Abstract

INTRODUCTION: Peliosis hepatis is characterized as a vascular condition in which blood-filled cystic cavities are distributed diffusely throughout the liver parenchyma. The condition is rare, with the pathogenesis poorly described in the literature. It is believed that this disease is secondary to an underlying malignancy, immune disorder, infection, or a drug/toxin mediated effect. We present a case of a patient diagnosed with peliosis hepatis complicated by the development of acute liver failure. CASE DESCRIPTION/METHODS: A 71-year-old man with a past medical history of coronary artery disease, hypertension, hyperlipidemia, and prostate cancer treated with radiosurgery was admitted to our hospital with symptoms of fatigue, dysphagia and anorexia. He was in his usual state of health until four weeks prior to admission, when he began experiencing early satiety with poor oral intake, nausea, diarrhea, right upper quadrant abdominal pain, and weight loss. He was evaluated by his primary care provider who prescribed him a five day course of levofloxacin with no resolution of symptoms. Upon admission, labs were notable for leukocytosis and a mild transaminitis. Imaging revealed hepatomegaly with hepatic hemangiomatosis and splenic hemangiomas. A liver MRI was performed which returned consistent with diffuse hepatic peliosis with splenic peliosis. He underwent an intensive hematologic/oncologic, rheumatologic, and infectious workup that was significant for a positive quantiferon TB gold and he was subsequently started on empiric TB therapy. Synthetic liver function continued to worsen consistent with acute liver injury, which progressed to acute liver failure. The patient continued to decline and ultimately passed from multi-organ system failure. DISCUSSION: The majority of patients with peliosis hepatis will present asymptomatically and are found incidentally, while a subset of patients will present with abdominal pain or stigmata of liver disease. A liver biopsy is useful for diagnosis and is used in the context of the clinical picture, laboratory data, and imaging findings. Once the underlying offending etiology is recognized and appropriately treated, symptoms can improve and regression of the hepatic lesions can be seen. Our patient is unique in that his presentation was atypical and rapid, and a true causal etiology was never concretely identified, leading to progression to acute hepatic failure.

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