Metabolism of Autologous and Homologous IgG in Rheumatoid Arthritis

Michael A. Catalano; Edwin H. Krick; David H. De Heer; Robert M. Nakamura; Argyrios N. Theofilopoulos; John H. Vaughan

doi:10.1172/JCI108779

Metabolism of Autologous and Homologous IgG in Rheumatoid Arthritis

Michael A. Catalano, Edwin H. Krick, David H. De Heer, Robert M. Nakamura, Argyrios N. Theofilopoulos, and John H. Vaughan

Published August 1, 1977 - More info

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Abstract

The metabolism of radioiodinated IgG was studied in 20 patients with rheumatoid arthritis and 11 normal controls using autologous IgG and homologous IgG pooled from normal donors. Fractional catabolic rates in the controls were 4.44% of the autologous- and 4.29% of the homologous-labeled protein per day. The corresponding rates in the rheumatoid patients were 9.67% of the autologous- and 8.64% of the homologous-labeled protein per day. Extravascular catabolism occurred only in the rheumatoid group and accounted essentially for the entire increased catabolism of IgG observed in these patients. 10 patients were especially hypercatabolic, with fractional catabolic rates for autologous IgG greater than 10%. Moreover, they catabolized their autologous IgG significantly faster than the homologous IgG (12.6 vs. 9.9%). The increment of catabolism of autologous over homologous IgG also occurred in the extravascular compartment. These highly hypercatabolic patients had a significantly increased number of manifestations of extra-articular disease.

The hypercatabolism of IgG could not be correlated with age, weight, sex, duration of disease, joint erosions, corticosteroid therapy, erythrocyte sedimentation rate, rheumatoid factor titer, serum IgG concentration, or circulating immune complexes as measured by the Raji cell radioimmunoassay.

Conceivable sites of extravascular catabolism and possible causes of faster catabolism of autologous (rheumatoid) than of homologous (normal) IgG are discussed.