Treatment of fibrosing cholestatic hepatitis with lamivudine Tak–Mao Chan*, Pui–Chee Wu‡, Fu–Keung Li*, Ching–Lung Lai*, Ignatius K.P. Cheng*, Kar–Neng Lai* Gastroenterology Volume 115, Issue 1, Pages 177-181 (July 1998) DOI: 10.1016/S0016-5085(98)70380-4 Copyright © 1998 American Gastroenterological Association Terms and Conditions
Fig. 1 Photomicrograph of liver biopsy specimen showing features of fibrosing cholestatic hepatitis characterized by marked hepatocyte balloon degeneration, focal hepatocyte loss, bile stasis, and pericellular fibrosis (H&E; original magnification 175×). Gastroenterology 1998 115, 177-181DOI: (10.1016/S0016-5085(98)70380-4) Copyright © 1998 American Gastroenterological Association Terms and Conditions
Fig. 2 Photomicrograph of liver biopsy specimen showing abundant HBcAg in both nuclei and cytoplasm by immunohistochemical staining (H&E; original magnification 175×). Gastroenterology 1998 115, 177-181DOI: (10.1016/S0016-5085(98)70380-4) Copyright © 1998 American Gastroenterological Association Terms and Conditions
Fig. 3 Photomicrograph of liver biopsy specimen showing HBsAg in the majority of hepatocytes by immunohistochemical staining (H&E; original magnification 175×). Gastroenterology 1998 115, 177-181DOI: (10.1016/S0016-5085(98)70380-4) Copyright © 1998 American Gastroenterological Association Terms and Conditions
Fig. 4 Diagram showing the serial levels of serum HBV DNA (□) and ALT (♢) and prothrombin time (○) in the patient. Lamivudine therapy was followed by a rapid reduction of HBV DNA and more gradual improvements in transaminasemia and liver function, the latter depicted by normalization of prothrombin time. Gastroenterology 1998 115, 177-181DOI: (10.1016/S0016-5085(98)70380-4) Copyright © 1998 American Gastroenterological Association Terms and Conditions