Changing Concepts of the Evolution of Chronic Hepatitis and the Role of Piecemeal Necrosis

Pópper, Hans

doi:10.1002/hep.1840030522

Cited by 25 publications

(12 citation statements)

References 31 publications

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“…The thin dissecting septa linking various structures of the liver are due to collapse of the original reticulin framework and ensuing fibrosis. Although piecemeal necrosis with gradual expansion and fibrosis of the portal triads may also lead to the development of cirrhosis (2,16,17), it may play only a minor role in the patients reported here because the duration prior to the development of cirrhosis was relatively short. This is consistent with the earlier observation of the Mayo group, that bouts of interlobular and multilobular necrosis, which lead to destruction of segments of lobules or groups of lobules, are more important in the pathogenesis of cirrhosis than piecemeal necrosis, and that cirrhosis develops directly without an intervening stage of CAH (periportal hepatitis) (1G12).…”

Section: Discussionmentioning

confidence: 81%

The prognostic significance of bridging hepatic necrosis in chronic type B hepatitis: a histopathologic study

Chen

Liaw

1988

Liver

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A histopathologic follow-up study was conducted in 207 consecutive patients to examine the prognostic significance of bridging hepatic necrosis (BHN) in chronic type B hepatitis. One hundred and eight patients showed BHN and the other 99 intralobular spotty necrosis (SN) on initial biopsy. A higher proportion of patients with BHN healed (45.4% vs 26.4%) or developed cirrhosis (18.3% vs 3%) than the patients with SN. In contrast, intralobular inflammation persisted or recurred more frequently in the SN than in the BHN group (40.4% vs 5.6%). These figures were statistically significant (P < 0.001). Alternatively, 87% of the patients who developed cirrhosis had had BHN as their initial histologic presentations. The estimated relative risk of cirrhotic progression for the BHN group compared to the SN group was 4: 1. We conclude that BHN is a paradoxical prognostic factor, either for healing, or cirrhotic progression.

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Section: Discussionmentioning

confidence: 81%

The prognostic significance of bridging hepatic necrosis in chronic type B hepatitis: a histopathologic study

Chen

Liaw

1988

Liver

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“…It has been underscored the inflammation and piecemeal necrosis of hepatic portal vein as well as the inflammation of hepatic lobules which are important indicators associated with poor prognosis. 21,22 Since then, Ishak et al reported about the modified HAI in 1995. 15 This has been used until now.…”

mentioning

confidence: 99%

Associations of Expressions of HBcAg and HBsAg with the Histologic Activity of Liver Disease and Viral Replication

Son¹,

Yoo²,

Kwon³

et al. 2008

Gut Liver

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Background/Aims: Subcellular localization of hepatitis B virus (HBV) core antigen (HBcAg) and HBV surface antigen (HBsAg) is known to be related to the activity of liver disease and the level of HBV replication. The aim of this study was to determine the correlation between histologic activity, viral replication, and the intracellular distributions of HBcAg and HBsAg. Methods: We enrolled 670 patients with chronic hepatitis B who underwent liver biopsy at Bundang CHA hospital between 1997 to 2007. The data from medical records were reviewed retrospectively. Results: The stage of fibrosis was higher (3.31±1.34 vs. 2.43±1.39, mean±SD, p＜0.01) and the grade of necroinflammatory activity was higher (9.39±3.11 vs. 6.13±3.40, p＜0.001) for the cytoplasmic expression of HBcAg (cHBcAg) than for the nuclear expression of HBcAg (nHBcAg). The serum HBV DNA level was 677.30±983.14 pg/mL in cHBcAg, 1274.46±1417.28 pg/mL in nHBcAg, 1121.01±1121.0 pg/mL in c-nHBcAg, and 229.47±678.92 pg/mL in negative (p＜0.001). HBeAg was seropositive in 74.7% of patients with cHBcAg, 90.6% in those with nHBcAg, 90.3% in those with n-cHBcAg, and 55.6% in those with negative (p＜0.001). The histologic stage and grade of hepatitis were not significantly correlated with the subcellular localization of intrahepatic HBsAg (p＞0.05). Conclusions: These observations suggest that the histologic activity of hepatitis is higher and viral replication is lower in cHBcAg positive patients than in those with nHBcAg. (Gut and Liver 2008;2:166-173)

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“…The clinical and pathological aspects of the acute exacerbation occurring in our cirrhotic patients were quite similar to those of chronic type B hepatitis (14). As the extent, frequency, severity and etiology of lobular hepatitis are determinants for progression in chronic type B hepatitis (5,24), perhaps the exacerbation occurring in cirrhosis might also play a role in the further progression or deterioration of cirrhosis. This notion is supported by the observation that all 5 patients who suffered from hepatic decompensation had experienced at least one episode of acute exacerbation.…”

Section: Years Of Follow-upmentioning

confidence: 99%

Natural course after the development of cirrhosis in patients with chronic type B hepatitis: a prospective study

Liaw

Lin

Chen

et al. 1989

Liver

152

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ABSTRACT— To examine the early stage of the natural course of liver cirrhosis, a prospective follow‐up study was conducted in a series of 76 patients with recent development of cirrhosis during the course of chronic type B hepatitis. During a mean follow‐up period of 34.4 months, 45 episodes of acute exacerbation were recorded; the majority of the episodes occurred within 2 years after entry. The calculated annual incidence of acute exacerbation was significantly higher in patients seropositive for hepatitis B e antigen (HBeAg) and/or hepatitis B virus (HBV)‐DNA (25.9%) than in those without these markers (11.9%). Three‐fourths of the acute exacerbations were attributable to the reactivation of HBV. Spontaneous HBeAg seroconversion to anti‐HBe also occurred in the early phase, but less than 30% of the events were preceded by acute exacerbation. Late hepatitis B surface antigen clearance occurred in two patients. Hepatic decompensation, esophageal variceal bleeding and hepatocellular carcinoma developed relatively late in the course of the disease with a calculated annual incidence of 2.3%, 2.3% and 2.8%, respectively. Seven patients (9.2%) died of hepatic failure or variceal bleeding, usually more than 3 years after entry. The estimated 5‐year survival rate was 80%. The results suggest that the natural events of chronic HBV infection, including exacerbation, seroconversion and its sequelae could occur after the development of cirrhosis. In addition, these events might be responsible for the clinicopathological changes and the outcomes of these cirrhotic patients.

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Changing Concepts of the Evolution of Chronic Hepatitis and the Role of Piecemeal Necrosis

Cited by 25 publications

References 31 publications

The prognostic significance of bridging hepatic necrosis in chronic type B hepatitis: a histopathologic study

The prognostic significance of bridging hepatic necrosis in chronic type B hepatitis: a histopathologic study

Associations of Expressions of HBcAg and HBsAg with the Histologic Activity of Liver Disease and Viral Replication

Natural course after the development of cirrhosis in patients with chronic type B hepatitis: a prospective study

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