Biomedical subjects

M Ichimaru

Publications and source records attributed to M Ichimaru.

At least 55 records · Page 3Linked to original sources

PubMed1990

[Serum deoxythymidine kinase in adult T-cell leukemia and its related disorders].

Using Prolifigen TK kit "Daiichi", the serum TK level were determined in patients with adult T-cell leukemia (ATL) and its related disorders. The mean level of serum TK at diagnosis was 279.9 U/l in acute type ATL, 27.8 U/l in chronic type ATL, 59.0 U/l in lymphoma type ATL, 3.1 U/l in pre-ATL and 2.4 U/l in HTLV-I carriers. In these patients, six other kinds of tumor markers such as lactic dehydrogenase, beta 2-microglobulin, immunosuppressive acidic protein, ferritin, tissue polypeptide antigen and carcinoembryonic antigen were also examined. Among the seven tumor markers, TK level showed the most significant difference among clinical subtypes of ATL. This indicates that the TK level is one of the promising parameters indicative of aggressiveness of ATL cells.

Adult↗

PubMed1990

[A Japanese family with hereditary HbH disease--a case report and its gene analysis].

Hereditary HbH disease was found in a Japanese family. The propositus showed hypochromic microcytic anemia and chronic hemolysis. HbH inclusion bodies were detected in red cells, and an abnormal band corresponding HbH was found in an isoelectric focusing of the hemolysate. Gene analysis of the propositus revealed double heterozygosity for alpha + and alpha zero thalassemias. Four of six his siblings shared the alpha zero thalassemia and one the alpha + thalassemia. Another one was normal. The alpha + thalassemia was of 3.7 kb-deletion type and alpha zero was close to Southeast Asian type. This is the fourth Japanese family with hereditary HbH disease.

Adult↗

PubMed1989

Changes in T wave morphology during hypercalcemia and its relation to the severity of hypercalcemia.

The effect of hypercalcemia on T wave morphology, polarity, and amplitude was studied in 14 patients with a primary diagnosis of malignant lymphoma (8 patients), adult T-cell leukemia (5 patients), and Hodgkin's disease (1 patient). Hypercalcemia was severe to extreme in 11 (14.9-22.8 mg/dl), moderate in 1 (13.4 mg/dl), and mild in 2 (11.8 and 12.2 mg/dl) patients. Ten of the 11 patients (91%) with severe hypercalcemia showed inverted, biphasic, and notched T waves, mainly in the chest leads. Notched T waves were observed in all 10 of these patients in anterior to lateral, mid to lateral, or lateral chest leads. Biphasic and/or inverted T waves in anterior or anterior to midchest leads were present in 4 of these 10 patients who had extreme hypercalcemia (greater than 16 mg/dl). Changes in T wave morphology were not observed in moderate or mild hypercalcemia. T wave amplitude showed significant inverse correlation with serum calcium (T mV vs Ca, r = -0.60, p less than 0.001; T/R ratio vs Ca, r = -0.68, p less than 0.001; n = 35). Decrease in T wave amplitude was marked in severe hypercalcemia (p less than 0.0001) and moderate hypercalcemia, but there was no change in mild hypercalcemia. Changes in T wave morphology, polarity, and amplitude either appeared with development of hypercalcemia or disappeared with normalization of serum calcium level. It was concluded that in addition to shortening the QT interval, severe to extreme hypercalcemia can cause development of inverted, biphasic, or notched T wave with a marked decrease in amplitude of T waves.

Adult↗

PubMed1989

High risk of mother-to-child transmission of HTLV-I in p40tax antibody-positive mothers.

A new enzyme-linked immunosorbent assay (ELISA) for detecting the antibody to a human T-lymphotropic virus type I (HTLV-I) tax gene product, p40tax, has been developed. By this ELISA method, we have investigated the relationship between the presence of p40tax antibody in HTLV-I-infected mothers and the virus transmission rate from mothers to their children. The rate of mother-to-child transmission of HTLV-I was higher in p40tax antibody-positive mothers than in antibody-negative ones. Thus, the presence of p40tax antibody may indicate an increased risk of vertical transmission of HTLV-I.

Adolescent↗

PubMed1989

Antibodies against p40tax gene product of human T-lymphotropic virus type-I (HTLV-I) under various conditions of HTLV-I infection.

