Inflammation of the gallbladder is known to occur in patients with primary sclerosing cholangitis... more Inflammation of the gallbladder is known to occur in patients with primary sclerosing cholangitis (PSC). However, the histological features of this form of cholecystitis have not been adequately defined. The aim of this study was to compare the inflammatory lesions of PSC-associated cholecystitis with those present in other cholecystopathies. The cases consisted of 11 gallbladders from patients with PSC who underwent liver transplantation. As controls, gallbladders from liver transplant patients with primary biliary cirrhosis (n = 4) and other chronic nonbiliary hepatopathies (n = 8), and 13 cholecystectomies from patients with chronic cholecystitis with (n = 10) and without (n = 3) lithiasis, were studied. The following histological features were tabulated on coded slides: presence, depth of involvement, and distribution of the inflammatory infiltrate, predominant cell type, presence of lymphoid aggregates, epithelial damage, metaplastic changes (pyloric or intestinal), fibrosis, smooth muscle hypertrophy, and presence of Rokitansky-Aschoff sinuses. At variance with the wide range of histological abnormalities present in other forms of chronic cholecystitis, most PSC-related cholecystitis showed a diffuse infiltrate (6 of 11) rich in plasma cells (6 of 11) predominantly confined to the lamina propria (9 of 11). The combination of these three features was present exclusively in PSC (5 of 11 PSC cholecystitis compared with 0 of 25 controls; P = .001). In conclusion, this study suggests that a characteristic form of cholecystitis may develop in patients with PSC.
Inflammation of the gallbladder is known to occur in patients with primary sclerosing cholangitis... more Inflammation of the gallbladder is known to occur in patients with primary sclerosing cholangitis (PSC). However, the histological features of this form of cholecystitis have not been adequately defined. The aim of this study was to compare the inflammatory lesions of PSC-associated cholecystitis with those present in other cholecystopathies. The cases consisted of 11 gallbladders from patients with PSC who underwent liver transplantation. As controls, gallbladders from liver transplant patients with primary biliary cirrhosis (n = 4) and other chronic nonbiliary hepatopathies (n = 8), and 13 cholecystectomies from patients with chronic cholecystitis with (n = 10) and without (n = 3) lithiasis, were studied. The following histological features were tabulated on coded slides: presence, depth of involvement, and distribution of the inflammatory infiltrate, predominant cell type, presence of lymphoid aggregates, epithelial damage, metaplastic changes (pyloric or intestinal), fibrosis, smooth muscle hypertrophy, and presence of Rokitansky-Aschoff sinuses. At variance with the wide range of histological abnormalities present in other forms of chronic cholecystitis, most PSC-related cholecystitis showed a diffuse infiltrate (6 of 11) rich in plasma cells (6 of 11) predominantly confined to the lamina propria (9 of 11). The combination of these three features was present exclusively in PSC (5 of 11 PSC cholecystitis compared with 0 of 25 controls; P = .001). In conclusion, this study suggests that a characteristic form of cholecystitis may develop in patients with PSC.
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