Sarcoidosis is a multisystemic inflammatory disease characterized by heterogeneous clinical manifestations and granuloma formation in the organs involved. Diagnosing systemic sarcoidosis requires a multidisciplinary approach and the exclusion of other pathologies; after diagnosis, organ involvement and disease extent are further assessed. Genetic factors influence not only the risk of sarcoidosis development but also the disease course, which is highly variable and unpredictable. The clinical course of systemic sarcoidosis is highly variable, ranging from a self-limited disease that does not require long-term therapy to a rapidly progressive, symptomatic disease requiring immunosuppression. The liver is a commonly affected organ in sarcoidosis; while most patients with systemic sarcoidosis have hepatic granulomas, a minority will experience significant liver disease. In hepatic sarcoidosis, granulomas can cause a cholestatic liver injury, exemplified by elevated serum alkaline phosphatase and gamma‐glutamyl transferase, though neither is pathognomonic and there are no hepatic sarcoid-specific biomarkers to monitor disease activity. Patients with ongoing hepatic inflammation require the initiation of the disease-modifying agents to prevent fibrosis and decompensation. This review article summarizes the existing literature on etiology, risk factors, pathogenesis, clinical features, and the management of hepatic sarcoid.
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Weinberg et al. (2025) studied this question.
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