Hepatopulmonary Syndrome and Portopulmonary Hypertension: Pulmonary Vascular Complications of Liver Disease

Valle, K.; DuBrock, Hilary M.

doi:10.1002/cphy.c210009

Cited by 9 publications

(13 citation statements)

References 152 publications

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“…Prereperfusion and total RBC transfusion were not significantly different between patients who died or survived. However, postreperfusion RBC transfusion was significantly higher in patients who died than those who survived (37 [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] vs. 25 [18.5-51.5], p = .010). The SMT patients were divided into three groups according to a custom of 12-unit delivery for SMT (postreperfusion RBC ≤24, 25-36, and >36 units).…”

Section: Resultsmentioning

confidence: 99%

“…Portopulmonary hypertension (POPH) is defined as pulmonary artery hypertension in the presence of portal hypertension, classified as group 1 PH by the 6th World Symposium on Pulmonary Hypertension. 20,21 Hemodynamically, POPH is characterized by an elevated mean pulmonary artery pressure (mPAP), elevated pulmonary vascular resistance (PVR), and normal pulmonary artery wedge pressure (PAwP). PH may also present in LT patients secondary to the hyperdynamic state and volume overload.…”

Section: Resultsmentioning

confidence: 99%

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Super‐massive transfusion during liver transplantation

Lapisatepun

Agopian

et al. 2023

Transfusion

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BackgroundMassive hemorrhage and transfusion during liver transplantation (LT) present great challenges. We aimed to investigate the incidence and risk factors for super‐massive transfusion (SMT) and survival outcome and factors that negatively affect survival in patients who received SMT during LT.Study Design and MethodsWe included adult patients undergoing LT from 2004 to 2019. SMT was defined as transfusion of ≥50 units of red blood cells (RBC) during LT. Independent risk factors were identified by multivariable logistic regression. Ninety‐day survival was recorded and factors that negatively affected survival were analyzed by the Cox survival test.ResultsOf 2772 patients, 158 (5.6%) received SMT during LT. Mean RBC transfusion was 72.6 (±23.4) units with a maximum of 168 units. Four variables (MELD‐Na score, previous upper abdominal surgery, portal vein thrombosis, and remote retransplant) were independent risk factors for SMT (odds ratio 1.800–8.274, 95% CI 1.008–16.685, all p < .005). The 90‐day survival rate in SMT patients was 81.6%. Preoperative pulmonary hypertension and massive postreperfusion transfusion negatively affected 90‐day survival (hazard ratio 2.658–4.633, 95% CI 1.144–10.130, and all p < .05).ConclusionsIn this large retrospective study, we found that SMT occurred in a small percentage of patients and was associated with relatively satisfactory short‐term survival. Identification of preoperative risk factors for SMT and factors that negatively affect survival improve our understanding of this unique LT patient population.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Super‐massive transfusion during liver transplantation

Lapisatepun

Agopian

et al. 2023

Transfusion

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“…The pathogenesis of HPS mostly involves pulmonary vascular dilatation in the context of chronic hepatic diseases ( 50 ). HPS is always accompanied by global inflammation and hemodynamic disturbance ( 51 ). Inflammation is one of the most important contributors to eGCX damage as well as to HPS occurrence.…”

Section: Potential Mechanisms Linking Egcx To the Pathogenesis Of Hpsmentioning

confidence: 99%

Endothelial glycocalyx in hepatopulmonary syndrome: An indispensable player mediating vascular changes

Cook

Liu

et al. 2022

Front. Immunol.

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Hepatopulmonary syndrome (HPS) is a serious pulmonary vascular complication that causes respiratory insufficiency in patients with chronic liver diseases. HPS is characterized by two central pathogenic features—intrapulmonary vascular dilatation (IPVD) and angiogenesis. Endothelial glycocalyx (eGCX) is a gel-like layer covering the luminal surface of blood vessels which is involved in a variety of physiological and pathophysiological processes including controlling vascular tone and angiogenesis. In terms of lung disorders, it has been well established that eGCX contributes to dysregulated vascular contraction and impaired blood-gas barrier and fluid clearance, and thus might underlie the pathogenesis of HPS. Additionally, pharmacological interventions targeting eGCX are dramatically on the rise. In this review, we aim to elucidate the potential role of eGCX in IPVD and angiogenesis and describe the possible degradation-reconstitution equilibrium of eGCX during HPS through a highlight of recent literature. These studies strongly underscore the therapeutic rationale in targeting eGCX for the treatment of HPS.

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“…The initial symptoms of PAH are shortness of breath, fatigue and angina. With the increase of pulmonary vascular resistance, the load of right ventricle (RV) increases, which is pathologically manifested as right ventricular hypertrophy, pulmonary endothelial dysfunction and pulmonary vascular remodeling, and ultimately leads to right ventricular failure and death (del Valle and DuBrock, 2021). According to the latest global epidemiological research, the incidence of PAH are crudely estimated at 5 cases per million adults (Hoeper et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Polydatin Glycosides Improve Monocrotaline-Induced Pulmonary Hypertension Injury by Inhibiting Endothelial-To-Mesenchymal Transition

Chen

Zhang

et al. 2022

Front. Pharmacol.

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Objective: To study the effect of polydatin on the injury of pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT).Methods: SD rats were induced to develop PAH injury by a single subcutaneous injection of MCT (60 mg/kg). From the second day, rats in the administration group were orally given sildenafil (20 mg/kg) and polydatin (30 or 60 mg/kg) for 3 weeks. At the end of the experiment, right ventricular hypertrophy (RVH) index of SD rats was calculated, pathological damage was assessed by HE staining, transcription levels of target genes were detected by RT-PCR and Elisa, and expression levels of Endothelial-to-mesenchymal transition (EndMT) related proteins were detected by immunohistochemistry (IHC) and immunofluorescence (IF). Finally, molecular docking analysis was used to verify the interaction of polydatin on the main targets.Results: Polydatin could significantly restore the body function, reduce MCT-induced PAH injury, reduce serum biochemical indices; polydatin could effectively inhibit EndMT process by decreasing the expression of N-cadherin, β-catenin and vimentin; polydatin could down-regulate TAGLN expression and increase PECAM1 expression to reduce pulmonary vascular remodeling. The interaction between polydatin and EndMT target was confirmed by molecular docking operation.Conclusion: Pharmacological experiments combined with Combining molecular docking was first used to clarify that polydatin can reduce the pulmonary endothelial dysfunction and pulmonary vascular remodeling induced by MCT by inhibiting EndMT. The results of the study provide new ideas for the further treatment of PAH injury.

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Hepatopulmonary Syndrome and Portopulmonary Hypertension: Pulmonary Vascular Complications of Liver Disease

Cited by 9 publications

References 152 publications

Super‐massive transfusion during liver transplantation

Super‐massive transfusion during liver transplantation

Endothelial glycocalyx in hepatopulmonary syndrome: An indispensable player mediating vascular changes

Polydatin Glycosides Improve Monocrotaline-Induced Pulmonary Hypertension Injury by Inhibiting Endothelial-To-Mesenchymal Transition

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