Profiles of autoantibodies in patients with scleroderma were reviewed and their possible clinical significance was discussed in this paper.
Many autoantibodies including antinuclear antibodies and rheumatoid factors are detected in patients with scleroderma, especially in those with hypergammaglobulinemia. Fluorescent antinuclear antibodies were found in 36-97% of the serum of patients with scleroderma. The specificities of these antinuclear antibodies have been actively investigated in various laboratories using various nuclear antigens and many specificities were recently identified. Among them, two new antibody systems; anti-Og (Scl-1/Scl-70) antibody and anti-centromere antibody, were found to be highly specific for this disorder. Anti-Og antibody was detected in 33% of scleroderma patients and the patients with this antibody tended to have relatively advanced dermal sclerosis and pulmonary fibrosis. Anti-centromere antibody was reported to be present in the serum of patients mainly with CREST syndrome. Other antinulcear antibody systems; e.g. anti-DNA, anti-RNP, and anti-SS·B, were also seen in patients with scleroderma. However, when the patients with overlap syndrome were excluded, anti-RNP antibody was major antibody system in scleroderma. In contrast to the patients with anti-Og antibody, those with antiRNP antibody tended to have much milder sclerodermatous skin change and better prognosis.
The presence of the serum autoantibodies in scleroderma patients and the association of these antibodies to patient's clinical characteristics suggest that these antibodies may play some significant roles in developping clinical features and/or might be closely related to the pathogenesis of this disease. Therefore it seems to be important to investigate these antibodies in order to clarify the pathogenesis of scleroderma.

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The presence of cryoglobulins which are usually mixed type, such as IgG-IgM, IgG-IgG has been reported in the serum of patients with collagen diseases and suggested as one of the evidence of circulating immune complex.
In this paper, we report the effect of D-Pc treatmen for 2 cases of RA and Sjögren syndrome with hyper-cryoglobulinemia.
Case 1, 54 years old woman, diagnosed as Sjögren syndrome, had mixed IgG-IgM cryoglobulinemia and microscopic hematuria with moderate proteinuria.
After 6 months of D-Pc therapy, the cryoprotein diminished and significant reduction of proteinuria was observed.
Her clinical symptomes and findings also were improved.
Case 2, 49 years old woman with odefinite RA had been treated with low dose (5 mg/ day) of prednisolone for long time. But many abnormal symptoms such as skin bleeding, erythema nodosum and muscle pain was seen and also high concentration of IgG-IgM mixed type cryoglobulin was detected in her serum.
After treatment with D-Pc, dramatic immunological changes and clinical improvement was also observed.
We consider that D-Pc therapy will be effective to some case of collagen diseases with cryoglobulinemia.

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Phospholipase A₂ (125 ng), arachidonic acid (50 ug), 8, 11, 14-eicosatrienoic acid (50 ug) and prostaglandin E2 (500 ng) exaggerated carrageenin-induced edema when administered subcutaneously with carrageenin to the rat paw. On the other hand, 11, 14, 17-eicosatrienoic acid, 6, 9, 12-octadecatrienoic acid, 9, 12-octadecadienoic acid and 4, 7, 10, 13, 16, 18-docosahexaenoic acid (each 50ug) did not potentiate the edemainducing activity of carrageenin.
Prednisolone, clidanac, indomethacin, phenylbutazone, aspirin, aminopyrine, tiaramide, quinacrine and theophylline administered orally to rats inhibited the carrageenin edema, but the profile of inhibitory effects on potentiating actions by phospholipase A₂, arachidonic acid and prostaglandin E₂ varied from compound to compound.

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Acute pulmonary hemorrhage has been associated with significant mortality in patients with systemic lupus erythematosus (SLE) . Clinical discriptions, however, are few in number and the etiology of pulmonary hemorrhage in lupus is still unclear.
We have observed two SLE patients with pulmonary hemorrhage, one was massive and fatal, and the other was focal. Causes of the hemorrhage were not clarified in our cases, showing no evidence of septemia, disseminated intravascular coagulation or arteritis. Circulating immune complexes may play a role for the hemorrhage, although their deposition was not demonstrated in the lung of one case (milder one) by the immunofluorecence method.

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It is said that jaw cysts enlarge as the cyst fluids increase because of inflammation. To gain a better understanding of pathogenesis of jaw cysts, the author examined the cyst fluids and the cyst walls on 126 cases and tried to control the inflammation by an irrigational method on 46 cases of them. As a result, in infected cysts, the values of polyunsaturated fatty acid and PO₂ decreased and those of lipoperoxides and free radical and leucocyte count increased. After the infection of the cyst disappeared, those values reached to those of non-infected cyst, and the cyst diminished in size. The enlargement of the cyst can be regarded as follows: O₂¹ is generated by phagocytosis; Polyunsaturated fatty acids peroxided by 0₂¹ generate prostaglandin, which absorbs bone in relation to cyclic AMP, and the cyst is enlarged. It can be said that the cyst may be due to the inflammation accompany with the infection of the cysts.

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