Clinical significance of a myeloperoxidase gene polymorphism and inducible nitric oxide synthase expression in cirrhotic patients with hepatopulmonary syndrome |
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Authors: | Yanying Wang Wenduo Wang Yanxia Zhang Xin Zhao Dongliang Yang |
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Institution: | 1. Department of Gastroenterology,Heilongjiang Provincial Hospital,Harbin 150036,China 2. Department of Infectious Disease,Tongji Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430030,China |
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Abstract: | The clinical significance of a myeloperoxidase (MPO) gene polymorphism and inducible nitric oxide synthase (iNOS) expression
in cirrhotic patients with hepatopulmonary syndrome (HPS) was explored. Enrolled subjects were divided into three groups according
to their disease/health conditions: the HPS group (cirrhotic patients with HPS; n=63), the non-HPS group (cirrhotic patients without HPS; n=182), and the control group (healthy subjects without liver disease; n=35). The distribution of the MPO −463 G/A genotype and its relationship with iNOS expression in a typical cell block from
ascitic fluid were detected by immunohistochemistry and polymerase chain reaction-restricted fragment length polymorphism
analysis (PCR-RFLP). In the HPS group, the partial pressure of oxygen in blood and ascitic fluid was significantly decreased
(8.95±1.58 kPa and 6.81±0.95 kPa, respectively; both P<0.01), while the partial pressure of carbon dioxide significantly increased (4.62±0.20 kPa and 5.92±0.45 kPa, respectively;
P<0.01). MPO and iNOS levels were significantly increased in the HPS group as compared with the non-HPS group. These increases
were even more remarkable in ascitic fluid (41.36±11.62 and 13.23±4.81 μg/L; 10.27± 3.20 and 4.95±1.12 μg/L) than in blood
(16.66±5.24 and 4.87±1.73 μg/L; 5.79±2.31 and 2.35±0.84 μg/L). The distribution of the MPO genotypes GG, GA, and AA were 76.2%,
22.2% and 1.6% in the HPS group, and 57.7%, 37.9% and 4.4% in the non-HPS group (P<0.05). The expression of iNOS was significantly higher in patients with the G alleles (G/G and G/A) (61.54%, 48/78) than
in patients with A alleles (G/A and A/A) (38.46%, 30/78) (P<0.01). It was suggested that the expression levels of iNOS and MPO were correlated with HPS-induced hypoxemia. The MPO-463
G/A mutation might be a protective factor that prevents the development of HPS. The MPO might be involved in the regulation
of iNOS expression. In humans, MPO pathways, the iNOS/NO system, and their interaction might have an impact on the occurrence
and development of HPS. |
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Keywords: | hepatopulmonary syndrome myeloperoxidase inducible nitric oxide synthase polymorphism |
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