RESUMO
Objetivo: Estudiar los polimorfismos IL1B-511 y TNF-A-308 asociaciados a lesiones precursoras de cáncer gástrico (CG) en una población infectada con Helicobacter pylori (H. pylori) de bajo riesgo de CG de Nariño. Material y método: De 105 pacientes con síntomas de dispepsia se incluyeron 81 infectados por H. pylori, (n=63) con gastritis no atrófica y (n=18) con lesiones precursoras de CG de Tumaco: población de bajo riesgo de CG. Las lesiones gástricas se clasificaron por el sistema de Sydney y H. pylori por tinción de Giemsa. Los polimorfismos de IL1B-511 y TNF-A-308 se genotipificaron por PCR-RFLP's. Los polimorfismos y su asociación con lesiones gastricas se evaluaron por análisis bivariado y regresión logística binomial. Resultados: Los pacientes portadores del alelo mutante T (IL-1B-511) no se encontraron a riesgo de lesiones precursoras de malignidad (OR=0,7). No se calculó el OR para TNF-A-308, por fijación del alelo normal G. Ser hombre y estar infectado por H. pylori incrementa 4,3 veces el riesgo de presentar lesiones precursoras de CG y no estar vinculado al régimen de salud aumenta 6,7 veces el riesgo de atrofia gástrica, (OR=4,27 y OR=6,72), respectivamente. Conclusión: El alelo mutante T (IL-1B-511) es un biomarcador de resistencia de los pobladores de Tumaco, de bajo riesgo de CG e infectados con H. pylori a padecer lesiones precursoras de CG.
Aim: To study the IL1B-511 and TNF-A-308 polymorphisms and their possible association with gastric cancer (GC) precursor lesions in a population infected with Helicobacter pylori (H. pylori) of low risk area of GC of Nariño. Material/method: 105 patients with symptoms of dyspepsia were included, 81 infected with H. pylori, (n=63) with non-atrophic gastritis and (n=18) with precursor lesions of GC of Tumaco: population of low risk of GC. Gastric lesions were classified by the Sydney System an H. pylori by Giemsa staining. The IL1B-511 and TNFA-308 polymorphisms were genotyped by PCR-RFLPs. Polymorphisms and their association with gastric lesions were evaluated by bivariate analysis and binomial logistic regression. Results: Patients carryng the mutant T allele (IL-1B-511) were not at risk of precursor lesions of malignancy (OR=0,7). The OR was not calculated for TNF-A-308, by fixing the normal allele G. Being a man and being infected with H. pylori increases 4,3 times the risk of presenting precursor lesions of GC and not being linked to the health regimen increases 6,7 times the risk of gastric atrophy, (OR=4,27 and OR=6,72), respectively. Conclusion: The mutant T allele (IL-1B-511) is a resistance biomarker of Tumaco residents, low risk of GC and infected with H. pylori to suffer precursor lesions of GC.
Assuntos
Humanos , Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Idoso , Helicobacter pylori , Neoplasias Gástricas , Fatores de Risco , Colômbia , Alelos , MutaçãoRESUMO
Chagas disease, named after Carlos Chagas, who first described it in 1909, exists only on the American Continent. It is caused by a parasite, Trypanosoma cruzi, which is transmitted to humans by blood-sucking triatomine bugs and via blood transfusion. Chagas disease has two successive phases: acute and chronic. The acute phase lasts six-eight weeks. Several years after entering the chronic phase, 20-35% of infected individuals, depending on the geographical area, will develop irreversible lesions of the autonomous nervous system in the heart, oesophagus and colon, and of the peripheral nervous system. Data on the prevalence and distribution of Chagas disease improved in quality during the 1980s as a result of the demographically representative cross-sectional studies in countries where accurate information was not previously available. A group of experts met in Brasilia in 1979 and devised standard protocols to carry out countrywide prevalence studies on human T. cruzi infection and triatomine house infestation. Thanks to a coordinated multi-country programme in the Southern Cone countries, the transmission of Chagas disease by vectors and via blood transfusion was interrupted in Uruguay in 1997, in Chile in 1999 and in Brazil in 2006; thus, the incidence of new infections by T. cruzi across the South American continent has decreased by 70 percent. Similar multi-country initiatives have been launched in the Andean countries and in Central America and rapid progress has been reported towards the goal of interrupting the transmission of Chagas disease, as requested by a 1998 Resolution of the World Health Assembly. The cost-benefit analysis of investment in the vector control programme in Brazil indicates that there are savings of US$17 in medical care and disabilities for each dollar spent on prevention, showing that the programme is a health investment with very high return. Many well-known research institutions in Latin America...