Immune Complexes and the Evolution of Lyme Arthritis: Dissemination and Localization of Abnormal C1q Binding Activity

John A. Hardin, Allen C. Steere, Stephen E. Malawista

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Abstract

In a prospective study of 78 patients with Lyme arthritis, abnormal serum C1q binding activity was present at the initial onset of erythema chronicum migrans in nearly all cases. The abnormal binding persisted in patients with subsequent nerve or heart involvement. In contrast, among those with only subsequent arthritis, it usually disappeared within three months (P = 0.018). However, in the synovial fluid of affected joints, abnormal binding was uniformly present, and always to a greater extent than in the circulation. The abnormally reactive material behaved like antigen-antibody complexes. It had a density of 19S or greater, dissociated below pH 4.2, and lacked antiglobulin activity. Cryoprecipitates containing immunoglobulin were good but insensitive predictors of its presence, but immune complexes themselves did not seem primarily responsible for cryoprecipitability. Thus, as judged by C1q binding, immune complexes remain disseminated in certain patients with Lyme arthritis but localize to joints in others. (N Engl J Med 301:1358–1363, 1979) LYME arthritis is an inflammatory disorder, typically episodic and confined to few joints or migratory, that may also involve the skin, nervous system, or heart.1 2 3 In some patients, knee involvement has become chronic and, as in rheumatoid arthritis, has progressed to pannus formation and cartilage erosion.4 Although the causative agent has remained elusive, the vector appears to be an ixodid tick,5,6 recently reclassified as Ixodes dammini.7,8 The clinical onset of disease is often marked by the appearance of an expanding skin lesion, erythema chronicum migrans (ECM), that follows the tick bite within three to 21 days and precedes the.

Original languageEnglish (US)
Pages (from-to)1358-1363
Number of pages6
JournalNew England Journal of Medicine
Volume301
Issue number25
DOIs
StatePublished - Dec 20 1979

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