[Secondary Immunodeficiency in Rheumatology]. / Sekundäre Immundefekte in der Rheumatologie.

ABSTRACT

Secondary Immunodeficiency in Rheumatology Abstract. For the treatment of autoimmune and autoinflammatory diseases an immunosuppressive therapy with conventional, small molecule or biological disease modifying anti-rheumatic drugs (DMARDS) plays a key role. This may lead to secondary immunodeficiency with an increased risk for infections, which we discuss in the present article. The risk for reactivation of chronic hepatitis B increases particularly with glucocorticoid dosages of ≥ 20mg/d for longer than four weeks, with B-cell-depleting therapies, followed by anti-TNF-α-inhibitors. The latter also represent a risk for the reactivation of latent tuberculosis. High doses of glucocorticosteroids for prolonged periods increase the risk for pneumonia with Pneumocystis jirovecii, especially if combined with other DMARDs. An elevated risk for Herpes zoster exists for B-cell depletion, TNF-α-inhibition and for JAK blockade. Severe immunosuppression (B-cell depletion, cyclophosphamide, mycophenolate mofetil, JAK inhibitors, prednisone ≥ 20mg/d or combination therapy) increase the risk for severe COVID-19 infections.