АА-amyloidosis: etiology, clinical features and efficacy of interleukin-6 inhibitors

In AA amyloidosis, the precursor of the amyloid fibrils is serum amyloid A (SAA) protein, an acute-phase reactant produced by the liver in response to inflammation. Therefore, systemic AA-amyloidosis is a complication of chronic inflammatory disorders, including rheumatoid arthritis, infections, autoinflammatory diseases, etc. AA-amyloidosis usually results from inadequate control of inflammation leading to persistently high SAA concentration. Isolated kidney disease is the most common clinical manifestation of AA-amyloidosis, whereas cardiomyopathy and peripheral neuropathy typical for AL- and ATTR-amyloidosis occur rarely. The incidence of AA-amyloidosis in rheumatoid arthritis has decreased over the last years due to the availability of effective anti-inflammatory and immunosuppressive therapies. However, rheumatoid arthritis remains one of the most common causes of AA-amyloidosis. The authors report a case of rheumatoid arthritis complicated by AA-amyloidosis and treated with levilimab, an IL-6 receptor inhibitor, and discuss the current etiology, clinical manifestations and approaches to treatment. IL-6 inhibitors may prevent or retard progression of AA-amyloidosis in rheumatoid arthritis patients due to their anti-inflammatory activity and ability to inhibit the production of SAA.