title: Anticardiolipin and anti-beta2 glycoprotein I antibodies and lupus-like anticoagulant: prevalence and significance in systemic sclerosis.
abstract: BACKGROUND
  It has been suggested that both anticardiolipin (aCL) and anti-beta(2) glycoprotein I (abeta(2)GPI) antibodies may play a critical role in the pathogenesis of systemic sclerosis (SSc)-related vascular impairment.
  
  
  OBJECTIVE
  To evaluate the prevalence of aCL and abeta(2)GPI antibodies and lupus-like anticoagulant (LAC) in patients with SSc and healthy controls. We also investigated a possible relationship between clinical and biological variables of patients with SSc and the presence of aCL/abeta(2)GPI antibodies and/or LAC.
  
  
  METHODS
  Measurements of aCL and abeta(2)GPI antibodies, and LAC were performed in 69 consecutive patients with SSc and 69 age- and sex-matched controls. Clinical and biological findings were compared between patients with and without antiphospholipid antibodies.
  
  
  RESULTS
  aCL and abeta(2)GPI antibodies and/or LAC were detected in 13 (19%) of 69 consecutive patients with SSc; in the healthy control group, aCL antibody was found in only one (2%) subject (P = 0.0007). None of the healthy controls had abeta(2)GPI antibody and/or LAC. Moreover, pitting scars, pulmonary arterial hypertension, macrovascular involvement as well as severity of capillary impairment (using nailfold videocapillaroscopy) were more frequent in SSc patients with aCL/abeta(2)GPI antibodies and/or LAC compared with those without.
  
  
  CONCLUSIONS
  Our findings suggest that antiphospholipid antibodies may have a role in the genesis of vascular involvement related to SSc. Finally, the assessment of antiphospholipid antibodies (aCL and abeta(2)GPI antibodies, as well as LAC) may contribute to a better recognition of clinical features in patients with SSc; in essence, the patients with aCL/abeta(2)GPI antibodies and/or LAC may require close monitoring of vascular changes, including in particular pulmonary arterial hypertension and digital infarcts.
authors.affiliation: Department of Internal Medicine, Rouen University Hospital, 76031 Rouen Cedex, France. isabelle.marie@chu-rouen.fr
authors.forename: I
authors.initials: I
authors.lastname: Marie
authors.forename: F
authors.initials: F
authors.lastname: Jouen
authors.forename: M-F
authors.initials: MF
authors.lastname: Hellot
authors.forename: H
authors.initials: H
authors.lastname: Levesque
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D017153:Antibodies, Anticardiolipin / Q000097:blood; D017152:Antibodies, Antiphospholipid / Q000097:blood*; D005260:Female; D005313:Fetal Death / Q000209:etiology / Q000276:immunology; D005385:Fingers / Q000473:pathology; D006801:Humans; D016682:Lupus Coagulation Inhibitor / Q000097:blood; D008297:Male; D008875:Middle Aged; D011247:Pregnancy; D012595:Scleroderma, Systemic / Q000150:complications / Q000276:immunology* / Q000473:pathology; D012883:Skin Ulcer / Q000209:etiology / Q000276:immunology / Q000473:pathology; D020246:Venous Thrombosis / Q000209:etiology / Q000276:immunology; D053482:beta 2-Glycoprotein I / Q000276:immunology
chemical_list: D017153:Antibodies, Anticardiolipin; D017152:Antibodies, Antiphospholipid; D016682:Lupus Coagulation Inhibitor; D053482:beta 2-Glycoprotein I