S2567 Hepatic Manifestations of Disseminated Histoplasmosis

Abstract

INTRODUCTION: Disseminated histoplasmosis is a fungal infection that can be severe in gastroenterology patients with weakened immune systems such as solid organ transplant patients and those on immunosuppression – corticosteroids or TNF-inhibitors. Treatment includes anti-fungal medication such as Itraconazole and amphotericin B. Here we present two patients with history of liver disease and disseminated histoplasmosis. CASE DESCRIPTION/METHODS: We have a 59-year-old male who presented with donor-derived disseminated histoplasmosis one month following simultaneous liver kidney transplant, after BAL cultures confirmed that donor’s lungs were positive for histoplasmosis. Patient had urine histoplasma antigen (Histo Ag) greater than 19 ng/mL. He was started on Itraconazole, recommended for a 12-month course; however, patient discontinued use after 4 months, at which point Histo Ag was 10.6 ng/mL. Two months after discontinuation, patient presented with a neck mass, positive for fungal yeast consistent with histoplasmosis. He was started on Isavuconazole. Histo Ag levels are decreasing steadily over 2.5-year period from 5.4 to less than 0.4 ng/mL. We have a 42-year-old male with history of ulcerative colitis (UC) who presented with disseminated histoplasmosis. For UC management, patient had received three infusions of Entyvio prior to discontinuation due to pruritus and blood pressure lability; and was subsequently started on methylprednisolone. After two weeks, patient presented with disseminated histoplasmosis, confirmed with liver biopsy showing lobular granulomas with intracellular budding yeast and Histo Ag of 5.9 ng/mL. He had positive serum 1,3-beta-d glucan and elevated alkaline phosphatase. Methylprednisolone was discontinued. Following 8 infusions of amphotericin B, he was transitioned to Itraconazole for 12 months. DISCUSSION: There is an increased risk of disseminated histoplasmosis in immunosuppressed patients – following a solid organ transplant or with corticosteroid medication, as seen in our two patients. Such patients are more susceptible to developing progressive forms of the infection, which can be severe and sometimes fatal if not treated. As these cases show, it is important to detect disseminated histoplasmosis early and to continue to monitor Histo Ag levels throughout treatment course to ensure infection is not progressing. Further studies may show how disseminated histoplasmosis can progress based on cause of infection and treatment course.