Title : Disseminated histoplasmosis presenting as isolated acute liver injury: A case report
Abstract:
The CNS, skin, and adrenal glands. We present a case of disseminated histoplasmosis in an immunocompromised host presenting with isolated acute liver injury.
The various manifestations of disseminated histoplasmosis can involve nearly any organ system, including a 59-year-old woman from Minnesota with a history of pulmonary sarcoidosis on methotrexate and infliximab presented with a 10-day history of fevers, myalgias, and generalized weakness.
Symptoms were associated with nausea and small volume emesis, without abdominal pain, constipation, or diarrhea. A week prior to presentation, she was evaluated in the urgent care setting with laboratory work demonstrating AST 106 IU/L, ALT 105 IU/L, total bilirubin 1 mg/dl, alkaline phosphatase 203 IU/L. Hepatic biochemistries had never previously been outside of normal range. She was initiated on a course of doxycycline for suspected sinusitis and continued on acetaminophen for symptom management, however, symptoms continued to worsen.
On presentation, she was febrile to 39.2oC, in moderate distress with marked nausea and dry heaves, mild conjunctival icterus, and unremarkable abdominal exam. Lab work revealed mixed hepatocellular and cholestatic liver injury with ALT 599 IU/L, AST 608 IU/L, total bilirubin of 2.3 mg/dl, ALP 585 IU/L, and INR 1.3.CT chest/abdomen/pelvis demonstrated splenomegaly along with stable features of pulmonary sarcoidosis. Right upper quadrant ultrasound revealed a normal-appearing liver with patent hepatic vasculature.
Prior medications were held due to concern for drug-induced liver injury. In the context of her immunosuppression, a broad infectious and autoimmune workup was performed, ultimately revealing positive histoplasmosis urine antigen further confirmed by consistent Histoplasma antigen and antibody positivity in the blood.Ferritin was also measured and found to be over 36,000 mcg/L, raising suspicion for Histoplasmosis-induced hemophagocytic lymphohistiocytosis. She clinically improved on IV amphotericin B and was transitioned to long-term itraconazole after two weeks.
