| Sažetak | Nositelji različitih krvnih grupa ABO sustava imaju drugačije koncentracije koagulacijskih čimbenika vWF i FVIII u krvnoj plazmi. Dosadašnjim istraživanjima dokazano je da ne-O krvne grupe doprinose većem riziku razvoja plućne embolije (PE). Cilj ove studije bio je ispitati povezanost ABO fenotipova, genotipova i alela s PE-om u hrvatskoj populaciji. Retrospektivna studija provedena je na 109 bolesnika s dijagnozom PE-a i 303 dobrovoljna darivatelja krvi bez koagulacijskih bolesti. Iz uzorka pune krvi izolirana je genomska DNA pomoću QIAamp DNA Blood Mini kita na QIAcube uređaju (QIAGEN, Njemačka). ABO genotipizacija provedena je “in house” PCR-SSP metodom na uređaju ABI 2720 (Applied Biosystems, SAD). Statističkom usporedbom dobivena je 1,86 puta veća vjerojatnost obolijevanja od PE u nositelja ne-O krvnih grupa (OR 1,86; 95 % CI 1,15-3,01). Utvrđeno je da B i AB krvne grupe najviše pridonose riziku uz omjere izgleda 1,94 te 3,68, dok za A krvnu grupu nema statistički značajne razlike (p=0,097). Nositelji genotipova A1A1, A1B i BB imaju veću vjerojatnost razviti PE od OO genotipa (OR 3,16, 95 % CI 1,21-8,19; OR 4,21, 95 % CI 1,75-10,03; OR 10,52, 95 % CI 1,94-56,95), stoga navedeni genotipovi predstavljaju čimbenike rizika za razvoj PE-a u hrvatskoj populaciji. B alel najviše doprinosi povećanju rizika, slijedi A1, dok O i A2 aleli ne utječu značajno na rizik. Dokazana je trostruko veća vjerojatnost razvoja PE u nositelja samo A i/ili B alela (OR 3,04; 95 % CI 1,76-5,25) u usporedbi s nositeljima barem jednog O alela. Rezultati ove studije u skladu su sa sličnim objavljenim istraživanjima te potvrđuju da su ne-O krvne grupe genetički čimbenik rizika za razvoj PE-a. Budućim istraživanjima treba u potpunosti razjasniti mehanizam kojim ABO sustav krvnih grupa utječe na razvoj PE-a. |
| Sažetak (engleski) | Carriers of particular blood types of the ABO system have different concentrations of vWF and FVIII in blood plasma. Previous research has shown that non-O blood types contribute to a higher risk of pulmonary embolism (PE). The aim of this study was to examine the association of ABO phenotypes, genotypes and alleles with PE in the Croatian population. A case-control study was conducted on 109 patients diagnosed with PE and 303 voluntary blood donors without any coagulation disorder as a control group. Genome DNA was isolated from a whole blood sample using the QIAamp DNA Blood Mini kit on a QIAcube device (QIAGEN, Germany). ABO genotyping was performed by “in house” PCR-SSP method on the ABI 2720 device (Applied Biosystems, USA). Statistical analysis has shown a 1.86-fold higher risk of the development of PE in non-O blood type carriers (OR 1.86; 95% CI 1.15–3.01). The strongest association with PE risk has been recorded for B and AB blood types with odds ratios of 1.94 and 3.68, while for blood type A there was no statistically significant difference (p = 0.097). Carriers of A1A1, A1B and BB genotypes are more likely to develop PE than OO genotypes (OR 3.16, 95% CI 1.21-8.19; OR 4.21, 95% CI 1.75-10.03; OR 10 , 52, 95% CI 1.94-56.95). Therefore, these genotypes represent risk factors for the development of PE in the sample of Croatian population. The B allele showed greatest contribution to the risk, followed by A1, while the O and A2 alleles do not significantly affect the risk. Carriers of A and/or B allele proved to be three times more prone to develop PE (OR 3.04; 95% CI 1.76-5.25) compared to carriers of at least one O allele. The results of this study are consistent with recently published studies and confirm that non-O blood types are a genetic risk factor for the development of PE. Future research should fully elucidate the mechanism by which the ABO blood group system influences the development of PE. |
