tion. The patients all had hepatic and systemic sarcoidosis. The Sarcoidosis often involves the liver with mild elevation of main clinical and morphological features are summarized in Table serum enzymes and granulomas histologically. Rarely, chronic 1. Tissue blocks were obtained from the peripheral parenchyma of cholestasis, portal hypertension, cirrhosis, or nodular hyper-both lobes, as well as from all major vessels and ducts. Sections plasia may be found. The pathogenesis of the portal hyperten-were stained with hematoxylin-eosin and elastic trichrome stains. sion and of the cirrhosis are not understood, in part because Selected blocks were stained with orcein, periodic acid-Schiff-dialarge samples of tissue have seldom been described. We de-stase, iron, and reticulin. Portal and hepatic veins were classified scribe the clinical and anatomic findings of four patients with as large if the outside diameter was larger than 3 mm, medium if sarcoid liver disease in whom the whole livers were available it was between 0.2 and 3 mm, and small if it was smaller than 0.2 mm. Granulomatous involvement was graded 0 through 3. Grade for examination. One patient had cirrhosis, one had diffuse and focal fibrosis were caused by ischemia secondary to pri-before death. A lung biopsy revealed sarcoid-type granulomas, and mary granulomatous phlebitis of portal and hepatic veins. The steroid therapy was begun. She died suddenly at home. portal hypertension in two patients was likely secondary to At autopsy, granulomas were found in many organs, including portal vein thrombosis, because cirrhosis was absent at the liver, spleen, lungs, heart, and lymph nodes. The liver parenchyma onset of variceal bleeding. (HEPATOLOGY 1997;26:554-560.) was grossly normal except for several localized regions of parenchymal extinction (Fig. 1). In grossly normal regions, granulomas were rarely seen, and most portal and hepatic veins were normal. In did not allow analysis of the form or histogenesis of sarcoid-involved, the medium portal or hepatic veins usually had lumina related liver disease. In the present study of four whole livers, that were compromised by intimal fibrosis, and small veins usually we show that granulomatous phlebitis of portal and hepatic had lumina that were obliterated by granuloma(s) or by fibrous veins may cause multifocal ischemia, leading to parenchymal tissue (Fig. 1). The granulomas in the large and medium hepatic extinction and cirrhosis.veins could be seen to involve intima, media, and adventitia. DuctsIt has been speculated that portal hypertension occurs as of all sizes were usually normal.Case 2. A 35-year-old black man with a 1-year history of congesa complication of cirrhosis or as a result of portal granulomas tive heart failure and dilated cardiomyopathy died suddenly.compressing and restricting blood flow through small portal At autopsy the liver showed moderate widespread chronic passive veins. [1][2][3][4][5][9][10][11][12] In our study, clinical portal hypertension was congestion with patchy sinusoidal...