotherapy regimens and now she is treated by low dose Ara C.

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We reported a case of 69-year-old femal presenting with clinically typical TTP which was treated with Ticlopidine and plasma exchanges four times in total and resulted in succesful improvement of her clinical state.
The first chromosomal analysis of lymphocytes in the peripheral blood of the patient revealed abnormal patterns of 45, XO/46, XX/47, XXX, the second, 45, XO/46, XX/47, XXX/47.XX, +21. Mesurement of FITC-labelled fibrinogen antibody against the fibrinogen combined with platelet glycoprotein GP IIb/IIIa complex using flow cytometry showed an apparently increased positive rate 76.2% for the platelet of the patient, compared with that of 31.9% for the control.
From the comparative study of the platelet agglutination of the platelet rich plasma (PRP) derived from the citrated-added complete blood taken from the patient to whom Ticlopidine was given, added with adenosine-5'-diphosphate (ADP), collagen or acetyl glyceryl ether phosphoryl choline (AGEPC) as the reagents and that of normal control, it was shown that for AGEPC increased. Thus, increased reaction specific to AGEPC in addition to activated platelet was demonstrated in the present study.

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A 71-year-old female was admitted to the Fukui Red Cross Hospital because of abnormal genital bleeding in Feb., 1987. She underwent gastrectomy for early gastric cancer (IIc) 5 years earlier, mastectomy for early breast cancer (stage I) 3 years earlier and radiation therapy (⁶⁰Co 350rad×25days) and chemotherapy (5FU, 200mg/day, orally) for uterine cancer (stage IIb) 2.5 years earlier. These 3 cancers had quite different histological features one from the other.
Laboratory investigation revealed leukocytosis (216,100/μl) with 90% blasts. The bone marrow was hyperplastic with 87% blasts. Although 90% of blasts had myeloperoxidase activity, surface marker analysis of the blasts revealed T-cell (CD2, CD3) phenotypes suggesting that the disease was so-called hybrid acute leukemia. She died of intracranial hemorrhage on the 2nd hospital day. An autopsy showed generalized leukemic infiltration and residual uterine cancer without metastasis to other sites. In our country, quadruplicate malignancies including hematological malignancy have been rarely described. The possible pathogenesis of multiple cancers has been discussed.

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A 56-year-old female, who was diagnosed as CML in 1983 and had been well controled with busulfan, was admitted to our hospital because of fever and iliac bone pain. Peripheral blood showed leukocytosis (WBC 70,000/μl and bone marrow was normocellular with 53% leukemic cells, suggesting that she was in the blastic crisis.
Chromosomal analysis of bone marrow cells at that time revealed t(9;22;12) and some additional abnormalities. The number of chromosomes ranged from 44 to 131 and the mode of chromosome number was 65.
She was treated with combination regimen consisting of vincristine, 6-mercaptopurine and prednisolone and right iliac tumor was irradiated. Three months after admission, she died of DIC and pulmonary insufficiency due to leukemic infiltration.

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In June 1987, a 20-year-old man was diagnosed as T-cell acute lymphoblastic leukemia. In August, at a nadir period of the remission induction chemotherapy, he complained of high fever and dry cough. A chest roentgenogram also showed a nodular area of increased density in the left upper lobe.
Since his clinical state deteriorated progressively despite the administration of broad-spectrum antibiotics, amphotericin B was administrated intravenously (with an initial dose of 5 mg/day, increased up to 25 mg/day). Concomitant with bone marrow recovery and continued antifungal therapy, he became soon afebrile and improved over the next 2 months. The infiltrates also began to resolve.
Then he abruptly coughed up about 800 ml of blood and suffered from acute respiratry failure. Bronchial arteriographic studies demonstrated active extravasation of contrast medium in the region of the cavity. After therapeutic embolization with Gelfoam, the extravasation was no longer obesrved. Active bleeding abruptly ceased and had not recurred until the left upper lobectomy which was performed 10 days after the embolization.
This case typically demonstrates the value of bronchial arterial embolization in treating massive hemoptysis.

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Malignant lymphoma of the central nervous system in a thirteen-year-old boy with immotile cilia syndrome (ICS) is reported. He had frequent upper respiratory tract infections, chronic sinusitis and pneumonia during in childhood. Bronchiectasis was demonstrated by bronchography. The diagonosis of ICS was confirmed by the lack of dynein arms of cila in the nasal mucosa with electronmicroscopy. In 1987, he complained of headache and vomiting and a space occupied mass lesion in the left frontoparietal lobe was found by head CT scan, which was subtotally resected. Histological studies showed large cell type non-Hodgikin lymphoma of B-cell phenotype. He received radiotherapy (41Gy) to the whole brain and systemic chemotherapy consisting of adriamycin, cyclophosphamide, vincristine, prednisolone, L-asparaginase and intrathecal methotrexate, and the patient maintained complete remission for eight months. However, relapse occurred and the patient died twelve months after the initiation of treatment.

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A case of extensive bone marrow necrosis due to cancer metastasis is reported.
A 55-year-old female, who had a history of subtotal gastrectomy for signet ring cell carcinoma of the stomach 7 years ago, was admitted to our hospital with a complaint of lumbago on October 25, 1987. Red blood cell count was 92×10⁴/μl, hemoglobin 2.7 g/dl, hematocrit 8.0%, platelet 6.4×10⁴/μl, and white blood cell count 13,400/μl with leukoerythroblastosis. Bone marrow aspiration of the sternum, left iliac crest, and bilateral posterior superior iliac supine showed extensive bone marrow necrosis. Serum ALP was increased to 7410IU/l, dominated isozyme of bone type. Hemostatic findings suggested a complication of consumption coagulopathy. Skull, vertebrae, iliac and pelvic bone X-ray showed multiple osteolytic lesions, and irregular isotope uptake was recognized on the bone scintigraphy using ^99mTc. Sixth bone marrow examination at the right iliac crest revealed signet ring cell carcinoma metastasis. In spite of detailed examinations, there was no evidence of primary carcinoma, including the remnant of stomach. We speculated that the signet ring cells were originated from the respected gastric cancer. The patient has received anti-cancer chemotherapy with UFT and OK432, and is still alive 9 months after diagnosis.

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A 67-year-old female was diagnosed as having classical pernicious anemia. Labolatory data included low serum vitamin B₁₂ concentrations, abnormal deoxyuridine suppression test, methylmalonic aciduria, atrophic gastritis, positive anti-intrinsic factor antibody and Schilling test results typical of pernicious anemia.
During hospitalization it was incidentally noted that her urine was green colored. Jaffe' reaction and Obermayer reaction for indicanuria were both positive. Dark purple crystalline material was obtained by centrifugation of her urine. The crystalline substance was soluble in methanol and its absorbance curve was identical to that of authentic indoxylsulphate potassium salt. Daily output of this substance was nearly 50 times normal. There was no increase in urinary excretion of monoamino-monocarboxyl amino acides. The exact reason for her indicanuria was not clear, although abnormal bacterial growth in the intestine remained as a possibility.

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