PMID- 9458202
OWN - NLM
STAT- MEDLINE
DCOM- 19980306
LR  - 20071114
IS  - 0315-162X (Print)
IS  - 0315-162X (Linking)
VI  - 25
IP  - 1
DP  - 1998 Jan
TI  - Effect of anticardiolipin/beta2-glycoprotein I complexes on production of 
      thromboxane A2 by platelets from patients with the antiphospholipid syndrome.
PG  - 51-6
AB  - OBJECTIVE: Antiphospholipid antibodies (aPL) reactive with anionic phospholipids 
      and beta2-glycoprotein I (beta2-GPI) are found in the sera of patients with 
      autoimmune diseases. Clinically, aPL/beta2-GPI complexes are associated with 
      arterial and venous thrombosis, fetal loss, and thrombocytopenia, i.e., the 
      antiphospholipid syndrome (APS). The mechanism of thrombosis is not known. We 
      hypothesized that aPL/beta2-GPI complexes could perturb the platelet membrane and 
      increase production of thromboxane A2 (TXA2, a proaggregatory prostanoid). 
      METHODS: We isolated an IgG fraction containing anticardiolipin antibody (aCL) 
      and the plasma cofactor, beta2-GPI, from a patient with a high titer of aCL and 
      thrombotic cerebrovascular disease. We then examined the effect of aCL, 
      beta2-GPI, and the aCL/beta2-GPI complex on platelet TXB2 (a stable metabolite of 
      TXA2) biosynthesis in vitro from 7 healthy controls. We also measured in vitro 
      platelet TXB2 biosynthesis in 7 patients with APS and in 8 controls. RESULTS: We 
      found: (1) significantly increased in vitro TXB2 production by platelets from 
      controls after incubation with aCL/beta2-GPI complexes; (2) moderately increased 
      TXB2 production by aCL alone; (3) no increase in TXB2 production by beta2-GPI 
      alone; and (4) significantly increased 11-dehydro-TXB2, a metabolite of TXB2 
      production in vivo, in the urine of patients with APS compared with controls. 
      CONCLUSION: These data suggest that aCL/beta2-GPI complexes play a role in 
      activating platelets to produce TXA2, which could contribute to the prothrombotic 
      state found in patients with APS.
FAU - Robbins, D L
AU  - Robbins DL
AD  - Department of Internal Medicine, University of California Davis, School of 
      Medicine, 95616, USA.
FAU - Leung, S
AU  - Leung S
FAU - Miller-Blair, D J
AU  - Miller-Blair DJ
FAU - Ziboh, V
AU  - Ziboh V
LA  - eng
GR  - AR30679/AR/NIAMS NIH HHS/United States
GR  - AR39831/AR/NIAMS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Canada
TA  - J Rheumatol
JT  - The Journal of rheumatology
JID - 7501984
RN  - 0 (Antibodies, Anticardiolipin)
RN  - 0 (Antibodies, Antiphospholipid)
RN  - 0 (Glycoproteins)
RN  - 0 (Immunoglobulin Fab Fragments)
RN  - 0 (Phospholipids)
RN  - 0 (beta 2-Glycoprotein I)
RN  - 54397-85-2 (Thromboxane B2)
RN  - 57576-52-0 (Thromboxane A2)
RN  - 67910-12-7 (11-dehydro-thromboxane B2)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Antibodies, Anticardiolipin/metabolism/*pharmacology
MH  - Antibodies, Antiphospholipid/metabolism
MH  - Antiphospholipid Syndrome/immunology/*metabolism
MH  - Autoimmune Diseases/immunology/*metabolism
MH  - Binding Sites
MH  - Blood Platelets/*drug effects/metabolism
MH  - Female
MH  - Glycoproteins/metabolism/*pharmacology
MH  - Humans
MH  - Immunoglobulin Fab Fragments/pharmacology
MH  - Male
MH  - Middle Aged
MH  - Phospholipids/metabolism
MH  - Thromboxane A2/*metabolism
MH  - Thromboxane B2/analogs & derivatives/urine
MH  - beta 2-Glycoprotein I
EDAT- 1998/02/11 00:00
MHDA- 1998/02/11 00:01
CRDT- 1998/02/11 00:00
PHST- 1998/02/11 00:00 [pubmed]
PHST- 1998/02/11 00:01 [medline]
PHST- 1998/02/11 00:00 [entrez]
PST - ppublish
SO  - J Rheumatol. 1998 Jan;25(1):51-6.