Antiphospholipid-Syndrome

A Nature Reviews Rheumatology review argues that the liver is an upstream player in autoimmune rheumatic disease and not only a bystander. Hepatocytes make β2-glycoprotein I, paraoxonase-1 (PON1), complement, CRP, hepcidin and most circulating antioxidants, and they process nutrients, drugs, toxins and gut microbial products. In lupus-prone mice, hepatic mitochondrial oxidative stress and mTOR activation come before autoantibodies, and loss of PON1 may let β2GPI become an immunogenic antigen in lupus and antiphospholipid syndrome. The review also covers lupus hepatitis versus autoimmune hepatitis, MASLD in rheumatic disease, how disease-modifying drugs affect the liver, when to biopsy, and liver-directed treatments, most of which are still experimental.

Reported incidence of antiphospholipid syndrome ranges from 0.75 to 6.49 per 100,000 person-years and prevalence from 6 to 50 per 100,000, but this Nature Reviews Rheumatology article shows that much of that spread comes from how a case is defined, which antibodies are measured, whether positivity is confirmed after 12 weeks, and who gets tested. It explains how the 1999, 2006 and 2023 criteria changed who counts as a case, why a single positive test is common and rarely means APS, and where APS is most likely to be found: unprovoked or recurrent venous thromboembolism, stroke in young adults and selected pregnancy complications.