Physioanatomic Considerations

Wanless, Ian R.

doi:10.1002/9781119950509.ch5

Cited by 6 publications

(5 citation statements)

References 150 publications

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“…The findings from the current study, which focused on chronic viral hepatitis, are not consistent with the view of pathogenesis LC posited by Wanless et al. , which asserts that the obstruction of the hepatic terminal venules and hepatic vein and accompanying congestion play an important role in parenchymal injury throughout the whole process from an early chronic liver disease to LC . The “parenchymal injury” described above are called parenchymal extinction lesions (PEL).…”

Section: Discussioncontrasting

confidence: 94%

Histological reassessment of the role of bridging fibrosis in the angioarchitectural features associated with lobular distortion of the liver in chronic viral hepatitis

Hano

Takasaki

Endo

et al. 2015

Hepatology Research

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Aim:To reassess the role of bridging fibrosis in the lobular distortion of the liver from an angioarchitectural aspect.Methods: Two tissue samples obtained from surgically resected livers with chronic hepatitis and one obtained from an autopsy case with chronic hepatitis were used for the threedimensional observation of angioarchitecture by histological reconstruction.Results: Samples showed bridging fibrosis with various degrees of severity, without cirrhotic changes. Two different types of portal-portal bridging fibrosis were found. In our samples, the type that developed in the bifurcation region of the portal tracts was more common than the type observed between the distal portions originating from different parent portal tracts. The angioarchitecture tended to be generally maintained in these lesions. Concerning portal-central bridging fibrosis, two types were observed. One type developed in the lesion with partial paucity of the third-step portal branches in the portal tract at a relatively early stage of chronic hepatitis. The other type developed in an advanced lesion with a complete loss of the normal angioarchitecture of the parenchymal portion of the portal veins. The former was likely developed after largescale necrosis, such as bridging necrosis, while the latter was presumed to be attributable to portal vein damage associated with long standing chronic inflammation. Conclusion:As has been previously noted regarding lobular angioarchitecture, portal-central bridging fibrosis clearly affects the lobular structure of the liver more than portal-portal bridging fibrosis. Therefore, portal vein damage may be a critical event in the eventual distortion of the lobular structure.

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Section: Discussioncontrasting

confidence: 94%

Histological reassessment of the role of bridging fibrosis in the angioarchitectural features associated with lobular distortion of the liver in chronic viral hepatitis

Hano

Takasaki

Endo

et al. 2015

Hepatology Research

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“…A focus of injury may heal by fibrosis. Advanced fibrosis occurs with the accumulation of many discrete lesions of parenchymal injury that heal by scarring 27 …”

Section: Discussionmentioning

confidence: 99%

Combining semiquantitative measures of fibrosis and qualitative features of parenchymal remodelling to identify fibrosis regression in hepatitis C: a multiple biopsy study

et al. 2012

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“…These factors include the liver’s dual blood supply, its fenestrated sinusoidal complex, secretion of soluble major histocompatibility complex antigens, and its ability to absorb antibody (Figure 2). In contrast to other solid organs, the microvascular network of the liver is sinusoidal and lined by fenestrated endothelium with a scant underlying basement membrane (Figure 2, g)[23]. This sinusoidal network is in contrast to other organs that not only have a single afferent blood supply, but also have standard capillary microvasculature that results in ischemia when occluded by complement activated immune complexes.…”

Section: The Liver Is An Immunologically Privileged Organmentioning

confidence: 99%

Revisiting liver’s role in transplant alloimmunity

Abrol¹,

Jadlowiec

Taner³

2019

WJG

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The transplanted liver can modulate the recipient immune system to induce tolerance after transplantation. This phenomenon was observed nearly five decades ago. Subsequently, the liver’s role in multivisceral transplantation was recognized, as it has a protective role in preventing rejection of simultaneously transplanted solid organs such as kidney and heart. The liver has a unique architecture and is home to many cells involved in immunity and inflammation. After transplantation, these cells migrate from the liver into the recipient. Early studies identified chimerism as an important mechanism by which the liver modulates the human immune system. Recent studies on human T-cell subtypes, cytokine expression, and gene expression in the allograft have expanded our knowledge on the potential mechanisms underlying immunomodulation. In this article, we discuss the privileged state of liver transplantation compared to other solid organ transplantation, the liver allograft’s role in multivisceral transplantation, various cells in the liver involved in immune responses, and the potential mechanisms underlying immunomodulation of host alloresponses.

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Physioanatomic Considerations

Cited by 6 publications

References 150 publications

Histological reassessment of the role of bridging fibrosis in the angioarchitectural features associated with lobular distortion of the liver in chronic viral hepatitis

Histological reassessment of the role of bridging fibrosis in the angioarchitectural features associated with lobular distortion of the liver in chronic viral hepatitis

Combining semiquantitative measures of fibrosis and qualitative features of parenchymal remodelling to identify fibrosis regression in hepatitis C: a multiple biopsy study

Revisiting liver’s role in transplant alloimmunity

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