Hepatopulmonary syndrome: More than just a matter of tone?

Fallon, Michael B.

doi:10.1002/hep.22198

Cited by 14 publications

(10 citation statements)

References 22 publications

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“…Moreover, in severely hypoxaemic patients with HPS, the concentration of exhaled NO is high [18]. Finally, administration of antagonists of NO synthesis, such as methylene blue or others, can enhance oxygenation [19][20][21][22][23].…”

Section: Case Reportmentioning

confidence: 99%

Hepatopulmonary syndrome following portopulmonary hypertension

Ioachimescu

Stoller³

2007

Eur Respir J

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Portopulmonary hypertension (PPHTN) and hepatopulmonary syndrome (HPS) are distinct clinical entities that may accompany liver disease.While PPHTN and HPS have been infrequently described as occurring in the same patient, to the present authors' knowledge, the order of occurrence has always been the initial onset of HPS, with pulmonary hypertension developing either concurrently or subsequently. In some instances, liver transplantation has been undertaken for HPS, followed by resolution of the HPS and subsequent development of pulmonary hypertension.The current case study presents a patient with hepatitis C-related cirrhosis in whom PPTHN developed initially, followed 2 yrs later by the development of the HPS.The current authors speculate that progressive imbalance in favour of endogenous vasodilators over vasoconstrictive factors led to normalisation of the pulmonary artery pressures.

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Section: Case Reportmentioning

confidence: 99%

Hepatopulmonary syndrome following portopulmonary hypertension

Ioachimescu

Stoller³

2007

Eur Respir J

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“…Chronic liver disease leads to altered vascular remodeling and angiogenesis in the hepatic, splanchnic, and systemic circulations . Hepatopulmonary syndrome (HPS) is one such vascular complication that develops when liver cirrhosis results in abnormal arterial gas exchange because of alveolar microvascular dilation and remodeling/angiogenesis . The occurrence of HPS ranges from 5% to 32% in cirrhotic patients evaluated for liver transplantation.…”

Section: Introductionmentioning

confidence: 99%

Role of splenic reservoir monocytes in pulmonary vascular monocyte accumulation in experimental hepatopulmonary syndrome

Zhang

et al. 2016

J of Gastro and Hepatol

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Background and AimPulmonary monocyte infiltration plays a significant role in the development of angiogenesis in experimental hepatopulmonary syndrome (HPS) after common bile duct ligation (CBDL). Hepatic monocytes are also increased after CBDL, but the origins remain unclear. Splenic reservoir monocytes have been identified as a major source of monocytes that accumulate in injured tissues. Whether splenic monocytes contribute to monocyte alterations after CBDL is unknown. This study evaluates monocyte distributions and assesses effects of splenectomy on monocyte levels and pulmonary vascular and hepatic abnormalities in experimental HPS.MethodsSplenectomy was performed in CBDL animals. Monocyte levels in different tissues and circulation were assessed with CD68. Pulmonary alterations of HPS were evaluated with vascular endothelial growth factor‐A (VEGF‐A) levels, angiogenesis, and alveolar–arterial oxygen gradient (AaPO2). Liver abnormalities were evaluated with fibrosis (Sirius red), bile duct proliferation (CK‐19), and enzymatic changes.ResultsMonocyte levels increased in the lung and liver after CBDL and were accompanied by elevated circulating monocyte numbers. Splenectomy significantly decreased monocyte accumulation, VEGF‐A levels, and angiogenesis in CBDL animal lung and improved AaPO2 levels. In contrast, hepatic monocyte levels, fibrosis, and functional abnormalities were further exacerbated by spleen removal.ConclusionsSplenic reservoir monocytes are a major source for lung monocyte accumulation after CBDL, and spleen removal attenuates the development of experimental HPS. Liver monocytes may have different origins, and accumulation is exacerbated after depletion of splenic reservoir monocytes. Tissue specific monocyte alterations, influenced by the spleen reservoir, have a significant impact on pulmonary complications of liver disease.

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“…Literature reported time spans for significant recovery vary widely, from several days to many months postoperatively [25, 26,28]. The common occurrence of delayed recovery supports the importance of vascular remodeling, rather than simple nitric oxide-based vasodilatation, as the dominant pathophysiologic mechanism underlying HPS [29].…”

Section: Managementmentioning

confidence: 97%