We measured myeloperoxidase (MPO), thiobarbituric acid reactive material (TBARM), and Type IV collagen 7S domain (7S collagen) in the plasma of 21 patients with acute lung injury (ALI). Sixteen healthy subjects served as a control group. There was no significant difference in MPO between the control and ALI groups. The TBARM and 7S collagen concentrations in ALI (TBARM; 3.05±0.65 nMol/ml, 7S collagen 9.06±5.96 ng/ml: Mean±SD) were significantly higher than those in the control group (2.54±0.33 and 3.43±1.05, p<0.05). TBARM and 7S collagen levels of deceased ALI patients were higher than those of surviving ALI patients (p<0.05). There were significant correlations between the plasma levels of these two parameters and the lung injury scores. Our findings suggest that plasma TBARM and 7S collagen are useful markers for the assessment of the severity of ARDS.
(Internal Medicine 33: 257-262, 1994)

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To investigate the pathological mechanisms of polymyositis, we performed immunohistochemical analyses with biopsied muscles. Comparative studies using specimens obtained from the same patient enabled us to analyze the pathological alterations at different sequential clinical phases without taking into account each immunogenetic difference. Expression of MHC (major histocompatibility complex) antigens, especially ectopic MHC-class-II antigens, in muscle fibers and infiltrating T-cells were shown to increase concomitantly with the clinically observed exacerbation. Moreover, other observations seem to support the possibilities that 1) administration of steroids lowers the number of invading CDS-positive cells, 2) induction of MHC-class-I antigens in muscle fibers precedes the inflammatory cell infiltration and that 3) remaining MHC-class-I antigens in muscle fibers may explain the recurrence of myositis often observed in the follow up period.
(Internal Medicine 33: 263-270, 1994)

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In 93 patients with inoperable non-small cell lung carcinoma who underwent chemotherapy including cisplatin, the prognostic value of 9 factors were determined using Cox's proportional hazard model. Univariate analysis revealed that patients with a performance status of grade 2 (p<0.01) or 3 (p<0.05), those with stage IV disease (p<0.05), those with a serum neuron specific enolase (NSE) level >7.0 ng/ml (p<0.001), and those with a low serum albumin level (p<0.05) had a significantly worse prognosis. Multivariate analysis showed that a performance status of 2 or 3 and a high NSE serum level were associated with a significantly worse prognosis. More attention should be paid to the serum NSE level in patients with non-small cell lung carcinoma, because it not only reflects the tumor volume, but is also a prognostic factor which is dependent on individual tumor characteristics.
(Internal Medicine 33: 271-276, 1994)

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Immunostaining of biopsied skeletal muscle of 4 Duchenne (DMD), 12 Becker muscular dystrophy (BMD) and 3 DMD carriers' was performed using monoclonal antibodies against dystrophin and utrophin. In DMD, dystrophin-negative staining was observed except for revertant fibers which showed different stain patterns for each antibody. In 7 BMDs, there was faint/patchy stain in cases of deletion between exons 45-52, while in one case there was deletion between exons 12-17 and no stain was noted relevant to the deletion site. Moreover, in 2 cases of undetectable deletion, antibodies which recognize a terminal portion of the C-terminal domain revealed the absent stain. In DMD, the utrophin-positive fibers corresponded to dystrophin-negative fibers. In BMD, this relationship did not necessarily occur in each fiber. In DMD carriers, a cluster of dystrophin-negative fibers which was positive for utrophin were prominent. In dystrophinopathy, the immunostaining of dystrophin and utrophin is useful, in combination with dystrophin gene analysis to make a definite diagnosis.
(Internal Medicine 33: 277-283, 1994)

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In our institute, one hundred sixty-four balloon dilatations of stenotic lesions in vascular access have been performed since November 1991. All of these procedures were done with high-pressure balloon catheters. In addition to seventy-four cases treated with only percutaneous transluminal angioplasty, there were thirty-four cases which were treated by thrombectomy and/or surgical revision with subsequent intraoperative balloon angioplasty. These angioplastic procedures were initially successful in 142 (87%) of 164 stenoses. The patency rate after 3 months was 68%; after 6 months, 42%; and after 1 year, 25%. There were no serious adverse reactions in our series. This procedure can be safely done with minimal traumatization and, although long-term patency rates are low, repeated dilatations can be performed with ease, when restenosis occurs, to keep a fistula functioning for a long time in appropriate patients.
(Internal Medicine 33: 284-287, 1994)

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Effects of leukemic cells (LC) on bone marrow stromal cells and myeloid progenitor cells (CFU-C) were studied in vitro, using LC lines with different lineage characteristics. LC and/or LC-conditioned medium (LC-CM) inhibited the growth of a stromal cell line, KM-101, and adherent cells of a long-term bone marrow culture (LTBMC) established from normal bone marrow. The inhibition was more prominent when LC were cocultured directly with KM-101 cells than when LC were cultured separate from the KM-101 cell layer via membrane nitration, or when LC-CM was added to KM-101 cells or LTBMC. LC-CM also exerted an inhibitory effect on the ability of LTBMC adherent cells to bind CFU-C. Furthermore, LC-CM inhibited the growth and survival of early and late CFU-C, but not the growth of LC. All these inhibitory effects were seen irrespective of the lineage characteristics of LC, but not seen with CM prepared from normal bone marrow immature granulocytes or peripheral blood lymphocytes. Neither tumor necrosis factor-α nor interferon-α was detected in these LC-CM. These findings suggest that LC suppress normal hematopoiesis through the release of undefined substance(s) inhibiting the growth and/or survival of stromal cells and hemopoietic progenitor cells as well as the function of stromal cells.
(Internal Medicine 33: 288-295, 1994)

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A 38-year-old female had felt exertional dyspnea for six months. Physical examination and laboratory data, including angiotensin-converting enzyme, failed to diagnose sarcoidosis. Her chest X-ray showed cardiomegaly but no hilar lymph node enlargement. Holter ECG showed nonsustained and sustained ventricular tachycardias, monomorphic or polymorphic tachycardia. Echocardiography and contrast left ventriculography showed left ventricular dilatation and generalized hypo- and akinesis. Endomyocardial biopsy revealed myocardial sarcoidosis. Administration of corticosteroids, metoprolol of 20 mg/day and cibenzoline of 300 mg/day was markedly effective for the treatment of ventricular tachycardia. This patient is alive for one year after treatment and the combination therapy seems to contribute to good prognosis.
(Internal Medicine 33: 296-299, 1994)

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Autoimmune hemolytic anemia is an autoimmune diseases which is reported to be caused by interferon treatment. A 33-year-old male with chronic hepatitis C developed Coombs-negative hemolytic anemia, probably due to administration of interferon-α2b. This is, to our knowledge, the first report of chronic hepatitis C complicated by Coombs-negative hemolytic anemia during interferon treatment.
(Internal Medicine 33: 300-302, 1994)

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We report a case of severe and fatal aplastic anemia during an episode of infectious mononucleosis caused by Epstein-Barr (EB) virus infection. The 13-year-old female patient had shown normal hematological findings and had previously undergone repeated chemotherapy and autologous bone marrow transplantation for refractory non-Hodgkin malignant lymphoma (NHL). She was probably in an immuno-suppressed condition prior to this episode of infection. The possible causal relationship of the EB virus infection in the pathogenesis of aplastic anemia was documented by the clinical course, demonstration of EB virus genome in the bone marrow cells, and an elevated plasma interferon (IFN)-γlevel.
(Internal Medicine 33: 303-307, 1994)

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