To study the effects of eicosapentaenoic acid (EPA) on the surface markers of peripheral lymphocyte, 200g of sardine was loaded daily to 12 healthy subjects with or without additional intake of 1.8g of EPA for 2 weeks. Fish diet resulted in a daily intake of 3.9g EPA. Serum concentration of EPA increased from 17.5±7.2μg/ml (mean±SD) to 195.0±53.9 in the group with fish diet (n=6) and it increased from 19.5±4.2 to 277.2±24.8 in the group with fish diet and additional EPA (n=6). In each groups, CD 4⁺ cells with IL-2 receptor and HLA-DR were increased and CD 8⁺ cells with T cell receptor were decreased. In the group with fish diet, CD 8⁺ cells with HLA-DR were increased. These results suggest that the load of EPA may influence the surface markers of lymphocyte in human.

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We performed a prospective study to clarify the incidence and characteristics of steroid myopathy. Of 52 patients who entered this study, 18 developed steroid myopathy (34.6%) and it occurred 30.1±13.5 (mean±SD) days after the start of corticosteroid therapy. The dose of prednisolone in the steroid myopathy group was higher than in the non steroid myopathy group (50.0 vs. 44.4mg/day, p<0.05). The incidence of steroid myopathy correlated significantly with corticosteroid dosage. Weight loss in the steroid myopathy group was more marked than in the non steroid myopathy group (-4.3 vs. -2.0kg, p<0.001). After starting therapy, no significant differences were exhibited between the steroid myopathy and non steroid myopathy groups in LDH and percent creatinuria levels. The serum cholinesterase level in the steroid myopathy group was significantly reduced. It appears that weight loss and a decreased cholinesterase level may be useful in the screening and diagnosis of steroid myopathy.

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The CD 4⁺CD 8^- helper T (TH) cells were cloned from childhood myasthenia gravis (MG) patients with negative or low level of anti-AChR antibody in sera. TH 1-like cell clones, which expressed IL-2 and IFN-γ mRNA, but not IL-4 or IL-5 mRNA, were established from peripheral blood lymphocytes (PBLs) of those patients. TH 2-like cell clones, expressing IL-4 and IL-5 mRNA, but not IL-2 or IFN-γ mRNA, were not established from PBLs of the same patients. Neither TH 1-like cell nor TH 2-like cell clone was found from PBLs of the healthy control children. Most of the established TH cell clones from healthy children expressed both IL-2 and IL-4 mRNA. There was the correlation between the number of TH 1-like cell clones from PBLs of childhood MG patients and the recurrence or the excerabation of clinical signs. As TH 1 cells were involved in the cellular immune responses in vivo, it is presumed that the cellular immune responses play the important role for the recurrence or the excerabation of the clinical signs of childhood MG patients.

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The levels of immune complex (IC) were studied by using two different methods in order to analyze the activation process of C_??_ in IC diseases. In vitro, heat aggregated IgG (HAG) in various concentrations was added to normal sera, and was incuvated at 37°C for 48 hours. IC levels were determined both by the C1q solid phase assay (ELISA) and by the anti-C1q antibody assay (ELISA). Meanwhile, changes in the concentration of (C_??_-C_??_) C_??_ inhibitor₂ complex were also determined (ELISA) as the indications of the levels of activated C1.
The levels of IC obtained by the C1q solid phase assay decreased in the temporal course after adding HAG. On the other hand, a gradual increase in the temporal course after adding HAG was observed in the levels of IC determined by the anti-C1q antibody assay, and in those of (C_??_-C_??_) C_??_ inhibitor₂ complex. The larger the amounts of added HAG, the greater the increase in the levels of IC and (C_??_-C_??_) C_??_ inhibitor₂ complex. The activation of C1 occurred after the connection of C1 with HAG, which was demonstrated by the clear differences in the aspect of C1 activity between the levels of IC measured by the C1q solid phase assay and by the anti-C1q antibody assay. These results suggest that the participation of C1 in the development and progress of IC diseases can be examined more clearly by both assays.
One ITP-patient was treated with steroid whose levels of IC determined by the anti-C1q antibody assay were continuously high and by the C1q solid phase assay were normal. During and after the treatment, his levels of IC, (C_??_-C_??_) C_??_ inhibitor₂ complex, and platelet-associated IgG were lowered, and the platelet counts and CH 50 levels were gradually improved. The results obtained by the in vitro study with HAG explain the discrepancies between the levels of IC determined by the C1q solid phase assay and by the anti-C1q antibody assay.

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A 61-year-old female presented with dry eyes and mouth in May 1991. The diagnosis of Sjögren's syndrome (SjS) was made based on positive results of the Schirmer's test, Rose-Bengal staining, salivary scintigraphy and lip biopsy. In January 1992, she complained of general malaise, loss of body weight, hair and memory, then she was hospitalized.
Physical examinations were within normal limits except goiter. Laboratory tests revealed high levels of blood sugar, no response of immuno-reactive insulin to oral glucose tolerance test, low levels of T₃, T₄ and high level of TSH, and anti-microsomal antibody as well as positive anti-nuclear antibody. The results for anti SS-A antibody and anti SS-B antibody were negative study.
Based on those clinical and laboratory data, she was diagnosed insulin-dependent diabetes mellitus (IDDM) and autoimmune thyroid disease (ATD).
The patient responded well to treatment with injectable insulin and oral T₄ medication.
Although the association of IDDM and ATD is not rare, there have been only two other cases reported in the literature in which IDDM, ATD and SjS occurred concomitantly.
This is a rare but valuable case because it may contribute to the understanding of the pathophysiology of SjS in regard to its association with other autoimmune diseases.

