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Activation of the alternative complement pathway accompanies disease flares in systemic lupus erythematosus during pregnancy

Buyon JP; Tamerius J; Ordorica S; Young B; Abramson SB
OBJECTIVE. To assess the activity of systemic lupus erythematosus (SLE) during pregnancy and to distinguish it from preeclampsia. METHODS. We prospectively measured the complement activation products Ba, Bb, SC5b-9, and C4d, as well as the conventional complement determinants C3, C4, and CH50, during pregnancy in 14 patients with SLE and 10 women with preeclampsia. RESULTS. Four of the 14 SLE patients were considered to have disease flares, 3 occurring in the second trimester and 1 postpartum. In these patients, significant abnormalities of Ba, Bb, SC5b-9, and CH50 were noted. In contrast, measures of C4d did not distinguish between pregnant patients who had flares and those whose SLE remained stable. Although decreased values of C3 were rarely seen in the patients with stable disease, normal values of C3 during lupus pregnancy were not reliably associated with stable disease. Three of 10 non-SLE patients with preeclampsia had elevated levels of Ba; however, in each case, the CH50 level was close to or within the normal range. This was in sharp contrast to the findings observed in the 4 patients with active SLE, in whom high levels of plasma Ba were always associated with low CH50 values. Moreover, the ratio of CH50 to Ba was significantly lower in the patients with lupus flares than in the non-SLE patients with preeclampsia. CONCLUSION. While a decline in the CH50 level alone could otherwise be attributed to decreased synthesis of complement components, these data demonstrate that ongoing activation of the alternative complement pathway can accompany disease flares in pregnant women with SLE
PMID: 1731815
ISSN: 0004-3591
CID: 9752

THE SHWARTZMAN PHENOMENON IN SYSTEMIC LUPUS-ERYTHEMATOSUS - A NOVEL MECHANISM OF VASCULAR INJURY [Meeting Abstract]

BELMONT, HM; BUYON, J; GIORNO, R; ABRAMSON, S
ISI:A1992JR15801046
ISSN: 0004-3591
CID: 51851

NITRIC-OXIDE INHIBITS HUMAN NEUTROPHIL SUPEROXIDE ANION PRODUCTION VIA DIRECT ACTION ON A MEMBRANE COMPONENT OF THE NADPH-OXIDASE [Meeting Abstract]

CLANCY, R; LESZCZYNSKAPIZIAK, J; ABRAMSON, S
ISI:A1992JR15800362
ISSN: 0004-3591
CID: 51846

CARDIAC RISK-FACTORS IN PATIENTS WITH SYSTEMIC LUPUS-ERYTHEMATOSUS (SLE) [Meeting Abstract]

KITSIS, EA; BELMONT, HM; SKOVRON, ML; ORNSTEIN, H; MCCULLAGH, E; PETER, JB; ABRAMSON, SB
ISI:A1992JR15800436
ISSN: 0004-3591
CID: 51847

INTRAVASCULAR NEUTROPHIL (PMN) ACTIVATION IN SLE - DISSOCIATION BETWEEN INCREASED CD11B/CD18 (CR3) AND DECREASED L-SELECTIN (LS) EXPRESSION ON NEUTROPHILS (PMNS) [Meeting Abstract]

MOLAD, Y; BUYON, J; ANDERSON, DC; ABRAMSON, SB; CRONSTEIN, BN
ISI:A1992JR15800927
ISSN: 0004-3591
CID: 51849

DIFFERENTIAL PHOSPHORYLATION OF CD11B/CD18 IN NEUTROPHIL SPECIFIC GRANULE AND PLASMA-MEMBRANES [Meeting Abstract]

BUYON, JP; SLADE, SG; LESZCYNSKAPIZIAK, J; PHILIPS, M; ABRAMSON, SB
ISI:A1992JR15800360
ISSN: 0004-3591
CID: 51845

ASSEMBLY OF HETEROTRIMERIC G-PROTEINS IN A LIPID BILAYER IS REQUIRED FOR THE INHIBITION OF NEUTROPHIL FUNCTION BY NONSTEROIDAL ANTIINFLAMMATORY DRUGS [Meeting Abstract]

ABRAMSON, SB; LESZCZYNSKAPIZIAK, J; CLANCY, RM; PHILIPS, M; WEISSMANN, G
ISI:A1992HN74100317
ISSN: 0009-9279
CID: 51975

NITRIC OXIDE-INDUCED ADP-RIBOSYLATION OF A 37KDA CYTOSOLIC PROTEIN IN HUMAN NEUTROPHILS PROMOTES ACTIN DEGRADATION [Meeting Abstract]

ABRAMSON, SB; LESZCZYNSKAPIZIAK, J; CLANCY, RM
ISI:A1992HN74100646
ISSN: 0009-9279
CID: 51987

NITRIC-OXIDE INHIBITS HUMAN NEUTROPHIL SUPEROXIDE ANION PRODUCTION VIA DIRECT ACTION ON THE NADPH-OXIDASE [Meeting Abstract]

CLANCY, RM; LESZCZYNSKAPIZIAK, J; MUSCAT, S; ABRAMSON, SB
ISI:A1992HN74100647
ISSN: 0009-9279
CID: 51988

NITRIC-OXIDE DERIVATIVE S-NITROSOGLUTATHIONE INHIBITS T-CELL PROLIFERATION AND INDUCES ACCUMULATION OF CYCLIC GUANOSINE 3,5'-MONOPHOSPHATE [Meeting Abstract]

MERRYMAN, PF; CLANCY, RM; HE, X; ABRAMSON, SB
ISI:A1992HN74100723
ISSN: 0009-9279
CID: 51993