EVALUATION OF THE -C592A PROMOTER POLYMORPHISM AND PUTATIVE HAPLOTYPES OF THE INTERLEUCIN-10 (IL-10) GENE IN SCHISTOSOMIC HIGH DIGESTIVE HEMORRHAGE IN PERNAMBUCO
Introduction: Portal Hypertension is a complication of periportal fibrosis in the terminal branches of the hepatic portal vein in schistosomiasis individuals that causes splenomegaly and the formation of varicose veins. The rupture of varicose veins causes Upper Digestive Bleeding (UDH). Single Nucleotide Polymorphisms and putative Haplotypes of the Interleukin-10 (IL-10) gene may be involved in modulating the immune response and development of the disease. Goal: To investigate the association between the polymorphism in the –C592A IL-10 region and the putative haplotypes of the IL-10 gene with the severity of UGIB in individuals with Schistosomiasis Mansoni treated at the Gastroenterology outpatient clinic at the Hospital das Clínicas of ``Universidade Federal de Pernambuco`` (HC-UFPE) in Pernambuco. Method: This is a cross-sectional study, which involved 124 individuals infected with Schistosoma mansoni, after specific treatment, to verify the association between the –C592A IL-10 genetic polymorphism and the putative haplotypes of the IL-10 gene with HDA. Results: There was no evidence of a statistically significant association between the - 592A IL-10 polymorphism and UGIB between the clinical groups (PR = 0.803, 95% CI = [0.29-1.25] and p = 0.120). There was no evidence of a statistically significant association between the putative haplotypes (-G1082A/-T819C/-C592A) IL-10 and UGIB. Conclusions: The results suggest that the IL-10 -C592A polymorphism and putative IL-10 promoter gene haplotypes were not associated with UGIB in this population.
EVALUATION OF THE -C592A PROMOTER POLYMORPHISM AND PUTATIVE HAPLOTYPES OF THE INTERLEUCIN-10 (IL-10) GENE IN SCHISTOSOMIC HIGH DIGESTIVE HEMORRHAGE IN PERNAMBUCO
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DOI: 10.22533/at.ed.15939723271110
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Palavras-chave: Schistosomiasis mansoni, Interleukin-10, Periportal fibrosis, Genetic polymorphism, Upper gastrointestinal bleeding.
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Keywords: Schistosomiasis mansoni, Interleukin-10, Periportal fibrosis, Genetic polymorphism, Upper gastrointestinal bleeding.
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Abstract:
Introduction: Portal Hypertension is a complication of periportal fibrosis in the terminal branches of the hepatic portal vein in schistosomiasis individuals that causes splenomegaly and the formation of varicose veins. The rupture of varicose veins causes Upper Digestive Bleeding (UDH). Single Nucleotide Polymorphisms and putative Haplotypes of the Interleukin-10 (IL-10) gene may be involved in modulating the immune response and development of the disease. Goal: To investigate the association between the polymorphism in the –C592A IL-10 region and the putative haplotypes of the IL-10 gene with the severity of UGIB in individuals with Schistosomiasis Mansoni treated at the Gastroenterology outpatient clinic at the Hospital das Clínicas of ``Universidade Federal de Pernambuco`` (HC-UFPE) in Pernambuco. Method: This is a cross-sectional study, which involved 124 individuals infected with Schistosoma mansoni, after specific treatment, to verify the association between the –C592A IL-10 genetic polymorphism and the putative haplotypes of the IL-10 gene with HDA. Results: There was no evidence of a statistically significant association between the - 592A IL-10 polymorphism and UGIB between the clinical groups (PR = 0.803, 95% CI = [0.29-1.25] and p = 0.120). There was no evidence of a statistically significant association between the putative haplotypes (-G1082A/-T819C/-C592A) IL-10 and UGIB. Conclusions: The results suggest that the IL-10 -C592A polymorphism and putative IL-10 promoter gene haplotypes were not associated with UGIB in this population.
- Taynan da Silva Constantino
- Ana Risoflora Alves de Azevedo
- Lucas Emanuel de Vasconcelos Cândido
- Letícia Moura de Vasconcelos
- Diogo Luiz Bacelar da Silva.
- Kayllane Kelssiney da Silva.
- Antônio José de Vasconcelos Neto.
- Aline de Melo Silva.
- Daniela Vieira Silvestre da Silva.
- Prof Dra Paula Carolina Valença Silva.
