SUN-740 Hepatitis C associated High Bone Mass Presenting with Bone Pain, Edentulism, and Neuropathy: A Rare Case Report

Abstract Disclosure: S.S. Dahir: None. C.R. Lichtenfeld: None. L.R. Rehm: None. L.T. Drake: None. K.M. Dahir: Alexion Pharmaceuticals, Inc., Ultragenyx. Background: Hepatitis C is an infection produced by a single-stranded RNA virus characterized by fatigue, nausea, upper right quadrant abdominal discomfort, and in acute cases, liver disease. Studies also link hepatitis C infections to high bone mass. Pathologic high bone mass disorders arise from dysregulated osteoclastic bone resorption and/or osteoblastic bone formation. Inherited osteopetrosis presents variably, with severe AR forms and milder AD cases. AD osteopetrosis, commonly caused by heterozygous CLCN7 mutations, impairs osteoclast function and bone resorption. Rarely, LRP5 gain-of-function mutations in the Wnt signaling pathway cause high bone mass. Clinical symptoms range from asymptomatic to severe complications like osteomyelitis, fractures, and bone marrow or organ involvement. Rarely, disorders of high bone mass are acquired. Here, we report a case of adult-onset high bone mass associated with hepatitis C. Case Description: A 53-year-old man with a history of treated hepatitis C presented for evaluation of generalized bone pain, fever, night sweats, and 30-pound unintentional weight loss and was found to have increased bone mass on an abdominal CT scan. He had a history of progressive loss of all adult teeth in his mid-40s, necessitating complete dentures, without a history of tori formation or dental encasement. He denied fractures, visual or auditory impairment, and had no family history of osteopetrosis. Imaging demonstrated increased bone density. Bone marrow biopsy showed hypercellular marrow with thickened trabeculae and increased cement lines. High bone mass panel genetic testing was negative for pathogenic variants or deletions. Labs showed no recurrence of hepatitis C. Apart from elevated bone resorption markers, labs were otherwise normal. DXA T-scores were +11.5 total spine; +6.6 in total femur: Imaging showed diffusely increased bone density with skull sparing. He was treated unsuccessfully with calcitonin. Conclusions: A broad differential diagnosis exists for acquired high bone mass. Several hypotheses surround the mechanism by which high bone mass is induced by hepatitis C, including that the hepatitis C virus may alter insulin-like growth factors and corresponding proteins leading to an increase in bone development. Diagnostic clues for earlier detection and treatment include obtaining a thorough history of prior disease exposures and a family history of bone diseases. Additionally, high bone turnover markers and high bone mass that specifically excludes the skull are key components to recognizing hepatitis C-associated high bone mass. Presentation: Sunday, July 13, 2025