We investigated antibodies against pX gene product, p40tax, by ELISA using recombinant p40tax protein in HTLV-I seropositive carriers as well as patients with adult T cell leukemia (ATL) and HTLV-I-associated myelopathy (HAM). Seventy (49.0%) out of 143 HTLV-I healthy carriers were found to be positive for antibody against p40tax antigen and the follow-up samples at two-year intervals revealed constant reactivity by ELISA in each carrier. The onset of antibody production was delayed 4 to 12 weeks as compared with anti-HTLV-I in primary infection cases. The anti-p40tax-positive rate (90%) in HAM patients was significantly higher than that of healthy carriers, acute and chronic ATL patients and their family members. Furthermore, HAM patients and a few healthy carriers showed high reactivities by ELISA. Children from mothers with anti-p40tax showed a higher anti-HTLV-I-positive rate than that of children from mothers without anti-p40tax (54.5% versus 12.5%). Two men without anti-p40tax and one female with low anti-p40tax developed ATL during follow-up studies. These results suggest that HTLV-I carriers could be divided into 2 or 3 sub-populations according to antibody response to p40tax. A smaller population with anti-p40tax, especially a high antibody reactivity, could have a high risk of developing HAM and of transmission from mother to child. In addition, ATL may occur in a population with low or absent anti-p40tax.

Carrier State↗

PubMed1989

Adult T cell leukaemia cells are of CD4+ CDw29+ T cell origin and secrete a B cell differentiation factor.

Cells from six cases of adult T cell leukaemia were studied with respect to phenotypical and functional features. All cells were reactive with anti-CD4 and anti-CDw29 monoclonal antibodies (antibody against helper inducer T cells) but were unreactive with anti-CD45R monoclonal antibody (antibody against suppressor inducer T cells). Functionally, these cells secreted a B cell differentiation factor detected by SKW6-CL4 cell differentiation to IgM-producing cells, this secretion being enhanced by culture with recombinant IL-2. Though these results indicate that adult T cell leukaemia cells are of mature helper inducer T cell origin, these cells strongly suppressed PWM-induced B cell differentiation in the absence of CD8+ suppressor effector T cells.

Aged↗

PubMed1989

Immunoglobulin classes of antibody for human T-lymphotropic virus type-I (HTLV-I) in healthy donors and HTLV-I-associated disorders.

Healthy blood donors, patients with adult T-cell leukemia (ATL) and HTLV-I-associated myelopathy (HAM) and recipients of unscreened blood (SR) who had seroconverted and were followed-up for more than 2 years were examined for HTLV-I antibodies of immunoglobulin G (IgG) and M(IgM) classes. The overall infection rate in donors was 4.9%, as determined by screening with a particle agglutination method (PA). The rate increased with increasing age. Positive sera with a low titer in the PA test (1/16, 1/32 and 1/64) contained IgM antibodies in 32.5% (titer 1/16) to 36.1% (titer 1/64) of the cases, but IgG antibodies were detected in only 5.6% of the sera with a titer of 1/16 and in 36.1% of the sera with a titer of 1/64. Conversely, in high titer sera (1/128 or higher) IgG antibodies were almost always detectable (99.0%) and IgM antibodies less frequently (25.5%). Sera from acute, chronic and pre-ATL, HAM and SR patients contained IgG antibodies in high titer in all cases. The incidence of IgM antibodies was 7.7, 30.0, 53.3, 72.3, and 77.8%, respectively. IgM antibodies were demonstrated repeatedly in some cases who were followed up for a year. Only IgM antibodies from HAM patients occurred in high titers and had strong reactivity to the p24 antigens of HTLV-I in Western blot testing. It is concluded that it is important to detect IgM antibodies not only in primary infections but also in persistent infections of HTLV-I.

Adolescent↗

PubMed1989

[Empiric therapy with aztreonam for febrile neutropenic patients with hematological malignancies].

Combination of aztreonam/amikacin/ticarcillin (AAT) and latamoxef/amikacin/ticarcillin (LAT) were compared in a prospective randomized trial of empiric therapy for febrile neutropenic patients with hematological malignancies. Low dose amphotericin B was also added to each regimen from the beginning. Of 45 evaluable episodes, 23 were treated with AAT and 22 with LAT. The response rates were 61 percent for AAT and 50 percent for LAT, statistically not significant. There was one infection-related death among patients assigned to AAT therapy and also one among those assigned to LAT therapy. Dose escalation of amphotericin B seemed to be effective for those patients who did not improve with initial therapy.

