Pilot study of anti-mitochondrial antibodies in antiphospholipid syndrome.

Abstract

Mitochondria are intracellular organelles of bacterial origin capable of stimulating the immune system when released into the extracellular milieu. We previously reported the expression of anti-mitochondrial antibodies (AMA) targeting whole organelles (AwMA), mitochondrial DNA (AmtDNA) or mitochondrial RNA (AmtRNA) in patients with systemic lupus erythematosus (SLE). Antiphospholipid syndrome (APS) is an autoimmune condition that may be independent of, or associated with, other diseases, usually SLE. This study aimed to detect AMA in patients with APS and to explore the association with clinical features of APS. AwMA-, AmtDNA- and AmtRNA-IgG and -IgM were detected in a pilot study (healthy controls n = 30 and APS patients n = 24) by direct ELISA, and their levels were associated with demographic and disease characteristics. AmtDNA-IgM and AmtRNA-IgG and IgM were elevated in APS compared to healthy controls (p = 0.009, p = 0.0005 and p = 0.01, respectively). AwMA-IgG were increased in patients positive for lupus anticoagulant (median ± interquartile range = 0.36 ± 0.31 vs. 0.14 ± 0.08, p = 0.008), and optical density values for AwMA-IgM were correlated with titres of IgM against cardiolipin (rs = 0.51, p = 0.01). An increment of 0.1 unit of AmtDNA-IgM levels was associated with reduced prior reporting of arterial events (odds ratio = 0.86; 95% confidence interval 0.74-1.00; p = 0.047). Our pilot study suggests that AMA are represented within the autoantibody repertoire in APS and may display different associations with the clinical manifestations of the disease. Further studies should focus on reproducing these preliminary results by following AMA levels through time in larger prospective cohorts.