| Sažetak | Cilj ovog istraživanja bio je istražiti povezanosti polimorfizama u genima za čimbenik nekroze tumora (TNF)-α –308G>A i –238G>A, interleukin (IL)-10 -1082G>A te IL-1α -889C>T s atopijskom astmom, rinitisom i dermatitisom (AD), uz kontrolu utjecaja čimbenika osobne osjetljivosti (spol, BMI, obiteljska alergološka anamneza) te čimbenika načina života i okoliša (pušenje, kontinentalno/primorsko i seosko/gradsko prebivalište, kontakt sa životinjama).
U prvom dijelu istraživanja sudjelovalo je 356 studenata prve godine studija Sveučilišta u Zagrebu kod kojih je provedeno prikupljanje osobnih podataka ispunjavanjem upitnika, ubodni kožni test sa najčešćim inhalacijskim alergenima, mjerenje ukupnog IgE u serumu, spirometrija s bronhodilatatornim testom i genotipizacija. Drugi dio istraživanja bila je studija praćenja ispitanika nakon razdoblja od 4-5 godina (N=121) s potpunim ili djelomičnim ponavljanjem protokola.
Polimorfizam TNF-α –308G>A je bio prisutan u oko 30 %, IL-1α –889C>T u oko 40%, TNF-α -238 G>A u <5 %, a IL-10 –1082G>A u >75 % ispitanika. Rezultati pokazuju negativnu povezanost polimorfizma TNF-α -308 G>A s AD i kožnim simptomima, uz kontrolu za čimbenike osobne osjetljivosti, načina života i okoliša. Polimorfizam TNF-α -308 G>A stimulira produkciju TNFα, što može povoljno djelovati na simptome AD pri kojemu je produkcija i aktivnost TNFα u koži manjkava. U razdoblju praćenja nisu uočene značajne povezanosti polimorfizama s promjenom rizika za prisutnost atopijskih bolesti, simptoma ili pokazatelja. |
| Sažetak (engleski) | The aim of this research was to assess the associations between polymorphisms in the genes for tumour necrosis factor (TNF)-α –308G>A and –238G>A, interleukin(IL)-10-1082G>A and IL-1α-889C>T and atopic asthma, rhinitis and dermatitis (AD), with adjustment for confounding personal (gender, BMI, parental history of atopic diseases), lifestyle, and environmental factors (smoking, continental/Mediterranean and urban/rural residency, exposure to pets).
The initial phase included 356 freshmen students from the University of Zagreb who underwent collecting a questionnaire, skin prick testing with common inhalatory allergens, total serum IgE measurement, spirometry with a bronchodilation test, and genotyping. A follow-up study, conducted 4-5 years later, included 121 subjects who repeated the protocol either completely or partially.
TNF-α –308G>A polymorphism was found in around 30%, IL-1α –889C>T in around 40%, TNF-α -238G>A in <5%, and IL-10 –1082G>A in >75% of subjects. These results point to a negative association between TNF-α –308G>A polymorphism and AD and skin symptoms, adjusted for personal, lifestyle, and environmental factors. TNF-α –308G>A polymorphism stimulates the production of TNF-α, which can be beneficial for the clinical course of AD, since part of AD pathogenesis is related to defective TNFα production and activity in the skin. There were no significant associations between the analysed polymophisms and time-related changes in the presence of atopic diseases, symptoms, and markers during the follow-up period. |
