Metabolism of autologous and homologous IgG in rheumatoid arthritis.
Metabolism of autologous and homologous IgG in rheumatoid arthritis.
复制标题
类风湿关节炎中自体和同源 IgG 的代谢。
DOI：
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发表时间：
1977
影响因子：
15.9
通讯作者：
John H. Vaughan
中科院分区：
文献类型：
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作者：
Michael A. Catalano;Edwin H. Krick;D. H. D. Heer;Robert M. Nakamura;A. Theofilopoulos;John H. Vaughan
本文用自体IgG和正常人IgG混合液对20例类风湿关节炎患者和11例正常人的放射性碘标记IgG代谢进行了研究。对照组的分解代谢率分别为4.44%的自体和4.29%的同源标记的蛋白质每天。类风湿患者的相应比率为每天9.67%的自体标记蛋白和8.64%的同源标记蛋白。血管外卡他汀仅发生在类风湿组，并基本上占在这些患者中观察到的IgG的全部增加的卡他汀。10例患者尤其是高分解代谢，自体IgG的分解代谢率分数大于10%。此外，它们分解代谢自身IgG的速度显著快于同源IgG（12.6%对9.9%）。在血管外室中，自体IgG的释放量也高于同源IgG。这些高分解代谢患者关节外疾病的表现数量显著增加。IgG的高浓度不能与年龄，体重，性别，病程，关节糜烂，皮质类固醇治疗，红细胞沉降率，类风湿因子滴度，血清IgG浓度，或循环免疫复合物的Raji细胞放射免疫测定。血管外catefiles和可能的原因更快catefiles的自体（类风湿）比同源（正常）IgG的设想网站进行了讨论。
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.