Case Presentation: A 43 year old man, with a past medical history of HIV diagnosed earlier this year, was referred to the hospital by his primary care doctor for a hemoglobin drop of 10 to 7 and epigastric pain, suspicious for GI bleed. Pt also reported subjective fever/chills for the past week. Physical exam was significant for palpable splenomegaly, as well as diffuse round purple ulcerations 6-7mm along upper and lower extremities, lower abdomen, and back. He had had these lesions in 2011, but they had receded after a few weeks without treatment. Labs on admission were significant for WBC 2.5, Hgb 7.7, Plt 157. He underwent endoscopy, and biopsy results from the duodenum and stomach showed small organisms (3-5 microns), morphologically consistent with leishmania species. Skin biopsy of one of his lesions, was consistent with cutaneous leishmaniasis. Bone marrow biopsy pathology was consistent with leishmaniasis as well. The patient was started on liposomal amphotericin B 250 mg IV, but after 2 doses, he had a rise in his Creatinine to 1.55 from 1, so the treatment was held. Creatinine started to decline to 1.82, so the patient was restarted on amphotericin with IVF hydration. His creatinine again rose to 2.2, so amphotericin was stopped. The patient was deemed safe for discharge, and the next week, he was started on miltefosine 50 mg tid per his ID clinic.
Discussion: This patient with leishmaniasis initially presented with a self-resolving cutaneous infection, and presented years later with both cutaneous and visceral disease. It is likely that the onset of HIV was the trigger that allowed for the parasite to take advantage of his immunocompromised state and to present as a visceral infection. This man presented with classic symptoms such as fever, splenomegaly, and pancytopenia. While it was unusual for the initial diagnosis to be found on endoscopy, it is not uncommon for someone with concurrent HIV infection and leishmaniasis to have disease in his gastrointestinal tract. This patient’s treatment course was also challenging. Firstly, while his symptoms were typical of leishmaniasis, other disease processes had to be ruled out such as primary hematologic malignancies causing pancytopenia, or other infectious diseases. More importantly, both amphotericin B and miltefosine have significant side effect profiles. Amphotericin commonly causes AKI, which occurred in this patient after receiving his first two doses of amphotericin, as well as with resumption of therapy, even with concurrent hydration. Miltefosine may cause significant vomiting and diarrhea, and transaminase elevations may be severe enough to warrant suspension of therapy. Furthermore, although miltefosine is oral and can be taken at home, it is important to administer miltefosine in the setting of clinician supervision, since patients need to take it for a full month for it to be effective. It is important to monitor patients during their treatment phases to watch for changes in kidney and liver function values.
Conclusions: This case represents an unusual initial diagnosis of leishmaniasis, via endoscopy, and the combination of both cutaneous and visceral disease in one individual. This case also demonstrates the side effect profiles of antimicrobials used to treat leishmaniasis, and the importance of monitoring such individuals throughout their treatment to manage AKI and other pathologies that arise.
