The classification of chronic hepatitis distinguishing benign chronic persistent hepatitis from severe chronic active hepatitis was constructed without knowledge of well-defined aetiological factors. Better understanding of the different hepatitis-viruses has shed new light on this subject. Chronic viral hepatitis B and C each show typical histological patterns. The validity of the conventional classification has been evaluated by a comparative study of chronic viral hepatitis B and C. 130 biopsies from 110 patients with chronic hepatitis C (CH-C) proven serologically by antibodies (second generation testing) were compared with 105 biopsies from 73 patients with chronic hepatitis B (CH-B). These were scored semi-quantatively. In CH-C, lymphoid follicles and/or aggregates were found in 88.5%, fatty degeneration in 51%, bile duct lesions in 46.2%, and Mallory body-like material in the hepatocytes in 9.2%. The portal lymphocytic infiltration generally predominated over the necro-inflammatory lesions of the parenchyma. Chronic persistent hepatitis (defined by the presence of portal hepatitis) was present exclusively in CH-C. Chronic lobular hepatitis was found exclusively in CH-B. We conclude that the histological criteria described for CH-C are highly suggestive of the diagnosis, that the artificial subdivision of chronic hepatitis into CPH and CAH is obsolete and that the histological assessment of chronic hepatitis should consist of a grading of inflammatory activity (minimal, mild, moderate, severe) and staging of fibrosis (extent of distortion of architecture). The final diagnosis should be based on the demonstration of the aetiological agent.

We analysed the value of the expression of beta 1,6 branching of asparagine-linked oligosaccharide chains and polysialic acid of the neural cell adhesion molecule (NCAM) in predicting malignant behaviour in human insulinomas, as these glycoconjugates have been associated with invasive growth and metastatic potential. Fifty-three insulinomas from patients with well-documented clinical and follow-up data were investigated. Lectin histochemical staining for beta 1,6 branches revealed that 11 (74%) of the 15 malignant insulinomas stained more strongly than normal beta cells. However, in as many as 23 (63.1%) of the 38 benign insulinomas with a disease-free follow up for 4-18 years (average 8 years), a staining intensity equivalent to that of malignant tumours was found. Two (13%) of the malignant insulinomas and 1 of the 4 liver metastases studied were unstained. None of the 53 insulinomas (and the rat RIN insulinoma) re-expressed polysialic acid as demonstrated by immunohistochemistry and Western blotting with the monoclonal antibody 735. Therefore, histochemical staining for beta 1,6 branches and immunohistochemistry for polysialic acid are unlikely to be of value as prognostic indicators for patients with insulinomas.

In the endocrine pancreas, chromogranins A and B as well as secretoneurin (a biologically active peptide processed endoproteolytically from secretogranin II) are most intensely expressed in alpha (glucagon) cells. We examined whether the functional status of neoplastic and nonneoplastic human alpha cells is reflected in the expression patterns of chromogranins/secretogranins. Neoplastic alpha cells were analysed immunocytochemically in six functioning glucagonomas and 37 nonfunctioning neuroendocrine tumours (29 with alpha cells) for their immunoreactivity to chromogranin A and B, as well as secretoneurin. There was no difference in the staining intensity for either peptide between glucagonomas and nonfunctioning, alpha cell containing tumours. Nonneoplastic alpha cells from patients with a functioning glucagonoma showed a decreased glucagon immunoreactivity, whereas the expression of chromogranin A (but not chromogranin B and secretoneurin) was as intense as in alpha cells not associated with glucagonoma syndrome. These results suggest that the expression of chromogranins/secretogranins in neoplastic alpha cells of the pancreas may be independently regulated from the cells' functional status. In nonneoplastic alpha cells there seems to be an association between glucagon production and chromogranin B and secretoneurin expression.

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