Measurement of Exhaled Nitric Oxide in Cirrhotic Patients with Esophageal and Gastric Varices.

Xiaoquan Huang,Shiyao Chen,Kaiqi Yang,Souksavanh Thansamay,Tiancheng Luo

doi:10.1155/2019/9673162

Abstract

Background and aims. This study aimed to detect exhaled nitric oxide (eNO) level in cirrhotic patients and explore the correlation between eNO levels and the severity of cirrhosis. Methods. Patients were enrolled to analyze the relationship of eNO with noncirrhosis, cirrhosis, and complications of decompensated cirrhosis. We explored the potential predictive values of eNO in different states of cirrhosis. Results. The eNO levels were significantly increased in cirrhotic patients compared with noncirrhotic patients (14 (10–18) vs 8 (6–13) ppb, P < 0.001). The eNO level was increased in those with ascites (15 (14–22) vs 13 (10–18) ppb, P=0.026), with portal vein thrombosis (19.5 (11.75–22) vs 13.5 (10–17) ppb, P=0.032), or with the mucosal red-color sign of esophageal and gastric varices (EGV) (16.5 (10–21.75) vs 13 (10–14.75) ppb, P=0.041). Among cirrhotic patients undergoing hepatic venous pressure gradient (HVPG) measurement, the eNO level was significantly increased in the high-HVPG group (HVPG >12 mm Hg) compared with the low-HVPG group (6 mm Hg ≤ HVPG ≤ 12 mm Hg) (15 (11.75–19.25) vs 10 (8–14) ppb, P=0.011). Conclusions. The eNO level was increased in cirrhotic patients, especially in those complicated with ascites, portal vein thrombosis, mucosal red-color sign of varices, and high HVPG.

Highlights

Cirrhosis is the end-stage chronic liver disease due to a variety of etiologies
Hypohepatia, portal hypertension (PHT), and various complications may occur in decompensated cirrhosis, including esophageal and gastric variceal bleeding, portal vein thrombosis (PVT), spontaneous bacterial peritonitis, and hepatic encephalopathy, severely affecting quality of life [1]. e increase in portal pressure in cirrhotic patients leads to dilatation of visceral arterial blood vessels of the whole body and hyperkinetic circulatory state accompanied by portosystemic collateral circulation
nitric oxide (NO) is a novel signaling molecule involved in inflammation and tissue damage, which can dilate visceral blood vessels, increase visceral blood flow, and aggravate PHT. e increase in inflammatory cytokines and endotoxins in the circulation of cirrhotic patients can stimulate pulmonary vascular endothelial cells to produce smallmolecule NO, which is exhaled outside the body from the respiratory tract [3]

Summary

Introduction

Cirrhosis is the end-stage chronic liver disease due to a variety of etiologies. Hypohepatia, portal hypertension (PHT), and various complications may occur in decompensated cirrhosis, including esophageal and gastric variceal bleeding, portal vein thrombosis (PVT), spontaneous bacterial peritonitis, and hepatic encephalopathy, severely affecting quality of life [1]. e increase in portal pressure in cirrhotic patients leads to dilatation of visceral arterial blood vessels of the whole body and hyperkinetic circulatory state accompanied by portosystemic collateral circulation. E increase in portal pressure in cirrhotic patients leads to dilatation of visceral arterial blood vessels of the whole body and hyperkinetic circulatory state accompanied by portosystemic collateral circulation. E increase in inflammatory cytokines and endotoxins in the circulation of cirrhotic patients can stimulate pulmonary vascular endothelial cells to produce smallmolecule NO, which is exhaled outside the body from the respiratory tract [3]. E increase in eNO is more common in patients with decompensated cirrhosis, such as intrapulmonary vascular dilatation complicated with hyperdynamic circulatory syndrome and hepatopulmonary syndrome. E excessive elevation of eNO is predominantly associated with an increase in the release from pulmonary vascular endothelial cells, airway epithelial cells, and peripheral inflammatory cells [2]. The increased NO levels in pulmonary small airways and alveolar regions can lead to an increase in the eNO concentration [7,8,9]. e increase in eNO is more common in patients with decompensated cirrhosis, such as intrapulmonary vascular dilatation complicated with hyperdynamic circulatory syndrome and hepatopulmonary syndrome. e excessive elevation of eNO is predominantly associated with an increase in the release from pulmonary vascular endothelial cells, airway epithelial cells, and peripheral inflammatory cells [2]. e concentrations of eNO from different sites, such as central airway and alveoli, can be detected using different expiratory flows and operational formulas [8, 10, 11]. e eNO test is a noninvasive, simple, and economical method that reflects systemic inflammatory state and endothelial cell function, which may be closely related to the progression of cirrhosis [7, 12, 13]. erefore, this study aimed to analyze the relationship of the eNO level with the severity of liver cirrhosis and evaluate the predictive value of eNO as a noninvasive marker for HVPG in patients with cirrhotic portal hypertension (CPH)

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