Aztreonam↗

PubMed1989

[Trisomy of chromosome 11 in a case of common ALL antigen-positive acute myeloblastic leukemia (FAB-M1)].

In February 1986, a 68-year-old woman was diagnosed as having acute myeloblastic leukemia (FAB-M1). At the time of diagnosis, 86.0% of the bone marrow cells were myeloblastoid, and 15% of these myeloblastoid cells were positive to myeloperoxidase. Surface marker analysis by flow cytometry disclosed granulocyte-associated antigen (MY7) and also lymphocyte-associated antigen (CALLA) on the leukemic cells. Chromosomal banding studies of bone marrow cells revealed trisomy 11 in 6 of 19 metaphases examined and normal karyotype in the others. Complete remission was attained after intensive combination chemotherapy, and has remained for 38 months. Only 19 patients with trisomy 11-associated acute nonlymphocytic leukemia (ANLL) including the present case have been reported. Morphologic analyses have revealed that the frequency of FAB-M1 is high. However, except for the present case, surface marker findings were apparent in only one M5a patient, in whom monocyte-macrophage-associated antigen was detected. Accordingly, careful surface marker studies will be needed to clarify the frequency of acute mixed lineage leukemia in such patients.

Aged↗

PubMed1989

[Translocation (8; 22) (q24; q11) and Epstein-Barr viral genome in a case of Burkitt's type of acute lymphoblastic leukemia (L3)].

A case of Burkitt's type of acute lymphoblastic leukemia (FAB L3) in an 80-year-old male patient is reported. At the time of diagnosis, 74% of the bone marrow cells were lymphoblastoid cells, which were large and homogeneous in size, and whose cytoplasm was abundant and intensely basophilic containing many vacuoles. Lambda-light chains were detected as surface immunoglobulin (Ig), but not heavy chains or kappa-light chains. Epstein-Barr (EB) viral genome was detected in the cultured bone marrow cells by spot hybridization method. Chromosomal banding studies of bone marrow cells revealed t(8; 22) (q24; q11) in all the 18 metaphases examined. This translocation brings the Ig lambda-light chain gene on chromosome 22q11 to chromosome 8q24 where the c-myc proto-oncogene is localized, which is thought to be closely associated with the leukemogenesis of this disorder, whereas EB viral genome is observed in African Burkitt's lymphoma. To our best knowledge, however, there have been no reported Japanese patients with L3 ALL in whom t(8; 22) or EB viral genome was observed.

Aged↗

PubMed1989

[Cytogenetic studies of healthy HTLV-I carriers (Report 1): Cytogenetic studies of an ATL family].

The chromosome 14q11 anomaly has been reported to be specific to adult T-cell leukemia (ATL) and this anomaly has also been confirmed in preleukemic state of ATL (pre-ATL) patients though the frequency is low. In an attempt to clarify if the same chromosome aberrations could be found also at the stage of HTLV-I carrier and if there is any cytogenetic difference from non-HTLV-I carriers, a cytogenetic study of lymphocytes stimulated with phytohemagglutinin in three HTLV-I healthy carriers and three non-HTLV-I carriers in an ATL family was performed. The results were as follows. 1. In three HTLV-I carriers, 7 of 311 cells examined (2.3%) showed chromosome aberrations, and 4 cells (1.3%) had 14q11 anomaly. 2. In three non-HTLV-I carriers, 4 of 260 cells examined (1.5%) showed chromosome aberrations, whereas no cells had 14q11 anomaly. These findings suggest that 14q11 anomaly is already present at the stage of HTLV-I carrier and seems to be an important cytogenetic clue to the pathogenesis of ATL.

Adult↗

PubMed1989

[Study on pathophysiology of the myelodysplastic syndromes (MDS)--pattern of dysmegakaryopoiesis related to leukemic transformation].

