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Biomedical subjects

Tomotaka Iguchi

Publications and source records attributed to Tomotaka Iguchi.

9 recordsLinked to original sources

[Subacute necrotizing lymphadenitis showing lymphatic blockade-mediated acute respiratory failure].

A 24-year-old woman was referred to our hospital with fever and cervical lymphadenopathy. On admission, her serum concentration of soluble IL-2 receptor had increased to 1,740 IU/ml, LDH was 2,889 IU/l, and ferritin was 2,389 ng/ml. Dyspnea became evident (PaO2 60 Torr) with a further increase of serum ferritin to 96,552 mg/ml on day 11. Chest CT findings showed the thickening of the interlobular septa, bilateral pleural effusion, and swelling of mediastinal lymph nodes, symptoms which were very similar to those associated with lymphangitis carcinomatosis. She received steroid pulse therapy (methylprednisolone, 1,000 mg/day for three days). This resulted in a rapid improvement of her dyspnea and disappearance of the lymphatic blockade-mediated pulmonary findings in two days. A cervical lymph node biopsy was performed on day 12, and revealed that she had subacute lymphadenitis (Kikuchi disease). This case suggests that acute respiratory failure should be considered in cases of Kikuchi disease when associated with a lymphatic blockade.

Acute Disease↗

Peripheral T-cell lymphoma together with myelofibrosis with elevated plasma transforming growth factor-beta1.

Myelofibrosis is usually observed in myeloproliferative disorders, such as chronic myeloid leukemia. However, there are only a few reports showing an association between T-cell lymphoma and myelofibrosis. We report a case of peripheral T-cell lymphoma, unspecified (diffuse large cell) type, involving the bone marrow that was associated with severe myelofibrosis. In the present case, the plasma concentration of transforming growth factor-beta1 (TGF-beta1) was increased to 8.95 ng/ml (normal range: 1.56-3.24 ng/ml). No lymphadenopathy or skin lesions were observed during the entire clinical course. Although the mechanism of secondary myelofibrosis is still unclear, elevated plasma TGF-beta1 might be involved in the pathogenesis of bone marrow fibrosis in the present case.

Aged↗

Combined treatment of leukemia cells with vitamin K2 and 1alpha,25-dihydroxy vitamin D3 enhances monocytic differentiation along with becoming resistant to apoptosis by induction of cytoplasmic p21CIP1.

Vitamin K2 (VK2) effectively induces apoptosis in leukemia cell lines, including HL-60 and U937. However, combined treatment of cells with VK2 plus 1alpha,25-dihydroxy vitamin D3 (VD3) resulted in suppression of VK2-inducing apoptosis and pronounced induction of monocytic differentiation as compared with that by VD3 alone. After achieving monocytic differentiation by pre-exposure to VK2 and VD3, the cells became resistant to various apoptotic stimuli including VK2- and H2O2-treatment and serum deprivation. Accumulation of cytoplasm p21CIP1 along with disappearance of nuclear p21CIP1 was detected in cells in response to 96-h treatment with VK2 plus VD3. A stable transfectant, U937-deltaNLS-p21CIP1, which lacked the nuclear localization signal of p21CIP1 and showed overexpression of cytoplasm p21CIP1 without monocytic differentiation, was resistant to apoptosis. These data suggest that a change of intracellular distribution of p21CIP1 from nucleus to cytoplasm along with differentiation appears to be anti-apoptotic. Clinical benefits of using VK2 for treatment of patients with leukemia and myelodysplastic syndrome (MDS) have been reported. Our data suggest that VK2 plus VD3 may be an effective combination for differentiation-based therapy for leukemia and also MDS whose cytopenias are mediated though apoptosis.

Apoptosis↗

[Primary diffuse large B-cell lymphoma of the esophagus].

A 64-year-old man with primary esophageal lymphoma suffered from dysphagia. An upper gastrointestinal examination revealed a partly ulcerated submucosal tumor in the upper portion of the esophagus. Histopathological and immunohistological examination of endoscopic biopsy specimens showed diffuse large B-cell lymphoma of the immunoblastic type. Improvement of the dysphagia and esophageal findings were noted after chemotherapy and radiotherapy. A review of the literature indicated that primary esophageal lymphomas account for less than 1% of all gastrointestinal lymphomas, and less than 0.1% of all malignant lymphomas. Because of the rarity of primary esophageal lymphoma, its clinical and biological characteristics are not currently well known. It is important to accumulate information on, and to further investigate patients with, primary esophageal lymphoma.

Esophageal Neoplasms↗

[Relapse of diffuse large B cell lymphoma to CD20-negative multiple cutaneous tumors immediately after anti-CD20 monoclonal antibody (rituximab) therapy].

