Ki Tae Suk1, Moon Young Kim2, Soung Won Jeong3, Jae Young Jang3, Yoon Ok Jang4, Soon Koo Baik5,6,7. 1. Department of Internal Medicine, Hallym University College of Medicine, Chuncheon, South Korea. 2. Department of Internal Medicine, Yonsei University Wonju College of Medicine, 20 Ilsan-ro, Wonju, 26426, South Korea. 3. Institute for Digestive Research, Digestive Disease Center, Department of Internal Medicine, Soonchunhyang University College of Medicine, Seoul, South Korea. 4. Cell Therapy and Tissue Engineering Center, Yonsei University Wonju College of Medicine, Wonju, South Korea. 5. Department of Internal Medicine, Yonsei University Wonju College of Medicine, 20 Ilsan-ro, Wonju, 26426, South Korea. baiksk@yonsei.ac.kr. 6. Cell Therapy and Tissue Engineering Center, Yonsei University Wonju College of Medicine, Wonju, South Korea. baiksk@yonsei.ac.kr. 7. Institute of Evidence Based Medicine, Yonsei University Wonju College of Medicine, Wonju, South Korea. baiksk@yonsei.ac.kr.
Abstract
BACKGROUND/AIMS: Hepatopulmonary syndrome (HPS) is characterized by a defect in oxygenation induced by pulmonary vascular dilatation in cirrhosis. While severe HPS is responsible for a high rate of mortality, the prevalence and pathophysiology of HPS are not fully elucidated. We evaluated the prevalence and pathophysiology of HPS in patients with cirrhosis. METHODS: A total of 142 patients with cirrhosis who underwent saline-agitated contrast echocardiography were enrolled in this prospective observational study. HPS was defined by positive findings on contrast echocardiography, cirrhosis, and the presence of an oxygenation defect (alveolar-arterial oxygen gradient > 15 mmHg). HPS grades from 0 to 3 were assigned based on the density and spatial distribution of microbubbles in the left ventricle. The primary endpoint was the prevalence of HPS. The secondary endpoints included clinical characteristics and levels of lipopolysaccharide (LPS), LPS-binding protein (LBP), nitric oxide, and endothelin-1 in HPS. RESULTS: Fifty-nine patients (41.5%) were diagnosed with HPS (grade 1: 24, grade 2: 23, and grade 3: 12 patients). The mean levels of LPS (0.36 ± 0.02, 1.02 ± 0.18, 2.86 ± 0.77, and 6.56 ± 1.46 EU/mL, p < 0.001) and LBP (7026 ± 3336, 11,445 ± 1247, 11,947 ± 1164, and 13,791 ± 2032 ng/mL, p = 0.045) were found to be increased according to HPS grade (negative, grade 1-3). Endothelin-1 levels were significantly elevated according to HPS grade (1.83 ± 0.17, 2.62 ± 0.22, 3.69 ± 0.28, and 4.29 ± 0.34 pg/mL, p < 0.001), demonstrating a significant difference between each grade (p < 0.05). CONCLUSIONS: HPS is a common complication with a prevalence of 41.5% in patients with cirrhosis. Bacterial translocation and portal pulmonary vascular dilatation are key mechanism involved in the progression of HPS.
BACKGROUND/AIMS: Hepatopulmonary syndrome (HPS) is characterized by a defect in oxygenation induced by pulmonary vascular dilatation in cirrhosis. While severe HPS is responsible for a high rate of mortality, the prevalence and pathophysiology of HPS are not fully elucidated. We evaluated the prevalence and pathophysiology of HPS in patients with cirrhosis. METHODS: A total of 142 patients with cirrhosis who underwent saline-agitated contrast echocardiography were enrolled in this prospective observational study. HPS was defined by positive findings on contrast echocardiography, cirrhosis, and the presence of an oxygenation defect (alveolar-arterial oxygen gradient > 15 mmHg). HPS grades from 0 to 3 were assigned based on the density and spatial distribution of microbubbles in the left ventricle. The primary endpoint was the prevalence of HPS. The secondary endpoints included clinical characteristics and levels of lipopolysaccharide (LPS), LPS-binding protein (LBP), nitric oxide, and endothelin-1 in HPS. RESULTS: Fifty-nine patients (41.5%) were diagnosed with HPS (grade 1: 24, grade 2: 23, and grade 3: 12 patients). The mean levels of LPS (0.36 ± 0.02, 1.02 ± 0.18, 2.86 ± 0.77, and 6.56 ± 1.46 EU/mL, p < 0.001) and LBP (7026 ± 3336, 11,445 ± 1247, 11,947 ± 1164, and 13,791 ± 2032 ng/mL, p = 0.045) were found to be increased according to HPS grade (negative, grade 1-3). Endothelin-1 levels were significantly elevated according to HPS grade (1.83 ± 0.17, 2.62 ± 0.22, 3.69 ± 0.28, and 4.29 ± 0.34 pg/mL, p < 0.001), demonstrating a significant difference between each grade (p < 0.05). CONCLUSIONS: HPS is a common complication with a prevalence of 41.5% in patients with cirrhosis. Bacterial translocation and portal pulmonary vascular dilatation are key mechanism involved in the progression of HPS.
Authors: Ki Tae Suk; Jung-Hwan Yoon; Moon Young Kim; Chang Wook Kim; Ja Kyung Kim; Hana Park; Seong Gyu Hwang; Dong Joon Kim; Byung Seok Lee; Sae Hwan Lee; Hong Soo Kim; Jae Young Jang; Chang-Hyeong Lee; Byung Seok Kim; Yoon Ok Jang; Mee Yon Cho; Eun Sun Jung; Yong Man Kim; Si Hyun Bae; Soon Koo Baik Journal: Hepatology Date: 2016-07-30 Impact factor: 17.425
Authors: Lin Chen; Yi Han; Yujie Li; Bing Chen; Xuehong Bai; Karine Belguise; Xiaobo Wang; Yang Chen; Bin Yi; Kaizhi Lu Journal: Cell Death Dis Date: 2019-11-07 Impact factor: 8.469