A series of 116 patients with MDS consisted of 74 cases of RA, 10 cases of RARS, 14 cases of RAEB, 9 cases of RAEB-T and 9 cases of CMML, were studied on the quantity and morphological abnormalities of megakaryocytes in relation to over all survival and leukemic change. The amount of megakaryocytes was graded into four groups; marked hypoplasia (O), moderate hypoplasia (L), normoplasia (N) and hyperplasia (H), RA cases showed heterogeneous pattern; containing 14 cases (18.9%) of group (O), 18 cases (24.3%) of group (L), 31 cases (41.9%) of group (N) and 11 cases (14.9%) of group (H). RARS, RAEB, RAEB-T and CMML cases were classified into group (N) or group (H). The heterogeneous pattern of RA did not relate to leukemic change, but over all survival tended to be shorter in group (N) cases. A significant number of young female cases of RA were involved in group (O). Morphological abnormalities of MDS megakaryocytes were classified into five types; I, mononuclear micromegakaryocytes, II, binuclear micromegakaryocytes, III, mononuclear small megakaryocytes, IV, multiseparated-nuclear megakaryocytes and V, megakaryocytes with bizzare nuclei. RAEB and RAEB-T cases uniformly showed marked dysmegakaryopoiesis ranging from type I to V. whereas RA, RARS and CMML cases showed mild dysmegakaryopoiesis. Only five cases (6.4%) of RA cases had type I micromegakaryocytes. Eight RA cases with type I on diagnosis or obtaining it during the clinical course tended to develop acute myeloid leukemia (5 cases) or to transform to RAEB sooner or later. In two cases of RAEB in which hematological improvement was obtained with low dose cytosine arabinoside regimen, disappearance of type I micromegakaryocytes was noted. A female case with 5q-anomaly surviving more than 10 years showed marked megakaryocyte hyperplasia and almost exclusively type III and IV megakaryocytes. These findings indicated that pattern of dysmegakaryopoiesis, especially appearance of type I, was closely related to leukemic change in MDS. Thus quantitative and qualitative evaluations of MDS megakaryocytopoiesis seemed important to understand the further heterogeneity of pathophysiology in MDS subtypes.

Aged↗

PubMed1989

[ATL (adult T-cell leukemia/lymphoma)].

128 cases of ATL (adult T-cell leukemia/lymphoma) were divided into 3 subgroups, 70 cases of acute type, 19 cases of chronic type and 39 cases of lymphoma type, and their prognosis were evaluated. Median survival time from the onset of acute type using Kaplan-Meier method was 8 months, that of lymphoma type was 14 months and that of chronic type was 50 months. Median survival time from the start of treatment of acute type was 5 months, that of lymphoma type was 11 months and that of chronic type was 22 months. Relatively short median survival time of chronic type may be due to they had some duration with observation only at first. No significant elongation of survival time could be obtained when acute type was divided into 2 stages, before and after 1982. Twelve patients with non-Hodgkins' lymphoma unresponsive to the first line combination chemotherapy were treated with combination therapy with cis-dichlorodiammineplatinum (CDDP). Ten patients were evaluable for response (4 cases of CR, 6 cases of PR). To stop the HTLV-1 carrier mothers milk for giving their children seems to be effective method to decrease the occurrence of ATL in future.

Adult↗

PubMed1989

[Analysis of EEG, respiration, and ECG by 24-hour polygraphic study in a case of aortitis syndrome associated with epilepsy].

The relationships between electroencephalographic changes and cardio-respiratory responses were analysed by using 24 hour ambulatory simultaneous monitoring of EEG, respiration, ECG in a patient with aortitis syndrome. Circadian changes of "absence" attacks, effects of anti-convulsive drugs on epileptic attacks, and respiratory arrest and abnormalities of the cardiorespiratory integration were clarified.

Adult↗

PubMed1989

[Chromosome 21 rearrangement in a case of therapy-related myelodysplastic syndrome in multiple myeloma].

A case of therapy-related myelodysplastic syndromes (t-MDS) in 66-year-old male patient is reported. The patient was diagnosed as having multiple myeloma in July 1983. Cyclophosphamide was given since September 1984, and melphalan was added since June 1986. Radiation therapy was not performed. Mild, slowly aggravating pancytopenia developed in July 1987. By December 1987, the hemoglobin level dropped to 6.0 g/dl, leukocytes to 2,800/microliters, and platelets to 15,000/microliters. At that time, 27% of the bone marrow cells were blasts and 23.3% monocytoid cells. Based on these findings, a diagnosis of t-MDS was made. He was managed by supportive care only, but the monocytoid cells increased rapidly in number and he died of pulmonary bleeding in March 1988. Chromosomal banding studies of the bone marrow cells revealed dir ins [inv (17) (p13q21); 21] (q21; p13q22) in all the 11 metaphases examined, but chromosomes No. 5 and 7 were normal. However, Keldsen et al reported that chromosome 21q rearrangements were nonrandomly associated with t-MDS and t-acute nonlymphocytic leukemia.

