The final diagnosis of granulomatous gastritis is based on morphological findings and clinical and laboratory data. Detailed analysis of the morphological features of the granulomas together with associated mucosal changes could generate more information on aetiology and pathogenesis. Biopsies from 71 patients diagnosed as having granulomatous gastritis were reviewed. Thirty-seven of these patients (52%) had Crohn's disease. In 18 patients (25%) an isolated granulomatous gastritis was diagnosed. In seven patients (10%) the final diagnosis was a foreign body reaction. Of the remaining cases, four (7%) corresponded to tumour-associated granulomas and one case each of sarcoidosis (1%), Whipple's disease (1%) and vasculitis-associated disease (1%). Two cases (3%) were unclassifiable. The granulomas were mainly found in the antrum (64% antrum only, 11% antrum and corpus, 6% transitional mucosa corpus-antrum). Granulomas were usually small. This was particularly true for those found in patients with Crohn's disease. Multiple granulomas were observed in the sarcoidosis, the Whipple's disease and vasculitis-associated cases. A pattern of chronic gastritis with atrophy was present in 95% of the biopsies (68/71 patients). Helicobacter pylori was detected in 92% of the biopsies (64/71 patients).

A cytokeratin immunohistochemical study was performed on 38 liver biopsies from cases of primary biliary cirrhosis, primary sclerosing cholangitis, extrahepatic biliary obstruction or drug-induced liver disease in order to analyse the cytoskeletal changes in detail. On paraffin sections of 27 cases, a variable number of hepatocytes were reactive with a polyclonal anti-cytokeratin antiserum that, in the normal liver, stains bile duct cells only. On cryostat sections of 23 cases, a variable number of hepatocytes were immunoreactive with a monoclonal antibody specifically directed against cytokeratin no. 7 and were most numerous in cases of long-standing cholestasis irrespective of the aetiology. In three cases of primary sclerosing cholangitis and two cases of primary biliary cirrhosis a few hepatocytes were also weakly positive with a monoclonal antibody specific for cytokeratin no. 19. Since cytokeratins no. 7 and no. 19 are, in the normal liver, restricted to bile duct cells, these results further support the concept of 'ductular metaplasia' of hepatocytes, the mechanism of which remains unclear.

The hypothesis presented in this paper suggests that, at birth, the basic lesion of congenital hepatic fibrosis corresponds to ductal plate malformation of interlobular bile ducts, resulting from faulty development, i.e. disturbance in epithelio‐mesenchymal inductive interactions. The immature bile ducts are subject to a progressive destructive cholangiopathy, resulting in a pattern of more or less advanced fetal type of biliary fibrosis. The destructive cholangiopathy may be of variable speed and duration in different patients. The renal lesions in autosomal recessive polycystic kidney disease, which is most often associated with congenital hepatic fibrosis, show a comparable pattern and evolution. The hypothesis that congenital hepatic fibrosis corresponds to a fetal type of biliary fibrosis would explain a number of disparate observations. According to this concept, congenital hepatic fibrosis does not correspond to a single clinical entity but to a broad, merging spectrum of conditions. All have in common that they represent some stage of biliary fibrosis, usually of the fetal type, rarely of the adult type, resulting from a slowly progressive, destructive cholangiopathy.

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