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Pleural Fluid Complement in Systemic Lupus Erythematosus and Rheumatoid Arthritis

GENE G. HUNDER, M.D., F.A.C.P.; FREDERIC C. MCDUFFIE, M.D., F.A.C.P.; and NORMAN G. G. HEPPER, M.D., F.A.C.P.
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Supported in part by USPHS research grant AM-11630 from the National Institutes of Health, Bethesda, Md., and a grant from the Minnesota Chapter, Arthritis Foundation, New York, N.Y.

▸Requests for reprints should be addressed to Gene G. Hunder, M.D., Mayo Clinic, Rochester, Minn. 55901.


Rochester, Minnesota


Ann Intern Med. 1972;76(3):357-363. doi:10.7326/0003-4819-76-3-357
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Whole hemolytic complement and three components (C1q, C4, and C3) were measured in pleural fluids obtained from 50 patients—23 with malignant disease, 6 with lupus erythematosus, 6 with rheumatoid arthritis, 3 with congestive heart failure, 3 with pulmonary embolism, and 9 in whom the cause of the pleural effusion was not ascertained. The mean values for whole complement and the three components were lowest in lupus erythematosus and rheumatoid arthritis patients. Compared with the malignant disease group, these differences were statistically significant (P < 0.01) for whole complement, C4, and C3. Anticomplementary activity was found in pleural fluids from some patients with lupus erythematosus or rheumatoid arthritis. This suggests that the pleural fluid complement depletion may be secondary to immunologic inactivation and that immune mechanisms may contribute to the development of Pleuritis in lupus erythematosus and rheumatoid arthritis.

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