Open AccessLupus pregnancy. II. Unusual pattern of hypocomplementemia and thrombocytopenia in the pregnant patient
Author(s) -
Lockshin Michael D.,
Harpel Peter C.,
Druzin Maurice L.,
Becker Carl G.,
Klein Renate F.,
Watson Rosemarie M.,
Elkon Keith B.,
Reinitz Elizabeth
Publication year - 1985
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.1780280110
Subject(s) - proteinuria , medicine , lupus anticoagulant , pregnancy , systemic lupus erythematosus , gastroenterology , immunology , lupus erythematosus , antibody , obstetrics , kidney , disease , biology , genetics
To explore the causes of complications in pregnant women with systemic lupus erythematosus (SLE), we prospectively evaluated 34 pregnancies in 28 SLE patients, and 2 additional pregnancies in patients with lupus anticoagulant and positive antinuclear antibody, but no other manifestations of SLE. Nineteen pregnancies (55%) were complicated by marked proteinuria, thrombocytopenia, and/or lupus anticoagulant. Hypocomplementemia occurred in 18 pregnancies (52%). Neither thrombocytopenia‐anticoagulant nor proteinuria was accompanied by an increase in antibody to double‐stranded DNA or by clinical signs of active SLE. Antibody to Ro antigen did not predict fetal death. Both thrombocytopenia and proteinuria appeared abruptly during pregnancy and disappeared quickly after delivery. Fetal death was the result in 7 of 9 (77%) pregnancies in patients with anticoagulant, 6 of 10 (60%) in patients with thrombocytopenia, 6 of 18 (33%) in patients with hypocomplementemia, and 3 of 11 (27%) in patients with proteinuria. Twenty of 29 (68%) children were identified as male. The pathogenesis of hypocomplementemia was evaluated by a new assay, C1s‐C1 inhibitor complex, which is thought to measure rate of complement activation by the classical pathway. Most pregnant patients with low CH50 levels and proteinuria had normal levels of C1s‐C1 inhibitor complex, whereas nonpregnant patients with equivalent proteinuria and hypocomplementemia had high levels, as did pregnant patients with hypocomplementemia who did not have SLE. Pregnant and nonpregnant hypocomplementemic patients with proteinuria had similar levels of C3 and C4. In pregnant patients with SLE, C1s‐C1 inhibitor complex was independent of CH50; in nonpregnant patients a linear relationship between C1s‐C1 inhibitor complex and CH50 was seen. We conclude that hypocomplementemia and probably thrombocytopenia (with anticoagulant) occur via different mechanisms in pregnant and nonpregnant patients with SLE.