Pathological Analysis of the Liver of Patients with Cirrhosis and Hepatopulmonary Syndrome Reveals a Vascular Pattern of Damages

Lejealle, C.; Paradis, Valérie; Francoz, Claire; Soubrane, O.; Lebrec, Didier; Valla, Dominique‐Charles; Durand, François; Rautou, Pierre‐Emmanuel

doi:10.1016/s0168-8278(16)00734-0

Cited by 1 publication

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“…Furthermore, NO inhibition by methylene blue administration transiently improves oxygenation, whereas NG-nitro-L-arginine methylester, via iNOS inhibition, did not prove to affect hypoxemia of HPS[ 41 - 43 ]. Interestingly, a recent biopsy study comparing explanted livers from 76 patients with cirrhosis found that focal parenchyma extinction as well as vascular lesions, such as intrahepatic portal vein thrombosis, thickening or obstruction of centrilobular veins and sinusoidal proliferation, were more prevalent in those patients with HPS compared to those without, suggesting an association between liver ischemia and the production of proangiogentic and vasodilatation factors[ 44 ].…”

Section: Pathogenesis and Pathophysiologymentioning

confidence: 99%

Review article: Update on current and emergent data on hepatopulmonary syndrome

Σουλαϊδόπουλος¹,

Cholongitas²,

Giannakoulas³

et al. 2018

WJG

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Hepatopulmonary syndrome (HPS) is a frequent pulmonary complication of end-stage liver disease, characterized by impaired arterial oxygenation induced by intrapulmonary vascular dilatation. Its prevalence ranges from 4% to 47% in patients with cirrhosis due to the different diagnostic criteria applied among different studies. Nitric oxide overproduction and angiogenesis seem to be the hallmarks of a complicated pathogenetic mechanism, leading to intrapulmonary shunting and ventilation-perfusion mismatch. A classification of HPS according to the severity of hypoxemia has been suggested. Contrast-enhanced echocardiography represents the gold standard method for the detection of intrapulmonary vascular dilatations which is required, in combination with an elevated alveolar arterial gradient to set the diagnosis. The only effective treatment which can modify the syndrome’s natural history is liver transplantation. Although it is usually asymptomatic, HPS imparts a high risk of pretransplantation mortality, independently of the severity of liver disease, while there is variable data concerning survival rates after liver transplantation. The potential of myocardial involvement in the setting of HPS has also gained increasing interest in recent research. The aim of this review is to critically approach the existing literature of HPS and emphasize unclear points that remain to be unraveled by future research.

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Section: Pathogenesis and Pathophysiologymentioning

confidence: 99%