Infections and the Antiphospholipid Syndrome

Abstract

Currently, the origin of autoimmune diseases is considered to be multifactorial. Genetic predisposition, immune system malfunction or even backfire, hormonal regulation, and environmental factors, i.e. infections, all play important roles in the pathogenesis of autoimmune diseases such as the antiphospholipid syndrome (APS). New drugs and strategies aimed at preventing infections could further improve the outcome of APS and other autoimmune diseases.

Prevalence of hepatitis C serum antibody in autoimmune diseases

“…To evaluate whether this observation is merely stochastic or possibly associated with anti-HCV treatment, a prospective study of a larger number of patients is warranted. Fourth, although many infectious agents were found to be associated with APS [56][57][58], we failed to observe an association between the presence of anti-HCV antibodies and pAPS, in agreement with previous studies [16,59]. However, 8% of patients with sAPS had detectable anti-HCV, similar to reported associations between HCV and atypical APS or catastrophic APS [60,61].…”

Presence of Antibodies Against Mycoplasma penetrans in Patients with Antiphospholipid Syndrome

“…This is the so-called "twohit theory" in which pathogenic anti-2GPI antibodies act as the first hit and inflammatory responses as the second. [Amital et al 2008;García-Carrasco et al 2009].  Antiphospholipid antibodies (aPL) may be demonstrated during the course of many infections in addition to occurring in conditions such as Systemic Lupus Erythematosus (SLE), APS, and a wide variety of other rheumatic diseases.…”

Is It Antiphospholipid Syndrome?

“…However, the differential diagnosis between IE and APS in individual cases may be difficult, as antiphospholipid antibodies are frequently positive during infections [10]. On the other hand, fever can be present in antiphospholipid syndrome, and cases of APS presenting as fever of unknown origin [11] or truly mimicking IE—the so-called pseudoinfective endocarditis [12]—have been described.…”

“…Leucocytosis was absent, and PCR was not raised, further suggesting a noninfectious process. The correct diagnosis was eventually made only two months later, after a high-dose corticosteroid course which might have contributed to the rapid growth of aortic vegetations, thus increasing the embolic risk of the patient [10]. However, a high degree of suspicion and strict adherence to diagnostic algorithms could have led to the correct diagnosis.…”