Reactivation of Cutaneous Leishmaniasis in a Rheumatoid Arthritis Patient Undergoing Tocilizumab Treatment
4 affiliations
- 1Laboratório de Parasitologia, São Paulo, Universidade de São Paulo Instituto de Medicina Tropical de São Paulo, São Paulo, Brazil
- 2Laboratório de Doenças Infecciosas e Emergentes, Pontifícia Universidade Católica do Paraná, Curitiba, Brazil
- 3Faculdade de Medicina, Departamento de Infectologia e Medicina Tropical, São Paulo, Universidade de São Paulo, São Paulo, Brazil
- 4Laboratório de Soroepidemiologia, São Paulo, Universidade de São Paulo Instituto de Medicina Tropical de São Paulo, São Paulo, Brazil
Abstract
Cutaneous leishmaniasis is a neglected vector-borne disease caused by Leishmania spp., with viable parasites potentially persisting after clinical cure. Immunosuppressive therapies may favor reactivation of latent infection. The case of a 62-year-old Brazilian woman with a 25-year history of rheumatoid arthritis who developed a painful ulcerative lesion on her right leg 1 month after initiating tocilizumab therapy is reported. Molecular testing confirmed Leishmania (Viannia) braziliensis, consistent with reactivated cutaneous leishmaniasis. Tocilizumab was discontinued, and liposomal amphotericin B was initiated but interrupted because of nephrotoxicity and hepatotoxicity. Despite incomplete treatment, the lesion gradually healed after withdrawal of immunosuppression without requiring additional antiparasitic therapy. Secondary prophylaxis with liposomal amphotericin B was subsequently initiated under close clinical and laboratory monitoring, and no recurrence has been observed during follow-up. This case highlights the importance of screening clinical history for prior leishmaniasis, maintaining vigilance for reactivation in patients from endemic areas, and promptly adjusting immunosuppressive therapy to optimize clinical outcomes.
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BibTeX
@article{souza2026reactivation,
title = {{Reactivation of Cutaneous Leishmaniasis in a Rheumatoid Arthritis Patient Undergoing Tocilizumab Treatment}},
author = {Regina Maia de Souza and Felipe Francisco Tuon and Antônio Carlos Nicodemo and Christini Takemi Emori and Beatriz Julieta Celeste and Maria Carmen Arroyo Sanchez and Valdir Sabbaga Amato},
journal = {The American Journal of Tropical Medicine and Hygiene},
year = {2026},
month = sep,
doi = {10.4269/ajtmh.26-0345},
url = {https://doi.org/10.4269/ajtmh.26-0345},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Reactivation of Cutaneous Leishmaniasis in a Rheumatoid Arthritis Patient Undergoing Tocilizumab Treatment
AU - Regina Maia de Souza
AU - Felipe Francisco Tuon
AU - Antônio Carlos Nicodemo
AU - Christini Takemi Emori
AU - Beatriz Julieta Celeste
AU - Maria Carmen Arroyo Sanchez
AU - Valdir Sabbaga Amato
PY - 2026
DA - 2026/09/15
JO - The American Journal of Tropical Medicine and Hygiene
DO - 10.4269/ajtmh.26-0345
UR - https://doi.org/10.4269/ajtmh.26-0345
AB - Cutaneous leishmaniasis is a neglected vector-borne disease caused by Leishmania spp., with viable parasites potentially persisting after clinical cure. Immunosuppressive therapies may favor reactivation of latent infection. The case of a 62-year-old Brazilian woman with a 25-year history of rheumatoid arthritis who developed a painful ulcerative lesion on her right leg 1 month after initiating tocilizumab therapy is reported. Molecular testing confirmed Leishmania (Viannia) braziliensis, consistent with reactivated cutaneous leishmaniasis. Tocilizumab was discontinued, and liposomal amphotericin B was initiated but interrupted because of nephrotoxicity and hepatotoxicity. Despite incomplete treatment, the lesion gradually healed after withdrawal of immunosuppression without requiring additional antiparasitic therapy. Secondary prophylaxis with liposomal amphotericin B was subsequently initiated under close clinical and laboratory monitoring, and no recurrence has been observed during follow-up. This case highlights the importance of screening clinical history for prior leishmaniasis, maintaining vigilance for reactivation in patients from endemic areas, and promptly adjusting immunosuppressive therapy to optimize clinical outcomes.
SN - 0002-9637
SN - 1476-1645
ER -