A 60-year-old male was referred to our hospital because of cervical lymphadenopathy and a left hilar abnormal shadow seen on chest X-ray in May 1999. The pathological findings of the cervical lymph nodes revealed that the patient had a malignant lymphoma, of the diffuse large B cell type, at clinical stage IIIB. Immunohistochemistry demonstrated that the lymphoma cells were positive for CD11a, CD19, CD20, CD23, CD25, CD45, IgM, IgD and lambda, but negative for CD5. Although a complete remission was obtained after 8 courses of CHOP therapy, the patient relapsed 32 months later. Two courses of a half dose of CHASE therapy consisting of CPM, ara-C, VP-16 and dexamethasone, followed by rituximab (600 mg/week x4) resulted in a transient re-induction of complete remission. However, multiple cutaneous tumors became apparent just 10 days after the last rituximab therapy. Immunohistochemistry of the cutaneous tumors revealed infiltration of CD20-negative lymphoma cells. A series of chemotherapy including high-dose MTX was ineffective, and the patient died in August 2003. Autopsy findings revealed the systemic intra-capillary infiltration of CD20 negative-lymphoma cells into multiple organs, including the lungs, liver, and kidneys. A CD20 negative-clone selected by rituximab therapy appeared to have expanded in this case.

Antibodies, Monoclonal↗

[Deletion of 13q in aplastic anemia after treatment with anti-thymocyte globulin].

A 31-year-old woman was given a diagnosis of aplastic anemia (AA) in 2000 and was treated with anti-thymocyte globulin (ATG) (horse serum), cyclosporine and granulocyte-colony stimulating factor (G-CSF). In 2002, she came to our hospital. The laboratory data revealed severe cytopenia according to the criteria by Camitta. A cytogenetic study revealed a normal female karyotype. We demonstrated CD55-negative and CD59-negative clones in her erythrocytes and granulocytes. HLA-DR 1501 was negative. After corticosteroid pulse therapy, the del(13q) (7/21 cells) was noted in her marrow cells. She was re-treated with ATG (rabbit serum), cyclosporine and G-CSF without particular cytogenetic changes after the therapy. Deletion of the 13q anomaly is rarely detected in patients with AA and its clinical significance in this disease is not well known. In the literature, AA patients with the del(13q) responded well to immunosuppressive therapy, irrespective of the timing of the appearance of the del(13q) anomaly. Further investigation will be needed to clarify the significance of del(13q) in AA.

Adult↗

[Autoimmune phenomena during interferon-alpha therapy for hematopoietic disorders].

The development of various kinds of autoimmune disease as a result of interferon-alpha (IFN-alpha) therapy has been reported among chronic myeloproliferative disorders(CMPD) including chronic myeloid leukemia(CML). Therefore, we investigated the frequency of autoimmune disorders in 33 patients with hematopoietic diseases treated with IFN-alpha in our department. Thirty-three patients (12 females, 21 males) included cases of CML (n = 23), essential thrombocythemia (ET) (n = 1), multiple myeloma (n = 8), and hypereosinophilic syndrome (HES) (n = 1). Autoantibodies (ANA, dsDNA, and RAPA), thyroid grand functions, and coagulant functions were examined. Twenty-five out of 33 patients were treated with natural IFN-alpha, and 8 patients were treated with recombinant IFN-alpha 2b (rIFN alpha-2b). Three patients were treated with IFN and anticancer agents. Antinuclear antibodies were detected in 2 of 33 patients. RAPA and anti-thyroglobulin antibody became positive in 3 and 4 patients, respectively. Ten patients showed low serum levels of either free T3 and/or free T4. However, none of them showed any clinical symptoms for developing autoimmune diseases. In addition, circulating anticoagulant antibodies were detected in 3 of 23 patients with CML treated with rIFN alpha-2b, but in no cases treated with natural IFN-alpha. Although none of the patients developed autoimmune diseases, we concluded that patients receiving IFN therapy should be carefully monitored for clinical signs and symptoms of autoimmune disorders.

Adult↗

De novo appearance of t(7;13)(q10;q33) in the leukemic phase of myelodysplastic syndrome: a case report.

Clonal cytogenetic abnormalities are found in about 50% of all patients with myelodysplastic syndrome (MDS) and the clinical implication of these abnormalities is now well documented. However, the de novo appearance of balanced translocations in MDS patients during the progression of the disease is rarely reported and the significance of the balanced translocation remain to be elucidated. We report here the first case of refractory anemia with excess blasts in transformation (RAEBt), in which a new chromosomal translocation, t(7;13)(q10;q33) appeared de novo in the AML phase. It has been revealed that rearrangements and deletions of chromosome 7, i.e. der(1;7)(q10;p10), are very complex and that multiple regions may contribute to the disease phenotype and progression. Our case suggests that the chromosomal region at 7q10, rather than 1p10, might be one of the hot spots for myeloid proliferative disorders, including MDS.

Acute Disease↗