The C1q binding assay in systemic lupus erythematosus

Inman, Robert D.; Fong, Jill; Pussell, Bruce A.; Ryan, P. J.; Hughes, G. R. V.

doi:10.1002/art.1780231109

Cited by 35 publications

(3 citation statements)

References 23 publications

(11 reference statements)

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“…We were not surprised by the lack of relationship between measures of serum complement and staphylococcal protein A immune complex binding, since this also has been noted by other investigators (9,11,42).…”

Section: Discussionsupporting

confidence: 79%

Hypocomplementemia with low Cls‐Cl inhibitor complex in systemic lupus erythematosus

Lockshin

Qamar

Redecha

et al. 1986

Arthritis & Rheumatism

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Ninety-three serum and plasma samples from 45 patients with systemic lupus erythematosus were analyzed for the complex formed by Cls and its inhibitor, as well as for C3, C4, C4a desarginine, and staphylococcal protein A-bound immune complexes. There were statistically significant correlations between Cls-C1 inhibitor complex and CH50, between Cls-C1 inhibitor complex and C4, and between Cls-C1 inhibitor complex and C4a desarginine. Serial studies were performed on 24 patients over a period of 6 months. Seven of 21 patients with hypocomplementemia had persistently normal levels of Cls-C1 inhibitor complex, 7 had transiently abnormal levels of Cls-C1 inhibitor complex, and 7 had sustained abnormal levels of Cls-C 1 inhibitor complex. Two of 3 pregnant patients with normal levels of complement had abnormal levels of Cls-Cl inhibitor complex. Staphylococcal protein A-bound immune complexes demonstrated no correlation with any of the complement assays. Complement activation, as measured by Cls-C1 inhibitor complex, is often a transient phenomenon in systemic lupus erythematosus patients with persistent hypocomplementemia. (SLE) is the assumption that serum complement, measured as CH50, C3, or C4, reflects the rate of in vivo complement activation (1-6). Testing of this hypothesis is cumbersome, however (7,s); it requires the administration, to patients, of radiolabeled complement components.Several assays for products of complement activation are now available. These assays measure the complex formed by Cls and the C1 inhibitor (9-12), C3d (13-15), C4d (16), C5a (17,18), membrane attack complex (19), and other products (20,21). Studies relevant to SLE have, in general, concluded that these assays correlate well with the clinically used measures of complement, CH50, C3, and C4.In contrast, in a previous study of pregnant SLE patients, we noted that Cls-C1 inhibitor complex did not reflect clinically measured hypocomplementemia (22). The serum specimens analyzed in our prior report were obtained from single patients at single points in time. These observations now are extended by findings on a new group of 45 SLE patients (27 nonpregnant, 18 pregnant), 24 of whom we have followed serially. In these patients, we compared levels of CIS-C1 inhibitor complex with levels of CH50, C3, C4, C4a desarginine, and staphylococcal protein A-bound immune complexes. Our results indicate that the levels of Cls-C1 inhibitor complex are frequently either normal or are only transiently abnormal when levels of CH50, C3, and C4 are persistently abnormal, which suggests that activation of the classical complement pathway occurs sporadically in patients with sustained hypocomplementemia. In addition, measurements of C4a desarginine and staphylococcal protein A binding correlate poorly with other complement measures.

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Section: Discussionsupporting

confidence: 79%

Hypocomplementemia with low Cls‐Cl inhibitor complex in systemic lupus erythematosus

Lockshin

Qamar

Redecha

et al. 1986

Arthritis & Rheumatism

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“…Several studies have shown that by comparing groups of patients with active disease with groups of patients with inactive disease, significant correlations between various laboratory parameters and disease activity can be found (16)(17)(18)29,30). Our study confirmed this.…”

Section: Discussionmentioning

confidence: 99%

The value of complement and immune complex determinations in monitoring disease activity in patients with systemic lupus erythematosus

Valentijn

Overhagen

Hazevoet

et al. 1985

Arthritis & Rheumatism

131

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Serial serum samples from 33 patients with systemic lupus erythematosus were tested for CH50, C3, C4, and circulating immune complexes. Circulating immune complexes were determined by 5 different assays. Disease activity was determined by a scoring system we devised. On an interpatient analysis, overall disease activity correlated significantly with levels of CH50, C3, and a positive result on Clq binding assay. However, with the exception of depressed C3 levels, the sensitivity, specificity, and predictive values of all the serologic tests were low. An intrapatient analysis revealed a patient-specific activity parameter in 11 of the 33 patients. We conclude that these serologic tests are not reliable in assessing disease activity in patients with systemic lupus erythematosus, although a small subgroup of patients will exhibit a patient-specific activity parameter.

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“…Yet despite their presence, it remains difficult to determine precisely the pathogenetic potential of immune complexes in systemic vasculitis since they are rarely detectable in 100% of these patients (Pussell et al, 1978), they may be present in otherwise normal tissues (Baart de la Faille-Kuyper et al, 1973) or, conversely, undetectable in tissues with typical vasculitic lesions (Conn et al, 1972), and disease activity may not correlate with measured levels (Inman et al, 1980). Problems in interpretation also arise since levels of immune complexes measured by different methods correlate poorly (Lambert et al, 1978).…”

Section: Immuno-pathogenetic Mechanisms Immune Complexes (A) Animal Mmentioning

confidence: 99%

The aetiology and pathogenesis of major systemic vasculitides

Savage

1986

Postgraduate Medical Journal

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The C1q binding assay in systemic lupus erythematosus

Cited by 35 publications

References 23 publications

Hypocomplementemia with low Cls‐Cl inhibitor complex in systemic lupus erythematosus

Hypocomplementemia with low Cls‐Cl inhibitor complex in systemic lupus erythematosus

The value of complement and immune complex determinations in monitoring disease activity in patients with systemic lupus erythematosus

The aetiology and pathogenesis of major systemic vasculitides

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