Chronic viral hepatitis B and C: an argument against the conventional classification of chronic hepatitis

Abstract

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for CH-C are highly suggestive of the diagnosis, that the artificial subdivision of chronic hepatitis into CPH and CAH is obsolete and that the histological assessment of chronic hepatitis should consist of a grading of inflammatory activity (minimal, mild, moderate, severe) and staging of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.

Liver iron and fibrosis during long‐term treatment with deferiprone in Swiss thalassaemic patients

“…Hepatic iron measurements by SQUID in mg/g wet weight were expressed in terms of mg/g dry weight, using an approximative conversion factor of 3.33. Grading of hepatic fibrosis was performed using the method of Schmid et al (1994 ): 0, none; 1, mild, portal fibrosis only; 2, portal fibrosis + incomplete septa; 3, septa bridging portal–portal; 4, septa bridging portal–central and/or focal incomplete cirrhosis; 5, diffuse incomplete or focal complete cirrhosis; 6, diffuse complete cirrhosis.…”

TUNEL-positive hepatocytes in alcoholic liver disease

“…Ballooning degeneration of hepatocytes, Mallory bodies (MB), granulocyte reaction around Mallory-body-containing hepatocytes and megamitochondria were recorded as either present or absent. Hepatic fibrosis was evaluated as previously described [28], with some modifications [45]. Perisinusoidal fibrosis in the pericentral (perivenular) acinar zone was registered as either present or absent.…”

“…Perisinusoidal fibrosis in the pericentral (perivenular) acinar zone was registered as either present or absent. For grading of portal tract and septal fibrosis, the system recently proposed by Schmid et al [45] was employed (grade 0, none; grade 1, mild, only portal tract fibrosis; grade 2, portal tract fibrosis plus incomplete septa; grade 3, fibrous septa bridging portal-portal; grade 4; fibrous septa bridging portal-central, and/or focal incomplete cirrhosis; grade 5, diffuse incomplete and/or focal complete cirrhosis; and grade 6, diffuse complete cirrhosis).…”

Quantitative assessment of fibrosis and steatosis in liver biopsies from patients with chronic hepatitis C

“…3 Hepatic fibrosis is one of the most important features of chronic hepatitis C. The accurate assessment of hepatic fibrosis is important to study the natural history and the prognosis of patients with chronic hepatitis C. Fibrosis is also seen in patients with alcoholic liver disease (ALD) [4][5][6] and other forms of nonalcoholic fatty liver disease (NAFLD). [7][8][9] Steatosis is another morphological feature that can be seen in patients with chronic hepatitis C, [10][11][12][13] ALD, 5 6 and NAFLD. 7 8 14 There are several methods for assessing hepatic fibrosis and the progression of fibrogenesis in clinical practice.…”