Aged↗

PubMed1989

[Marked dysmyelopoiesis after induction chemotherapy in a case of acute myelomonocytic leukemia (M 4) with t(6; 11)].

A case of AML (M 4) with t(6; 11) showed recovery to myelodysplastic syndrome (MDS)-like bone marrow after one course of DCMP regimen. Dysplastic changes of three cell-lineages were observed and micromegakaryocytes were markedly increased in number. Recovering hematopoiesis was incomplete. During MDS-like phase, t(6; 11) disappeared, reverting to normal karyotypes. Low dose ara-C regimen did not show any effect. AML soon relapsed with reappearance of t(6; 11). MDS-like abnormal hematopoiesis has recently been reported to occur after remission induction therapy or at the time of relapse. G-6PD isozyme study revealed in a remission case of AML that hematopoiesis still consisted of abnormal clone in spite of karyotypic normalization. The abnormal hematopoiesis observed in our case can be referred to such a clonal disorder predominating after disappearance of blastic component of AML. It seems important to reveal what proportion of de novo AMLs shows such an abnormal hematopoiesis and to establish suitable therapeutic approach.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed1989

CML-T1: a cell line derived from T-lymphocyte acute phase of chronic myelogenous leukemia.

Most data suggest that malignant transformation in chronic myelogenous leukemia (CML) occurs in hematopoietic stem cell that is the progenitor of myelopoiesis and of B but not T lymphopoiesis. We established a T-lymphoid cell line (CML-T1) from a person with Ph-chromosome-negative CML in acute phase. Evidence of its T-lymphocyte origin includes the pattern cytochemical reactivity, reactivity with anti-T-cell monoclonal antibodies (MoAbs), and rearrangement of the beta-T-cell receptor (TCRB) gene. CML-T1 cells have features of type IV thymocytes. Cytogenetic analyses indicate a 47,XX, del(11), t(6;7)(q23;q24), +mar karyotype. CML-T1 cells exhibit molecular changes typical of CML, including translocation of the ABL protooncogene from chromosome 9 to 22, rearrangement of the BCR gene, and transcription of a chimeric BCR-ABL messenger RNA (mRNA). The ABL insertion on chromosome 22 appears interstitial, similar to other cases of Ph-chromosome-negative CML. These data clearly indicate that T cells can be involved in acute-phase CML. CML-T1 should be useful in studying this process as well as that underlying Ph-chromosome-negative CML.

Adult↗

PubMed1989

[Effects of low dose Ara-C regimen in acute leukemias and RAEB].

Recent increase of leukemia among elderly patients prompted us to investigate the types of leukemia which can be induced into remission by low-dose Ara-C (LDAC) regimen. LDAC regimen was performed in 30 cases with overt acute leukemia (A), hypoplastic leukemia (B), and RAEB (C); Group A consists of M1 (1 case), M2 (4 cases), M3 (1 case), M4 (4 cases), M6 (1 case), and ALL (2 cases), Group B AML (8 cases), ALL (2 cases), and null (1 case), Group C RAEB (2 cases), and RAEB-T (4 cases). Complete remission (CR) rate was 23% (3/13) in group A, 64% (7/11) in group B, 0% (0/6) in group C. Partial remission rate was 33% (2/6) in group C. In group A, patients with M2 were induced into CR. In group B, both AML and ALL were induced into CR. Hypocellular marrow indicating low leukemic burden related to good sensitivity to Ara-C. Duration of CR was rather short; mean duration being 5.3 months. In group C, 2 PR cases of RAEB showed partial hematological recovery. LDAC regimen is effective especially for most of hypoplastic leukemia and some of M2. Side effects were tolerable, but all CR cases passed through bone marrow hypoplasia and needed supportive cares.

Acute Disease↗