The effect of aspirin and indomethacin on prostacyclin and thromboxone production by placental tissue incubated with immunoglobulin G fractions from patients with lupus anticoagulant

Alan M Peaceman*, Karen A. Rehnberg

*Corresponding author for this work

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

OBJECTIVE: We investigated the hypothesis that nonsteroidal antiinflammatory agents can influence the abnormal prostanoid production associated with antiphospholipid antibodies. We specifically assessed whether aspirin or indomethacin could eliminate the increased placental thromboxane production previously observed with immunoglobulin G fractions from patients with lupus anticoagulant without adversely affecting prostacyclin production. STUDY DESIGN: Immunoglobulin G fractions were prepared from the plasma of eight nonpregnant patients with antiphospholipid antibody syndrome and demonstrable lupus anticoagulant. Samples from each patient were then placed in incubation wells containing explains from normal term pregnancies and 10−4 mol/L aspirin, 10−7 mol/L indomethacin, or no added drug. Aliquots were removed all intervals up to 48 hours of incubation and assessed for placental prostacyclin and thromboxane production by radioimmunoassay of the stable metabolites prostaglandin F and thromboxane B2. RESULTS: The addition of aspirin to wells contaiing immunoglobulin G from patients with lupus anticoagulant was associated with a significant decrease in thromboxane production compared with wells without added drug, but prostacyclin production was unaffected. In contrast, the addition of indomethacin also decreased thromboxane production significantly, but prostacyclin production was also diminished, so the ratio of thromboxane to prostacyclin was unaffected. CONCLUSION: These results support a role for the use of aspirin for antiphospholipid antibody-related pregnancy loss through a mechanism similar to that postulated for preeclampsia, namely, selective inhibition of thromboxane production.

Original languageEnglish (US)
Pages (from-to)1391-1396
Number of pages6
JournalAmerican Journal of Obstetrics and Gynecology
Volume173
Issue number5
DOIs
StatePublished - Jan 1 1995

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Lupus Coagulation Inhibitor
Thromboxanes
Epoprostenol
Indomethacin
Aspirin
Immunoglobulin G
Antiphospholipid Antibodies
Pregnancy
Thromboxane B2
Antiphospholipid Syndrome
Non-Steroidal Anti-Inflammatory Agents
Pre-Eclampsia
Pharmaceutical Preparations
Prostaglandins
Radioimmunoassay

Keywords

  • aspirin
  • indomethacin
  • Lupus anticoagulant
  • prostacyclin
  • thromboxane

ASJC Scopus subject areas

  • Obstetrics and Gynecology

Cite this

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title = "The effect of aspirin and indomethacin on prostacyclin and thromboxone production by placental tissue incubated with immunoglobulin G fractions from patients with lupus anticoagulant",
abstract = "OBJECTIVE: We investigated the hypothesis that nonsteroidal antiinflammatory agents can influence the abnormal prostanoid production associated with antiphospholipid antibodies. We specifically assessed whether aspirin or indomethacin could eliminate the increased placental thromboxane production previously observed with immunoglobulin G fractions from patients with lupus anticoagulant without adversely affecting prostacyclin production. STUDY DESIGN: Immunoglobulin G fractions were prepared from the plasma of eight nonpregnant patients with antiphospholipid antibody syndrome and demonstrable lupus anticoagulant. Samples from each patient were then placed in incubation wells containing explains from normal term pregnancies and 10−4 mol/L aspirin, 10−7 mol/L indomethacin, or no added drug. Aliquots were removed all intervals up to 48 hours of incubation and assessed for placental prostacyclin and thromboxane production by radioimmunoassay of the stable metabolites prostaglandin F1α and thromboxane B2. RESULTS: The addition of aspirin to wells contaiing immunoglobulin G from patients with lupus anticoagulant was associated with a significant decrease in thromboxane production compared with wells without added drug, but prostacyclin production was unaffected. In contrast, the addition of indomethacin also decreased thromboxane production significantly, but prostacyclin production was also diminished, so the ratio of thromboxane to prostacyclin was unaffected. CONCLUSION: These results support a role for the use of aspirin for antiphospholipid antibody-related pregnancy loss through a mechanism similar to that postulated for preeclampsia, namely, selective inhibition of thromboxane production.",
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T1 - The effect of aspirin and indomethacin on prostacyclin and thromboxone production by placental tissue incubated with immunoglobulin G fractions from patients with lupus anticoagulant

AU - Peaceman, Alan M

AU - Rehnberg, Karen A.

PY - 1995/1/1

Y1 - 1995/1/1

N2 - OBJECTIVE: We investigated the hypothesis that nonsteroidal antiinflammatory agents can influence the abnormal prostanoid production associated with antiphospholipid antibodies. We specifically assessed whether aspirin or indomethacin could eliminate the increased placental thromboxane production previously observed with immunoglobulin G fractions from patients with lupus anticoagulant without adversely affecting prostacyclin production. STUDY DESIGN: Immunoglobulin G fractions were prepared from the plasma of eight nonpregnant patients with antiphospholipid antibody syndrome and demonstrable lupus anticoagulant. Samples from each patient were then placed in incubation wells containing explains from normal term pregnancies and 10−4 mol/L aspirin, 10−7 mol/L indomethacin, or no added drug. Aliquots were removed all intervals up to 48 hours of incubation and assessed for placental prostacyclin and thromboxane production by radioimmunoassay of the stable metabolites prostaglandin F1α and thromboxane B2. RESULTS: The addition of aspirin to wells contaiing immunoglobulin G from patients with lupus anticoagulant was associated with a significant decrease in thromboxane production compared with wells without added drug, but prostacyclin production was unaffected. In contrast, the addition of indomethacin also decreased thromboxane production significantly, but prostacyclin production was also diminished, so the ratio of thromboxane to prostacyclin was unaffected. CONCLUSION: These results support a role for the use of aspirin for antiphospholipid antibody-related pregnancy loss through a mechanism similar to that postulated for preeclampsia, namely, selective inhibition of thromboxane production.

AB - OBJECTIVE: We investigated the hypothesis that nonsteroidal antiinflammatory agents can influence the abnormal prostanoid production associated with antiphospholipid antibodies. We specifically assessed whether aspirin or indomethacin could eliminate the increased placental thromboxane production previously observed with immunoglobulin G fractions from patients with lupus anticoagulant without adversely affecting prostacyclin production. STUDY DESIGN: Immunoglobulin G fractions were prepared from the plasma of eight nonpregnant patients with antiphospholipid antibody syndrome and demonstrable lupus anticoagulant. Samples from each patient were then placed in incubation wells containing explains from normal term pregnancies and 10−4 mol/L aspirin, 10−7 mol/L indomethacin, or no added drug. Aliquots were removed all intervals up to 48 hours of incubation and assessed for placental prostacyclin and thromboxane production by radioimmunoassay of the stable metabolites prostaglandin F1α and thromboxane B2. RESULTS: The addition of aspirin to wells contaiing immunoglobulin G from patients with lupus anticoagulant was associated with a significant decrease in thromboxane production compared with wells without added drug, but prostacyclin production was unaffected. In contrast, the addition of indomethacin also decreased thromboxane production significantly, but prostacyclin production was also diminished, so the ratio of thromboxane to prostacyclin was unaffected. CONCLUSION: These results support a role for the use of aspirin for antiphospholipid antibody-related pregnancy loss through a mechanism similar to that postulated for preeclampsia, namely, selective inhibition of thromboxane production.

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