Elsevier

Autoimmunity Reviews

Volume 7, Issue 4, February 2008, Pages 272-277
Autoimmunity Reviews

Review article
Antiphospholipid antibodies, antiphospholipid syndrome and infections

https://doi.org/10.1016/j.autrev.2007.10.001Get rights and content

Abstract

Since the association between antiphospholipid antibodies (aPL) and syphilis was first described, many other viral, bacterial and parasitic infections have been shown to induce antiphospholipid antibodies, notably anticardiolipin antibodies (aCL). A review of the literature shows that while aCL occur frequently in viral infections, particularly in HIV (49.75%), HBV (24%) and HCV (20%), it is very rarely associated with anti-β2 glycoprotein I antibodies (anti-β2GPI) and is not correlated with thrombosis risk or hematological manifestations of the antiphospholipid syndrome (APS). Concerning bacterial infections, aCL is often present in leprosy (42.7%), where it is frequently associated with the presence of anti-β2GPI (44.8%), and in syphilis infections (8 to 67%), though without correlation with thrombotic events. Though few individual patients with unequivocal infection-induced aPL satisfy criteria for APS, the lack of statistical association with thrombotic events strongly argues against the identification of a true APS subset in this context. However, physicians should keep in mind the fact that an infection, generally bacterial, in patients with confirmed APS, may lead to catastrophic antiphospholipid syndrome with a possible fatal outcome.

Section snippets

HCV infection

Since the discovery of the hepatitis C virus (HCV) and the availability of serological screening and diagnostic tests, many manifestations, labeled extra-hepatic, have been reported to be associated with this infection, including the presence of aPL and APS.

Bacterial, mycobacterial and parasitic infections

Among bacterial infections, leprosy is probably the one whose association with aCL is the best explored. The mean prevalence of aCL in lepromatous or borderline leprosy is of around 43%, ranged from 21 to 67%. Contrary to viral infections, the mean prevalence of anti-β2GPI antibodies is as high as 45%, ranging from 2.9 to 89% [25], [34], [35]. However, these anti-β2GPI antibodies differ appreciably from those associated with APS by 1) their ability to recognize human and bovine β2-GPI

Infections and the catastrophic antiphospholipid syndrome

Beyond the mere relation of causality, the association of aPL, APS and infections also has major relevance in clinical practice in reference to a distinct form of APS known as the catastrophic antiphospholipid syndrome (CAPS). CAPS is defined as the rapid onset of APS mainly affecting microvasculature, leading to multiorgan failure through renal, pulmonary, cardiac, central nervous system or gastrointestinal impairment, resulting in an overall mortality of close to 50% [3]. Infections have been

Conclusion

The presence of aPL occurs very frequently in viral and bacterial infections. However, in nearly all studies, these “infectious” aPL are neither accompanied by anti-β2GPI antibodies, hematological manifestations nor thrombotic events which define APS. Finally, though few individual patients with unequivocal infection-induced aPL satisfy criteria for APS, the lack of statistical association with thrombotic events strongly argues against the identification of a true APS subset in this context.

Take-home messages

  • •

    Antiphospholipid antibodies are frequently present during HCV, HIV and HBV infections, and some bacterial infections (leprosy, syphilis).

  • •

    In such situations, antiphospholipid antibodies are usually not associated with anti-beta2 glycoprotein antibodies and thrombotic events.

  • •

    The catastrophic form of the antiphospholipid syndrome can be induced by acute infections.

References (40)

  • R.A. Asherson et al.

    Catastrophic antiphospholipid syndrome: international consensus statement on classification criteria and treatment guidelines

    Lupus

    (2003)
  • J.E. Hunt et al.

    A phospholipid-beta 2-glycoprotein I complex is an antigen for anticardiolipin antibodies occurring in autoimmune disease but not with infection

    Lupus

    (1992)
  • Y. Shoenfeld et al.

    Infectious origin of the antiphospholipid syndrome

    Ann Rheum Dis

    (2006)
  • P. Cacoub et al.

    Anticardiolipin, anti-beta2-glycoprotein I, and antinucleosome antibodies in hepatitis C virus infection and mixed cryoglobulinemia. Multivirc Group

    J Rheumatol

    (1997)
  • H. Guglielmone et al.

    Cofactor dependence and isotype distribution of anticardiolipin antibodies in viral infections

    Ann Rheum Dis

    (2001)
  • Z.M. Sthoeger et al.

    Anticardiolipin autoantibodies in serum samples and cryoglobulins of patients with chronic hepatitis C infection

    Ann Rheum Dis

    (2000)
  • J. Ordi-Ros et al.

    Anticardiolipin antibodies in patients with chronic hepatitis C virus infection: characterization in relation to antiphospholipid syndrome

    Clin Diagn Lab Immunol

    (2000)
  • V. Leroy et al.

    Prevalence and significance of anticardiolipin, anti-beta2 glycoprotein I and anti-prothrombin antibodies in chronic hepatitis C

    Br J Haematol

    (1998)
  • K. Zachou et al.

    Anti-cardiolipin antibodies in patients with chronic viral hepatitis are independent of beta2-glycoprotein I cofactor or features of antiphospholipid syndrome

    Eur J Clin Investig

    (2003)
  • G.N. Dalekos et al.

    Increased incidence of anti-cardiolipin antibodies in patients with hepatitis C is not associated with aetiopathogenetic link to anti-phospholipid syndrome

    Eur J Gastroenterol Hepatol

    (2000)

    • Cited by (0)

    View full text
    Copyright © 2007 Elsevier B.V. All rights reserved.