New aspects of piecemeal necrosis

Desmet, V J

doi:10.1007/978-94-009-4904-1_21

Cited by 6 publications

(1 citation statement)

References 83 publications

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“…The immunohistochemical analysis of the various lymphocyte subsets comprising the portal and zone 1 infiltrate in chronic HBV infection has been reported extensively (3,(6)(7)(8)(9)(10)(11)(12). All these studies have demonstrated the predominance of OKTs+ suppressor/cytotoxic T lymphocytes in these inflammatory lesions.…”

Section: Discussionmentioning

confidence: 99%

In situ characterisation of the (peri)portal inflammatory infiltrate in acute hepatitis A

Sciot

Wolf‐Peeters

Desmet

1986

Liver

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ABSTRACT— The portal and acinar zone 1 (periportal) inflammatory infiltrate in acute hepatitis A (HA) strongly resembles piecemeal necrosis (PMN) in chronic hepatitis B (HB). The latter infiltrate has been characterized in detail previously, and a predominance of suppressor/cytotoxic T cells has been demonstrated. For comparison we analyzed the infiltrate in acute HA in three liver biopsies, applying a broad panel of monospecific and monoclonal antibodies. In two cases, helper/inducer T cells surrounded by B lymphoid cells represented the main lymphoid subset in all portal areas. In the third liver biopsy, a case of acute HA superimposed on a pre‐existing chronic HB, the cellular composition of the inflammatory infiltrate varied from one portal tract to another. Despite the morphological resemblance between the inflammatory infiltrate in acute HA and PMN in chronic HB, a clear‐cut difference in the composition of both infiltrates is obvious from our results. By virtue of the presence of numerous suppressor/cytotoxic T cells, PMN in chronic HB represents the morphological expression of a cellular immune response, whereas the predominance of helper/inducer T cells, admixed with B cells and plasma cells in acute HA represents the morphological expression of a humoral immune response.

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Section: Discussionmentioning

confidence: 99%

In situ characterisation of the (peri)portal inflammatory infiltrate in acute hepatitis A

Sciot

Wolf‐Peeters

Desmet

1986

Liver

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The nature of cell death in piecemeal necrosis: Is order emerging from chaos?

Powell

1987

Hepatology

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Electron microscopic studies of acidophilic or Councilman‐like bodies in the liver show that they are manifestations of apoptosis. The morphology and biochemistry of apoptosis suggest a process of active cellular self‐destruction rather than degeneration. The incidence of apoptosis indicates that it is normally involved in the regulation of organ size and, in addition, may be triggered by specific pathological stimuli. Cell death produced in vitro by various types of cell‐mediated immune injury occurs by apoptosis The occurence of apoptosis in hepatic disease is illustrated and discussed. That it constitutes the only clearly identifiable mode of cell death in most types of acute and chronic hepatitis and in primary biliary cirrhosis is in accord with current concepts of the pathogenesis of these conditions. Furthermore, the morphological features of apoptosis may explain long‐standing enigmas in the histology of hepatitis–‐the cryptic nature of the cell death in piecemeal “necrosis” and the apparent drop‐out of large numbers of hepatocytes in many cases of acute hepatitis without overt evidence of necrosis. Apoptosis represents rapid budding of a cell to form numerous globules, the largest of which appear to be acidophilic bodies. All apoptotic fragments are quickly removed by adjacent cells without evident inflammation, permitting the process to occur inconspicuously.

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Acute Viral Hepatitis Hepatitis B

Desmet

1989

Modern Concepts of Acute and Chronic Hepatitis

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New aspects of piecemeal necrosis

Cited by 6 publications

References 83 publications

In situ characterisation of the (peri)portal inflammatory infiltrate in acute hepatitis A

In situ characterisation of the (peri)portal inflammatory infiltrate in acute hepatitis A

The nature of cell death in piecemeal necrosis: Is order emerging from chaos?

Acute Viral Hepatitis Hepatitis B

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