Functional variants of eNOS and iNOS genes have no relationship to the portal hypertension in patients with liver cirrhosis
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Cytokines blood MeSH
- DNA Primers chemistry MeSH
- Adult MeSH
- Enzyme-Linked Immunosorbent Assay MeSH
- Genetic Variation MeSH
- Genotype MeSH
- Liver Cirrhosis complications genetics MeSH
- Middle Aged MeSH
- Humans MeSH
- Polymerase Chain Reaction methods MeSH
- Hypertension, Portal etiology genetics MeSH
- Aged MeSH
- Case-Control Studies MeSH
- Severity of Illness Index MeSH
- Nitric Oxide Synthase Type II genetics MeSH
- Nitric Oxide Synthase Type III genetics MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Cytokines MeSH
- DNA Primers MeSH
- NOS2 protein, human MeSH Browser
- NOS3 protein, human MeSH Browser
- Nitric Oxide Synthase Type II MeSH
- Nitric Oxide Synthase Type III MeSH
OBJECTIVE: Nitric oxide is an important vasoactive mediator. Changes in NO production, caused by functional variants of both endothelial and inducible NO synthase (eNOS, iNOS), might play a role in portal hypertension. The aim was to study the significance of functional eNOS and iNOS gene variants in cirrhotic patients and their interrelationship to both inflammatory and endothelial activation parameters. MATERIAL AND METHODS: One hundred and thirty-two patients with liver cirrhosis (age 36-72 years) and 101 controls were examined for functional variants of eNOS (E298D, 27bpintr4, 786T/C) and iNOS (R221W, S608L) genes. Inflammatory (IL6, IL8, IL10) and vasoactive (sVCAM-1, E-selectin) cytokines were measured using ELISA kits. RESULTS: The frequency of E298D (GG 12%, GT 41%, TT 47%), 28bpintr4 (AA 6%, AB 28%, BB 66%), 786T/C genotypes (CC 17%, CT 45%, TT 38%), as well as R221W (CC 93%, CT 7%, TT 0%), and S608L (CC 65%, CT 32%, TT 3%) genotypes in cirrhotic patients did not differ from the controls (p > 0.05 for all comparisons). No relationship was found between the frequency of these genotypes and the severity of portal hypertension, or either inflammatory or vasoactive cytokines. A positive correlation was found between hepatic venous pressure gradient and cytokine concentration: sVCAM-1, IL6, IL8, IL10. CONCLUSIONS: Examined eNOS and iNOS variants have no relationship to pathogenesis of liver cirrhosis. Severity of portal hypertension was associated with the changes in endothelial activation.
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