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The discovery of a macroscopic lymphoproliferative lesion in the liver is an uncommon occurrence, which evokes diagnostic difficulties for the pathologist. Differentiating reactive lymphoid hyperplasia (RLH) from low-grade lymphomas may not always be possible on histologic evaluation alone. Reactive lymphoid hyperplasia should not be confused with intrahepatic lymphoid follicles, sometimes seen with well-formed active germinal centers, that can occur in autoimmune hepatitis, primary biliary cirrhosis, and chronic hepatitis B and C infection.1It is also difficult to differentiate from other rare entities, such as ectopic spleen, solitary plasmacytoma, or unicentric Castleman disease (angiofollicular hyperplasia) involving the liver.2Nonneoplastic nodules may include focal nodular hyperplasia, nodular regenerative hyperplasia, compensatory hyperplasia of the liver, pseudonodule of the liver demonstrable by angiography, partial nodular transformation, focal fatty change, cirrhotic large regenerative nodule with variable atypia, anoxic pseudolobular necrosis, intrahepatic bile duct adenoma, biliary and mesenchymal hamartoma, and mesenchymal nodular lesions, such as inflammatory pseudotumor and pseudolymphoma, pseudolipoma, peliosis hepatis, solitary necrotic nodule, and so on.3Some of these develop preferentially in noncirrhotic or cirrhotic livers, while others occur with similar prevalence in cirrhotic and noncirrhotic livers. Some occur multiply or diffusely and others singly. Inflammatory myofibroblastic tumors, or inflammatory pseudotumors or plasma cell granulomas, may manifest morphologic features similar to RLH.
Image of the Month—Diagnosis. Arch Surg. 2008;143(8):806. doi:10.1001/archsurg.143.8.806
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