Biology of portal hypertension

McConnell, Matthew; Iwakiri, Yasuko

doi:10.1007/s12072-017-9826-x

Cited by 83 publications

(90 citation statements)

References 139 publications

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“…The latter refers to the lost of fenestrae and development of a basement membrane by these cells as a consequence of liver fibrosis. In cirrhosis, these features make hepatic sinusoids less leaky and prevent the passage of proteins to the space of Disse and from here to the peritoneal fluid [81]. Other less reliable findings in cardiac ascites are higher LDH levels and higher red blood cell counts due to leaking of red blood cells into the ascites via lymph tissue, with resulting lysis [80].…”

Section: Clinical Presentation and Diagnosismentioning

confidence: 99%

Cardiac Hepatopathy

Fortea¹,

Puente²,

Cuadrado³

et al. 2021

Liver Pathology

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Liver disease resulting from heart disease has generally been referred as "cardiac hepatopathy." The two main forms of cardiac hepatopathy are acute cardiogenic liver injury (ACLI) and congestive hepatopathy (CH). ACLI most commonly occurs in the setting of acute cardiocirculatory failure, whereas CH results from passive venous congestion in the setting of chronic right-sided heart failure (HF). Both conditions often coexist and potentiate the deleterious effects of each other on the liver. In CH, the chronic passive congestion leads to sinusoidal hypertension, centrilobular fibrosis, and ultimately, cirrhosis ("cardiac cirrhosis") and hepatocellular carcinoma. The differentiation between congestion and fibrosis currently represents an unmet need and a growing research area. Although cardiac cirrhosis may only arise after several decades of ongoing injury, the long-term survival of cardiac patients due to advances in medical and surgical treatments is responsible for the increased number of liver complications in this setting. Eventually, the liver disease could become as clinically relevant as the cardiac disease and further complicate its management.

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Section: Clinical Presentation and Diagnosismentioning

confidence: 99%

Cardiac Hepatopathy

Fortea¹,

Puente²,

Cuadrado³

et al. 2021

Liver Pathology

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“…Intrahepatic resistance, portal tributary blood flow, and formation of spontaneous shunts determine portal pressure 116 , 138 . Intrahepatic resistance has a structural (fibrosis, alteration of the vascular architecture) and a non-structural (intrahepatic vascular tone) component.…”

Section: Modulation Of the Intestinementioning

confidence: 99%

“…Gut-derived stimuli such as certain pathogen-associated molecular patterns (PAMPS) (lipopolysaccharide, endotoxin) may play an important role in this interplay. They impair intrahepatic endothelial function by influencing nitric oxide release 138 , 139 or stimulate signaling pathways of intrahepatic contractile cells and of fibrogenesis by inducing inflammation, e.g. activation of Kupffer cells and other macrophages 140 , 141 using sensing protein families such as Nod-like receptors or Toll-like receptors 142 , 143 .…”

Section: Modulation Of the Intestinementioning

confidence: 99%

Managing portal hypertension in patients with liver cirrhosis

2018

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Portal hypertension is one cause and a part of a dynamic process triggered by chronic liver disease, mostly induced by alcohol or incorrect nutrition and less often by viral infections and autoimmune or genetic disease. Adequate staging - continuously modified by current knowledge - should guide the prevention and treatment of portal hypertension with defined endpoints. The main goals are interruption of etiology and prevention of complications followed, if necessary, by treatment of these. For the past few decades, shunts, mostly as intrahepatic stent bypass between portal and hepatic vein branches, have played an important role in the prevention of recurrent bleeding and ascites formation, although their impact on survival remains ambiguous. Systemic drugs, such as non-selective beta-blockers, statins, or antibiotics, reduce portal hypertension by decreasing intrahepatic resistance or portal tributary blood flow or by blunting inflammatory stimuli inside and outside the liver. Here, the interactions among the gut, liver, and brain are increasingly examined for new therapeutic options. There is no general panacea. The interruption of initiating factors is key. If not possible or if not possible in a timely manner, combined approaches should receive more attention before considering liver transplantation.

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“…Portal hypertension is a clinical syndrome affecting patients with or without cirrhosis, in which hemodynamic changes in the portosystemic circulation lead to complications such as variceal bleeding, ascites, and portosystemic encephalopathy. [1][2][3] Upper gastrointestinal bleeding caused by esophageal varices is its most serious complication, with an annual bleeding rate of 5-15% and a rebleeding rate of 60% within 1 year. 4 The surgical treatment of portal hypertension primarily aims to prevent esophageal variceal bleeding.…”

Section: Introductionmentioning

confidence: 99%

Efficacy Analysis of Gastric Coronary Venous TH Glue Embolization with Splenectomy for Treating Cirrhotic Portal Hypertension

Li¹,

Wang²,

Chen³

et al. 2019

Exploratory Research and Hypothesis in Medicine

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Background and aims: To evaluate the effects of gastric coronary venous embolization with TH glue (developercontaining octyl-α-cyanoacrylate) in combination with splenectomy for the treatment of cirrhotic portal hypertension and gastroesophageal varices. Methods: From April 2002 to July 2016, 81 patients with cirrhotic portal hypertension who underwent this procedure were subject to perioperative (within 2 weeks), short-term (within 2 weeks to 1 month) and long-term (1 month thereafter) efficacy analyses. Complications, rebleeding rate, and long-term survival rate were evaluated. Results: No patients developed embolism caused by TH glue ectopia. Eleven patients experienced perioperative complications, including high esophageal expenditure blood (1%), subphrenic effusion (1%) and abdominal infection (1%), which affected one case each respectively. Pulmonary infection (2%) and portal system thrombosis (2%) affected two cases respectively. There were 4 patients who experienced ascites (5%). All patients had small amounts of melena and were healed after conservative medical treatment. The 1-, 3-, 5-and 10-year postoperative rebleeding rates were 4.9%, 8.6%, 11.1% and 18.5% respectively. The 1-, 3-, 5-and 10-year postoperative survival rates were 97.5%, 92.6%, 90.1% and 80.2% respectively. No hepatic encephalopathy occurred within 1 year after operation in any case. Conclusions: The postoperative rebleeding rate was lower than that reported in the literature and the subjects achieved good perioperative, short-term and long-term effects. The method of operation in the treatment of cirrhotic portal hypertension and gastroesophageal varices is characterized by a good safety profile, less invasiveness, rapid postoperative recovery, and a lower rebleeding rate than other devascularization procedures. Thus, it is an option that can be first considered by patients requiring emergency surgery to stop bleeding or patients with poor liver function, and even some patients with Child-Pugh grade C.

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Biology of portal hypertension

Cited by 83 publications

References 139 publications

Cardiac Hepatopathy

Cardiac Hepatopathy

Managing portal hypertension in patients with liver cirrhosis

Efficacy Analysis of Gastric Coronary Venous TH Glue Embolization with Splenectomy for Treating Cirrhotic Portal Hypertension

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