Complement in Human Disease

Schur, Peter H.; Austen, K. Frank

doi:10.1146/annurev.me.19.020168.000245

Cited by 111 publications

(46 citation statements)

References 50 publications

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“…In our study C' titers during the primary attack were often elevated and tended to be stable during febrile episodes. Rises in C' activity have been noted in other infectious diseases and this has been attributed to a nonspecific response in acute inflammatory states (18).…”

Section: Discussionmentioning

confidence: 98%

Relationship of Serum Complement Levels to Events of the Malarial Paroxysm

et al. 1974

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Section: Discussionmentioning

confidence: 98%

Relationship of Serum Complement Levels to Events of the Malarial Paroxysm

et al. 1974

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“…Evidence of the involvement of these two factors in RA is mainly derived from studies of the joint spaces with demonstration of depressed synovial fluid complement levels and presence of immune complexes in the synovium and in synovial fluid (1)(2)(3)(4) (4)(5)(6). However, the level of complement components is generally normal or increased in plasma from BA patients (1,7,8). This finding has been explained by an increased synthesis of complement components associated with the inflammatory syndrome in RA and masking a possibly increased catabolism (8,9 …”

Section: Introductionmentioning

confidence: 99%

“…However, the level of complement components is generally normal or increased in plasma from BA patients (1,7,8). This finding has been explained by an increased synthesis of complement components associated with the inflammatory syndrome in RA and masking a possibly increased catabolism (8,9 …”

Section: Introductionmentioning

confidence: 99%

“…The complement activation in RA is suggested by the finding of depressed levels and/or hemolytic activities of Cl, C4, C2, C3, properdin factor B, and properdin in synovial fluids (1,23). In the circulating blood, immune complexes have been demonstrated (4, 5) but an increased synthesis of certain complement components secondary to the inflammatory syndrome in RA often may mask a possible increase in their catabolism, therefore resulting in a normal or even augmented conventional complement profile (1,7,8). Indeed, with turnover studies, it was seen that complement was hypercatabolized not only in synovial fluid but also in blood from RA patients (9,10).…”

mentioning

confidence: 99%

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Circulating complement breakdown products in patients with rheumatoid arthritis. Correlation between plasma C3d, circulating immune complexes, and clinical activity.

Nydegger¹,

Zubler²,

Gabay³

et al. 1977

J. Clin. Invest.

112

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“…Increased levels of complement components and hemolytic activity are frequently found in inflammatory disorders, and striking decreases have been reported in diseases such as systemic lupus erythmatosus (SLE)' acute glomerulonephritis, membranoproliferative glomerulonephritis (MPGN), liver disease, and congenital deficiency of complement components (1)(2)(3).…”

Section: Introductionmentioning

confidence: 99%

Complement breakdown products in plasma from patients with systemic lupus erythematosus and patients with membranoproliferative or other glomerulonephritis.

Perrin¹,

Lambert²,

Miescher³

1975

J. Clin. Invest.

255

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A B S T R A C T A dynamic estimation of the involvement of the complement system in various diseases was obtained by the direct quantitation of breakdown products of C3 and of properdin factor B. The methods used were based, first, on the separation of native and fragmented molecules according to their molecular size through a precipitation with polyethylene glycol and, secondly, on an immunochemical quantitation, using specific antisera for the major antigens of C3 and factor B. The sensitivity and the specificity of these methods were demonstrated by activation of complement in vitro with generation of C3 and factor B fragments.A clinical investigation was carried out in 41 patients with systemic lupus erythematosus (SLE), 31 with membranoproliferative glomerulonephritis (MPGN), 26 with other types of glomerulonephritis, and 6 with severe alcoholic cirrhosis of the liver. The following observations were made: (a) an elevated plasma level of C3d fragment of C3 was found in 68% of SLE patients, in 87% of MPGN patients, in 62% of patients with other hypocomplementemic nephritis, and in 15% of those with normocomplementemic nephritis, but in only 33% of patients with liver cirrhosis and very low levels of C3; (b) a significant difference was observed between the levels of C3 obtained with either anti-"native" C3 or anti-C3c sera for immunochemical quantitation, in patients with SLE or MPGN, indicating the presence of "altered" or fragmented C3 in plasma; (c) an elevated plasma level of Ba fragment of properdin factor B was found in 46% of SLE patients, in 67% of MPGN patients, in 50% of patients with otherThis work was presented in part at the European Complement Workshop, Heidelberg, May 1974.Dr. Lambert's address is: Centre de Transfusion, HopitalCantonal, 1211 Geneva 4, Switzerland. Received for publication 9 December 1974 and in revised form 18 March 1975. hypocomplementemic nephritis, and in 9% of patients with normocomplementemic nephritis, while the level of properdin factor B was only slightly decreased in these diseases; (d) in SLE and MPGN there was an inverse correlation between the levels of C3d and Ba and the level of C3 in plasma. The level of these fragments was directly correlated with the clinical manifestations of SLE; (e) some patients with a normal C3 level exhibited an elevated plasma concentration of C3 and factor B fragments, suggesting the coexistence of an increased synthesis with a hypercatabolism of complement components.

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Complement in Human Disease

Cited by 111 publications

References 50 publications

Relationship of Serum Complement Levels to Events of the Malarial Paroxysm

Relationship of Serum Complement Levels to Events of the Malarial Paroxysm

Circulating complement breakdown products in patients with rheumatoid arthritis. Correlation between plasma C3d, circulating immune complexes, and clinical activity.

Complement breakdown products in plasma from patients with systemic lupus erythematosus and patients with membranoproliferative or other glomerulonephritis.

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