Physioanatomic Considerations

Wanless, Ian R.

doi:10.1002/9781119251316.ch4

Cited by 4 publications

(2 citation statements)

References 140 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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. [15][16][17] The "parenchymal injury" described above are called parenchymal extinction lesions (PEL). While lesions with PEL expand and are replaced by fibrosis, surviving parenchymal tissue regenerates expansively with the consequence of regenerative nodule formation.…”

Section: Discussionmentioning

confidence: 99%

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

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 99%

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

View full text Add to dashboard Cite

show abstract

“…Dermal fibrosis is observed in the lower legs with chronic congestive heart failure. In the liver, fibrosis of parenchymal, capsular, and vascular compartments results from chronic venous outflow obstruction . Onion‐skin fibrosis of medium bile ducts may represent organization of edematous walls after chronic biliary obstruction (Wanless, unpublished observation). The study of Benias et al demonstrates that the interstitial spaces are partially lined by spindle cells, which are positive on immunohistochemical stains for CD34 and vimentin (as well as for D2‐40 in bile ducts).…”

mentioning

confidence: 99%

The Interstitial Space Takes Shape

Hytiroglou

Wanless

2019

Hepatology

Self Cite

View full text Add to dashboard Cite

In March 2018, Benias et al. published a study, entitled "Structure and distribution of an unrecognized interstitium in human tissues"(1), which received extensive news coverage. The authors utilized a variety of methods, including in vivo and ex vivo confocal laser endomicroscopy, frozen and routine histologic preparations, immunohistochemistry, electron microscopy and second harmonic generation microscopy, to provide novel information on the structure and function of the interstitial space. This article is protected by copyright. All rights reserved.

show abstract

The Role of Vascular Injury and Congestion in the Pathogenesis of Cirrhosis: the Congestive Escalator and the Parenchymal Extinction Sequence

Wanless

2020

Curr Hepatology Rep

Self Cite

View full text Add to dashboard Cite

Purpose of Review Current research into the pathogenesis of cirrhosis is largely dominated by investigations of hepatocellular injury and fibrogenesis, mostly in short-term experimental models. Cirrhosis in the human evolves for decades with histologic features that are very different from the models studied, dominated by hepatic vein obstruction and congestion. This is a clue that the mechanisms operating in the human are different from those in most animal models. Recent Findings This paper presents an updated "vascular hypothesis" with previously unpublished observations that provide a more complete understanding of the pathogenesis of chronic liver disease in the human: (1) a definition of parenchymal extinction emphasizing the importance of sinusoidal destruction, (2) analysis of the temporal evolution of parenchymal extinction lesions, (3) new data to quantify hepatic vein obstruction, (4) a "congestive escalator" hypothesis to explain how vascular obstruction occurs, beginning with sinusoidal endothelial cell injury, fluid translocation, and vascular compression by mechanics known as "compartment syndrome," (5) a "nested cone model" of hepatic vein anatomy that predisposes to compartment syndrome in the human, and (6) a proposal for the mechanism of collagen formation in response to congestion ("congestive fibrosis"). Summary The guiding principle in this model is that flow has to be vented to keep pressure gradients within the physiological range. Vascular obstruction causes tissue congestion which induces further vascular obstruction that drives a congestive escalator leading to progressive parenchymal extinction. This model may be applicable to all types of cirrhosis found in the human.

show abstract

Physioanatomic Considerations

Cited by 4 publications

References 140 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

The Interstitial Space Takes Shape

The Role of Vascular Injury and Congestion in the Pathogenesis of Cirrhosis: the Congestive Escalator and the Parenchymal Extinction Sequence

Contact Info

Product

Resources

About