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Value of the assay for IgA-containing circulating immune complexes in Henoch-Schönlein purpura
Using a modified Raji cell radioimmunoassay, IgA- and IgG-containing circulating immune complexes (IgA-CIC, IgG-CIC) were examined in the sera of 10 patients with Henoch-Schönlein purpura (HSP) and compared with those in the sera of patients with systemic lupus erythematosus (SLE), erythema multiforme (EM), erythema nodosum (EN) and Schamberg's disease. The mean level of IgA-CIC in HSP (233 micrograms/ml) was statistically higher than that in samples from healthy blood donors (14 micrograms/ml; p less than 0.05). In the other diseases, the mean values of IgA-CIC (SLE, 72 micrograms/ml; EM, EN, 0 microgram/ml; Schamberg's disease, 5 micrograms/ml) were not statistically different from that of normal controls. The IgA-CIC level in HSP rose markedly during the active phase of the cutaneous manifestation (233 micrograms/ml), declining to the normal range during remission (4 micrograms/ml; p less than 0.05). On the contrary, IgG-CIC did not increase during either phase. There was an isolated patient in whom IgA-CIC seemed to correlate with the clinical events of cutaneous and systemic involvement. The timing was such that a change in the level of IgA-CIC generally preceded disease activity. These findings suggest that IgA-CIC may be an etiologic factor in the cutaneous and systemic involvements of HSP, and the laboratory test for IgA-CIC is not only useful as a research tool, but also valuable as a predictive indicator of disease activity.
Using a modified Raji cell radioimmunoassay, IgA- and IgG-containing circulating immune complexes (IgA-CIC, IgG-CIC) were examined in the sera of 10 patients with Henoch-Schönlein purpura (HSP) and compared with those in the sera of patients with systemic lupus erythematosus (SLE), erythema multiforme (EM), erythema nodosum (EN) and Schamberg's disease. The mean level of IgA-CIC in HSP (233 micrograms/ml) was statistically higher than that in samples from healthy blood donors (14 micrograms/ml; p less than 0.05). In the other diseases, the mean values of IgA-CIC (SLE, 72 micrograms/ml; EM, EN, 0 microgram/ml; Schamberg's disease, 5 micrograms/ml) were not statistically different from that of normal controls. The IgA-CIC level in HSP rose markedly during the active phase of the cutaneous manifestation (233 micrograms/ml), declining to the normal range during remission (4 micrograms/ml; p less than 0.05). On the contrary, IgG-CIC did not increase during either phase. There was an isolated patient in whom IgA-CIC seemed to correlate with the clinical events of cutaneous and systemic involvement. The timing was such that a change in the level of IgA-CIC generally preceded disease activity. These findings suggest that IgA-CIC may be an etiologic factor in the cutaneous and systemic involvements of HSP, and the laboratory test for IgA-CIC is not only useful as a research tool, but also valuable as a predictive indicator of disease activity.