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Infection and Drug-Induced Antiphospholipid Antibodies

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Conclusions

Our observations, and those from others, give further support to our hypothesis that “autoimmune aPL” may be generated by immunization with products from bacteria or viruses after incidental exposure or infection. We also were able to generate APS-like syndrome in a strain of mice susceptible to autoimmunity, indicating that other factors are likely to be involved, such as genetic predisposition. Furthermore, not all aPL generated were pathogenic. Based on the clinical experience and on the numerous reports indicating presence of aPL in large number of infectious diseases, it may be expected that not all aPL produced during infection will be pathogenic. A limited number aPL induced by certain viral/bacterial products would be pathogenic in certain genetically predisposed individuals. Further studies to identify the agents responsible for induction the pathogenic aPL are needed. Identification of those bacterial and/or viral agents may help finding strategies for the prevention of production of aPL “pathogenic” antibodies. Alternatively, free peptides may be used to induce tolerance against aPL production or to abrogate their pathogenic effects.

Drugs such as procainamide and phenothiazines can also induce aPL. The prevalence and pathogenicity of drug-induced aPL is generally low and has been discussed in this chapter.

Keywords

  • Anticardiolipin Antibody
  • Systemic Lupus Erythemato
  • Hughes Syndrome
  • Lupus Anticoagulant Activity

These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

In memory of A.E. Gharavi who passed away on Oct 13, 2004.

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Pierangeli, S.S., Gharavi, A.E. (2006). Infection and Drug-Induced Antiphospholipid Antibodies. In: Khamashta, M.A. (eds) Hughes Syndrome. Springer, London. https://doi.org/10.1007/1-84628-009-5_42

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