Biomedical subjects

S Shimodaira

Publications and source records attributed to S Shimodaira.

23 records · Page 2Linked to original sources

PubMed1996

Regulation of serum thrombopoietin levels by platelets and megakaryocytes in patients with aplastic anaemia and idiopathic thrombocytopenic purpura.

To clarify the regulatory mechanism of thrombopoietin (TPO, c-Mpl ligand) in chronic thrombocytopenic conditions, we determined TPO levels in the sera of patients with aplastic anaemia (AA; n = 26) and idiopathic thrombocytopenic purpura (ITP; n = 32) by an enzyme-linked immunosorbent assay. Despite a similarity in platelet counts, serum TPO levels in the AA group were markedly higher than those in the ITP group: 20.41 +/- 9.71 f mol/ml (mean +/- SD) and 1.66 +/- 0.55 f mol/ml, respectively, both of which were significantly elevated compared to normal subjects (n = 41; 1.22 +/- 0.37). In both groups, serum TPO level showed an inverse correlation with the platelet count. We determined the megakaryocyte volume using bone marrow clot section and found that it was markedly small in the AA group; while in the ITP group it was augmented with a correlation to serum TPO level. Our findings suggest that TPO levels may be regulated not only by platelets but also megakaryocytes in AA and ITP.

Adolescent↗

PubMed1996

Serum thrombopoietin (c-Mpl ligand) levels in patients with liver cirrhosis.

To clarify the role of c-Mpl ligand (thrombopoietin: TPO) in liver cirrhosis (LC), we examined serum TPO levels (sTPO) in patients with LC (N = 44), chronic hepatitis (CH; N = 13) and healthy controls (N = 41) by an enzyme-linked immunosorbent assay. Although platelet counts of all LC patients (89 +/- 59 x 10(9)/l; mean +/- SD) were lower than those of controls and CH patients, sTPO levels in LC patients (1.23 +/- 0.51 fmol/ml) were the same as those in controls (1.22 +/- 0.37) and CH patients (1.18 +/- 0.36). Platelet counts were significantly higher in splenectomized patients than in unsplenectomized patients, but the sTPO level did not differ between these two groups. In LC patients, the sTPO level was not correlated with the platelet count, but was correlated with prothrombin time, activated partial thromboplastin time, and total bilirubin, indicating that production of TPO in the liver decreases slightly with the development of liver dysfunction. Our findings suggest that production of TPO is maintained in LC patients and their thrombocytopenia is not due to a defect in platelet production.

Case-Control Studies↗

PubMed1995

The detection of clonal proliferation in granular lymphocyte-proliferative disorders of natural killer cell lineage.

The clonal proliferation of large granular lymphocytes can be detected in patients with T-cell-lineage granular lymphocyte-proliferative disorders (T-GLPD) by Southern blotting T-cell receptor genes. However, this cannot be applied to patients with natural killer-cell-lineage GLPD (NK-GLPD) as it lacks a clonal marker. We therefore investigated the use of two other diagnostic techniques in evaluating clonal proliferation in Japanese patients with NK-GLPD (n = 4) and T-GLPD (n = 3) by chromosomal analysis of peripheral blood mononuclear cells (PBMC) stimulated with either interleukin-2 or phytohaemagglutinin, and Epstein-Barr viral (EBV) genomic DNA analysis. Chromosomal analysis revealed abnormal karyotypes in the PBMC of three of four patients with NK-GLPD, whereas EBV analysis showed a monoclonal terminal configuration in the PBMC in the fourth patient. Southern blots revealed rearrangements of the TCR genes in all three patients with T-GLPD but in none of those with NK-GLPD. It is suggested that these methods may be useful in detecting the abnormal proliferation of large granular lymphocytes in NK-GLPD.

Adult↗

PubMed1993

Eosinophilia in myelodysplastic syndrome with a (12;21)(q23;q22) translocation.

Cytogenetic analysis of bone marrow (BM) cells from a patient with myelodysplastic syndrome (MDS) associated with eosinophilia showed a 45,XY,t(12;21)(q23;q22), -17 karyotype. We performed clonal and suspension cultures using the patient's BM mononuclear cells to clarify the mechanism of eosinophilia. Eosinophil colonies formed in the presence of interleukin-5 (IL-5) and granulocyte-macrophage colony-stimulating factor (GM-CSF), but not in the presence of IL-3. When BM cells were cultured in suspension in the presence of IL-5, they differentiated to mature eosinophils, and chromosome analysis identified the 45,XY,t(12;21)(q23;q22), -17 karyotype in all metaphases. The patient's serum did not stimulate eosinophil proliferation or differentiation in comparison with normal serum, however, these data suggest that the abnormal clone with 45,XY,t(12;21)(q23;q22), -17 karyotype may have an increased responsiveness to IL-5 and GM-CSF, resulting in eosinophilia.

Aged↗

PubMed1993

Aggressive granular lymphocyte leukemia of natural killer cell type in an elderly patient.

A 75-year-old man was admitted to our hospital because of intermittent fever. His peripheral blood picture showed granular lymphocyte (GL) proliferation. The GLs were immunologically and functionally phenotyped as natural killer cells. Chromosomal analysis of peripheral lymphocytes with interleukin-2 stimulation revealed an inversion of chromosome 9 with an unusual breakpoint, showing abnormal monoclonal proliferation of the GLs. Progressive increase of GL count and hepatosplenomegaly necessitated the start of combined chemotherapy. His condition was complicated by icterus and renal failure, and he died finally of respiratory failure. Autopsy revealed disseminated intravascular coagulation and infiltration of GLs in the bone marrow, spleen, and liver.

Aged↗