The patient’s travel history included trips to Italy [more than 15 journeys (approximately 14 d each time) at different seasons and to various places in the last 10 y],

Greece (every year 1 wk to Crete for the last 15 y), Spain (2003), Morocco (2001), and Egypt (2000). Microscopical investigation of a mucosal biopsy confirmed the presumptive diagnosis of “mucosal leishmaniasis (ML)” (Figure 1). Polymerase chain reaction (PCR) identified Leishmania infantum as the species.1,2 As the patient lives in Switzerland outside Leishmania endemic regions, she must Obeticholic Acid cell line have acquired the infection while traveling in an L infantum endemic region (in her case: Italy, Greece, Spain, or Morocco).3 The patient was put on intramuscularly administered pentavalent antimonial treatment (meglumine antimoniate 20 mg/kg body weight/d). After 7 days of treatment, the patient developed a pronounced pruritic, partly erythematous, partly papulo-urticarial rash on the trunk and the inner thighs, which responded to oral antihistamine and topical corticosteroid treatment. On follow-up on day 12 of treatment the laboratory check-up Talazoparib showed severe hypokalemia (2.3 mmol/L) and an elevated serum amylase level (300 U/L). Additionally, we found a newly developed prolonged QTc interval (600 ms) on electrocardiogram (ECG). Due to the severe hypokalemia, treatment with meglumine antimoniate

was immediately suspended. After aborting treatment and starting potassium substitution, the potassium level and the QTc interval showed rapid normalization (as did the serum amylase level and skin rash). With the consent of the patient, we decided to

change the antileishmanial treatment to oral miltefosine [2.5 mg/kg body weight/d = 50 mg three times a day (TID)] for 30 days. After starting miltefosine treatment, the patient complained about pronounced nausea with repeated vomiting and presented with clinical signs of dehydration. Laboratory tests showed impaired kidney function (creatinine 160 µmol/L, uric acid 839 µmol/L) and hypokalemia (2.5 mmol/L). After suspending miltefosine treatment and administering oral rehydration, the symptoms subsided and the serum potassium Terminal deoxynucleotidyl transferase and kidney function tests showed rapid normalization. Finally, it was possible to complete the 30-day miltefosine treatment in conjunction with supportive antiemetic treatment with domperidone. After completion of treatment, the oral mucosal lesions healed completely without signs of recurrence on follow-up visits over the next year (Figure 1). ML—the least common clinical form of leishmaniasis—is mostly caused by the New World species, Leishmania braziliensis and Leishmania panamensis in the Americas and the Old World species, L infantum, which is endemic in the Mediterranean region, the Middle East, Central Asia, and China. Most cases of ML arise from lymphatic or hematogenous spread of cutaneous leishmaniasis (CL) and are found in the Americas.