Jozélio Freire de CARVALHO, Cezar Augusto Muniz CALDAS
Rheumatology Quarterly - 2026;4(3):140-147
Leishmaniasis-particularly visceral leishmaniasis (VL)-is marked by profound immune dysregulation, including polyclonal hypergammaglobulinemia, cytopenias, and broad autoantibody positivity, often mimicking autoimmune diseases (AID) such as systemic lupus erythematosus (SLE) and autoimmune hepatitis (AIH). In addition, immunosuppressive and biologic therapies used in AID may increase susceptibility to opportunistic leishmaniasis. This narrative review synthesizes primary studies and relevant literature to examine (i) autoimmune-like clinical and serological features of VL and other forms of leishmaniasis; (ii) occurrence in patients with AID receiving immunosuppressive therapy; (iii) underlying immunological mechanisms; and (iv) clinical implications for diagnosis and management. Evidence consistently shows frequent autoantibody positivity in VL, including antinuclear antibodies, anti-extractable nuclear antigen antibodies, rheumatoid factor, and direct Coombs positivity, often reversible after antiparasitic treatment. Clinical presentations resembling SLE or AIH are well documented. Increased cases are reported in patients receiving anti-tumor necrosis factor therapy, particularly in endemic areas. These findings highlight diagnostic overlap and reinforce the need to consider VL in autoimmune-like syndromes. Visceral leishmaniasis may induce "reactive autoimmunity" and simulate AID; thus, screening, exclusion of active infection, and post-treatment reassessment are essential to prevent misdiagnosis and inappropriate immunosuppression.
