Serum CA 19-9 (2-3 sialyl Le^a) is a marker of malignant disorder such as pancreas or gall bladder cancers. It has been reported that sera from patients with interstitial pneumonia show elevated level of CA 19-9. To investigate the relationship between the elevation of serum CA 19-9 (sCA 19-9) and the presence of pulmonary fibrosis, we examined the level of sCA 19-9 in sera from patients with rheumatic diseases with or without interstitial pneumonia (IP). The sCA 19-9 level was determined by enzymelinked immunosorbent assay (ELISA).
Fourteen sera of 129 (10.9%) patients with rheumatic diseases without malignant disorders were positive for sCA 19-9 when normal range was determined as less than 100 U/ml (mean±5 SD), and 26.7% of sera from poly/dermatomyositis (PM/DM) and 11.8% of systemic sclerosis (PSS) were positive for CA 19-9. Whereas only 8.0% of rheumatoid arthritis (RA) was positive.
Twelve (28.6%) of 42 rheumatic patients with IP showed positive levels for sCA 19-9 (mean 142.5±363.0U/ml), whereas only two (2.3%) of 87 without IP were positive (mean 33.9±65.8U/ml; p<0.05).
The correlation between the level of sCA 19-9 and pulmonary diffusing capacity (%DLCO) revealed an inverse correlation in 32 rheumatic patients with IP (r=-0.43, p<0.05). Furthermore, the elevated sCA 19-9 levels decreased after treatment with corticosteroid and/or cyclophosphamide or cyclosporin A. Therefore, elevation of the level of sCA 19-9 seems to be involved in the pathogenesis of IP and sCA 19-9 will be a useful parameter for IP. It has been reported that the CA 19-9 is produced from the bronchial glands and suggested that during chronic fibrotic process of the lung, the metaplastic change of the bronchial glandular cells occur and the cells produce CA 19-9.

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Indometacin farnesil (Indo-F) is a prodrug of indomethacin designed to reduce the occurrence of side-effects by esterification of the carboxyl group on indomethacin with farnesol. We have examined the pharmacological kinetics and action of Indo-F in peripheral blood mononuclear cells (PBMNC) and polymorphonuclear leukocytes (PBPNL) from patients with rheumatoid arthritis (RA). PBMNC and PBPNL were obtained from 31 RA patients. Indo-F was incubated with PBMNC or PBPNL in the presence or absence of granulocyte-macrophage colony stimulating factor (GM-CSF) (100pg/ml) for 37 days, after which the concentrations of Indo-F and indomethacin in the culture supernatants or in the cytoplasm extracts were measured with HPLC. The levels of Indo-F in the culture supernatants were significantly decreased in the presence of PBMNC or PBPNL from either normal individuals or RA patients. Indo-F was found to be taken up by PBMNC as well as by PBPNL from RA patients. Conversion of Indo-F into indomethacin was significantly enhanced by GM-CSF in the presence of PBMNC, but not PBPNL. The results indicate that Indo-F is taken up by peripheral blood leukocytes from RA patients. Moreover, the data suggest that monocyte-lineage cells might play an important role in the conversion of Indo-F into indomethacin since GM-CSF markedly facilitated the conversion in the presence of PBMNC, but not PBPNL.

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A 77 year-old woman was admitted to the hospital because of nasal obstraction on March 1994. Tumorectomy of the nasopharyngeal tumor disclosed non-Hodgkin's lymphoma (LSG: diffuse, medium sized). The patient was treated with local radiotherapy to nasopharyngeal region and combined chemotherapy (2 courses of CHOP) to reduce residual tumor. On July, the pericardial effusion appeared and the large granular lymphocyte (LGL) like lymphoma cells were observed in the effusion. Flow cytometic analysis of these cells showed that they expressed CD 2, CD 7, CD 56 and HLA-DR, but did not express CD 3. T-cell receptor gene (TCRβ) rearrangement was not observed and natural killer activity was detected in these lymphoma cells. The patient was treated with ProMACE and the pericardial infusion of methotrexate, carboplatin and prednisolone, but the patient died of heart failure. Monoclonarity of lymphoma cells in the pericardial effusion was determined by southernblot analysis, useing the terminal repeat of Epstein-Barr virus (EBV) for probe. It was suggested that EBV participated in tumorgenesis in this case.

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We herein report a case of chronic hepatitis C where the patient developed severe thrombocytopenia during interferon therapy. The patient was a 61-year-old woman, who received interferon therapy on April 27, 1993 under the diagnosis of C type chronic active hepatitis. After 4 weeks, her platelet count had decreased to 18, 000/μl and intraoral hemorrhage had begun. Although she received 250mg of methylprednisolone and 20U of platelet transfusion three times, her platelet count continued to decrease to 4, 000/μl on both May 28, and on June 3, 1993, and so she was transferred to our hospital on June 4. On her second admission to our hospital, although the platelet-associated IgG (PA-IgG) had increased markedly and the megakaryocytes in her bone marrow had decreased, her platelet count had already increased to 37, 000/μl, and this gradually returned to a normal level accompanied with a decrease of PA-IgG within one month.
In this case, although we found immunological abnormalities (high level of IgG, positive ANA and positive anti-smooth muscle antibody) prior to interferon treatment, we could not diagnose the patient as having suffered from autoimmune disease, including autoimmune hepatitis, because she did not satisfy the necessary criteria and because she did not have any symptoms suggesting autoimmune disease. We consider that there may be the possibility that interferon induced only an anti-platelet antibodies that caused the high level of PA-IgG

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We describe a case of interstitial pneumonitis associated with polymyositis who responded well to cyclosporine therapy. In October, 1993, a 49-year-old female was admitted to our hospital because of fever, muscle weakness and progressive dyspnea. Interstitial pneumonitis with polymyositis was diagnosed and daily oral steroid therapy was started. As the therapy was ineffective, pulse intravenous steroid therapies followed by oral cyclophosphamide and steroid therapy was given. Whereas serum levels of muscle enzymes decreased, she became progressively hypoxemic. No effect was observed in series of therapy including additional pulse steroid therapy, pulse intravenous cyclophosphamide therapy, oral azathioprine and oral bethametazone therapy. In April, 1994, oral cyclosporine was started. After daily oral cyclosporine was combined with steroid, her symptoms, chest X-ray, chest CT and pulmonary function tests significantly improved. Her disease became stable and there was no signs of recurrence since then.
It is suggested that cyclosporine is useful for the treatment of progressive interstitial pneumonitis associated with polymyositis.

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We reevaluated the efficacy of enzyme-linked immunosorbent assay (ELISA) with ultraviolet (UV) -treated polystyrene microtiter plates (UV-ELISA) for the detection of human serum anti-dsDNA antibodies. The subjects consisted of 38 patients with systemic lupus erythematosus (SLE). The titers of IgG serum anti-dsDNA antibodies by UV-ELISA were significantly (p<0.01) higher in sera from 26 active SLE patients than in those from 12 inactive SLE patients. ELISA with poly-L-lysine coated microtiter plates (PLL-ELISA) revealed the similar results. However, the background ratio was only 1.0±0.9% by UV-ELISA, which was significantly (p<0.01) lower than that by PLL-ELISA (16.8±10.8%). These results demonstrated the efficacy of ELISA with UV-treated polystyrene microtiter plates for the measurement of human serum anti-dsDNA antibodies in patients with SLE.

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