A Rare Case of Hepatic Sarcoidosis Caused By Hepatitis B Virus and Treatment-Induced Opportunistic Infection

The association between hepatitis C virus (HCV) and sarcoidosis is well-documented, but in this case report, we shall discuss an interesting association between hepatitis B virus (HBV) and sarcoidosis, presenting with non-specific symptoms and confirmed with liver biopsy and immunologic markers. The case was complicated by treatment with immunosuppressive medication that led to colonic histoplasmosis. A 58-year-old woman, from the western part of India, who has a past medical history of HBV-related cirrhosis of the liver for six months, hypertension, and type 2 diabetes presented to our clinic with bilateral pedal edema, anorexia, and mild epigastric discomfort. She had been on entecavir for the last six months. The patient denied any significant surgical, social, or family history. Abdominal ultrasonography revealed hepatosplenomegaly and mesenteric lymphadenopathy. She had a 21.3kPa liver stiffness on elastography and an HBV deoxyribonucleic acid (DNA) level of 89 copies/ml. Liver biopsy showed multiple noncaseating granulomas consisting of Langerhans cells in the parenchyma and portal tract, associated with moderate inflammation. A chest computed tomography (CT) scan showed upper and middle lobe fibrosis of the lungs; this diagnosis was further confirmed with elevated angiotensin-converting enzymes. She was started on prednisone; within a period of three months, she experienced weight loss, diarrhea, and fever. Colonoscopy was done after an abdomen CT showed mural thickening of the ascending colon and terminal ileum, which on biopsy was confirmed as histoplasmosis. Prednisone was stopped, and the patient was treated with hydroxychloroquine and amphotericin B, followed by itraconazole. The patient improved symptomatically, and repeated colonoscopy findings were normal. Studies are scarce to prove the association between hepatitis B and sarcoidosis; however, we reasonably hypothesized that the alterations in the pool of cytokines and immune cells caused by HBV infection might have had a vicious influence on immune regulation and could be a trigger for granuloma. Further studies can impact the future to provide for a better understanding of the pathophysiology of sarcoidosis, HBV correlation, and treatment options.