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A 62-year-old Japanese female with Sjögren's syndrome (SS) was admitted to our hospital because of fever, weight loss and parotid swelling. She has been diagnosed of having pseudolymphoma 1 year prior to the admission because of pulmonary lesion. Biopsy specimen obtaind from the parotid gland, lymph node and lung tissue demonstrated no apparent invasion of malignant cells but severe infiltration of lymphoid cells. Formation of myoepithelial islands was also observed. Analysis of immunoglobulin gene rearrangement by Southern blotting revealed a rearranged band in the parotid gland DNA. Furthermore, polymerase chain reaction (PCR) amplification clearly showed an appearance and expansion of monoclonal B cell population in the biopsy specimen from the lymph node and the lung. However, parotid swelling spontaneously regressed and pulmonary lesions almost disappeared without any treatment. We here discussed the importance of immunoglobulin gene analysis in the course of SS and the significance of monoclonal B cell expansion in SS.

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This report presents a 2-year-old boy with Wiskott-Aldrich syndrome, who developed membranoproliferative glomerulonephritis. The patient presented microhematuria, prote-inuria and hypertension at one year old when the patient developed recurrent episodes of respiratory infection. A histological study on the renal biopsy specimen revealed a diffuse and global double contour lesion in the capillary wall by light microscopy, but C 3 deposits were not recognized by immunofluorescent study.
There have been reports of nephropathy development in some patients with Wiskott-Aldrich syndrome after treatment with a transfer factor; however, our patient developed renal disease without the use of a transfer factor. The patient improved with methylpred-nisolone, at an alternate day regimen. This case provides valuable information of the clinical features of renal involvement in the course of Wiskott-Aldrich syndrome especially in relation to recurrent respiratory infections.

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A 53-year-old woman suffered from a dry cough and dyspnea in Jan. 1987. On the basis of Raynaud's phenomenon, proximal sclerosis, pigmentation and depigmentation of skin, bone resorption at the finger tips, dilation of the esophagus, pulmonary hypertension and pulmonary fibrosis, she was diagnosed as having progressive systemic sclerosis (PSS). In Feb. 1991, fever and sputum appeared, and the cough and dyspnea became severe. A friction rub appeared and the Velcro rales worsened. Laboratory data showed arterial hypoxemia, leukocytosis, positive anti-nuclear antibody, positive anti-Scl-70 antibody and circulating immune complexes. Serum complement levels were normal, and anti-centromere antibody, anti-DNA antibody and anti-RNP antibody were all negative. Chest X-ray, UCG and CT revealed a marked pericardial effusion as well as pulmonary hypertension and fibrosis. She was treated with prednisolone, besides receiving oxgen, diuretics, a calcium antagonist and digitalis.
Although massive pericardial effusion associated with PSS is thought to bo rare and indicates a poor prognosis, nonsurgical treatment was thought to have been effective in our case.

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We report a case of AIDS with remarkable symptoms of central nervous system. The patient was a 40-year-old man. Route of infection of HIV is unknown. He had dementia, left hemiplegia, bulbar palsy, progressed to rigid decorticate posture and died of respiratory arrest due to involvement of the brain stem, despite of treatment including use of 3'-azido-2', 3'-dideoxythymidine (AZT). Magnetic resonance (MR) images showed progressive cerebral atrophy and a diffuse high signal intensity area of cerebral white matter on T₂-weighted MR images, suggesting the diagnosis of HIV-induced encephalopathy. Beta-2-microglobulin concentration in the cerebrospinal fluid was high. p 24 band was gradually decreased in the course of time, which was revealed by Western blot analysis. In autopsy, marked atrophy of systemic lymphapparatus and marked decrease of CD 4 positive T cells in these tissues were found. Craniotomy was not allowed.

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A 31-year-old woman of 5 years-history of general malaise admitted because of lassitude, arthralgia, headache and blepharoptosis. Her symptoms and history indicate the diagnosis of chronic fatigue syndrome, according to the critenia from the Centers for Disease Control, USA, although differential diagnosis of Sjögren's syndrome and myasthenia gravis was needed in this case. While no autoantibodies were detected, gum test and Schirmer test were positive.
As to myasthenia gravis, blepharoptosis and ophtalmoplegia were observed in addition to a positive result of tensilon test. However, an evoked potential of electromyogram and anti-acethylcholine receptor antibody were negative, suggesting the diagnosis of myasthenia gravis to this patient is not definite at this moment. This case report may suggest that chronic fatigue syndrome shows several symptoms and signs which may associate with other autoimmune diseases.

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