Abstract

Leishmanias is an anthropozoonosis caused by the Leishmania protozoa. The manifestation of the disease varies depending on the type of Leishmania and the immunestatus of the patient. Tumor Necrosis Factor (TNF)-I± antagonists were introduced in the late 1990s and have had a marked impact on rheumatic diseases. Tumor necrosis factor plays an important role in the immune systems defense against intracellular infections and the use of TNF-I± antagonists is linked with an increased frequency of infections. We here present a case of cutaneous leishmaniasis relapse following treatment with miltefosine and amphotericin B, in a patient undergoing treatment with a TNF-I± antagonist.

Highlights

  • Leishmaniasis is an infection caused by the parasite Leishmania, a protozoan zoonosis transmitted by sandflies

  • Tumor Necrosis Factor (TNF)-α antagonists are potent inhibitors of cytokines that play an important role in the formation of granulomas and the host’s defense against intracellular infections such as tuberculosis and legionellosis

  • We believe that repeated treatment failure of Cutaneous Leishmaniasis (CL) in this case was explained by the use of TNF-α antagonists

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Summary

Introduction

Leishmaniasis is an infection caused by the parasite Leishmania, a protozoan zoonosis transmitted by sandflies. Worldwide cutaneous leishmaniasis is the most common presentation of leishmania infection with an estimated annual incidence of 0.7-1.2 million cases (Alvar et al, 2012). We report a case of a patient with AS treated with ADA, who presented with a case of relapsing CL after treatment with miltefosine and amphotericin B. Upon his return to Denmark in July, the patient was seen at the Department of Dermatology. 16 doses of l-AmB 200 mg were administered with 48 hours interval Following this the patient was seen at the Department of Infectious Diseases and it was concluded that treatment, after pausing ADA, had been successful (Fig. 2B). The pausing of ADA was well tolerated for the duration of the CL treatment

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