6533b825fe1ef96bd1282977

RESEARCH PRODUCT

Myocardial infarction marker levels are influenced by prothrombin and tumor necrosis factor-α gene polymorphisms in young patients.

Salvatore NovoMarco CarusoLoredana VaccarinoM BovaMarisa PalmeriGiusi I Forte 1Vitale FrancescoSilvana VitaleMaria Fatima MassentiDomenico LioCalogero CarusoLetizia Scola

subject

AdultMalePro-thrombinGenotypeImmunologyMyocardial InfarctionSNPSingle-nucleotide polymorphismAcute myocardial infarctionPolymorphism Single NucleotideBiochemistryYoung AdultGene FrequencyGenotypeTroponin IGenetic predispositionCreatine Kinase MB FormHumansImmunology and AllergyMedicineGenetic Predisposition to DiseaseMolecular BiologyAllele frequencyInflammationbiologyTumor Necrosis Factor-alphabusiness.industryAge FactorsFibrinogenHematologyMiddle AgedTroponinTumor necrosis factor-a.TroponinGenotype frequencyImmunologyHaematochemical parameterbiology.proteinProthrombinCreatine kinasebusinessBiomarkers

description

Polymorphisms of genes encoding key factors for the control and activation of inflammatory response and coagulation cascade regulation may play a role in genetic susceptibility to acute myocardial infarction (AMI). This study sought to analyze the effect of TNF - 308G/A and pro-thrombin (FII) 20210G/A polymorphisms on the laboratory parameters of young patients affected by AMI. Results indicated that TNF - 308A positive genotype frequencies were increased in these patients and that a genetically determined higher production of TNF-alpha is associated in young subjects to a more severe cardiac damage as depicted by higher levels of troponin, Creatine kinase-MB Isoenzyme (mCK-MB) and a significant increased plasma fibrinogen levels. Similar and probably additive effects on might have a genetically determined increased production of pro-thrombin even if no significant differences in genotype frequencies of pro-thrombin (FII) 20210G/A polymorphisms were observed in this study. All together these results, indicating the relationship among genetically determined TNF alpha and FII production and increased levels of tissue damage markers of AMI, suggest that a complex genetic background, might be involved in susceptibility to AMI in young men influencing the extension and severity of the disease.

yearjournalcountryeditionlanguage
2012-05-30
10.1016/j.cyto.2012.09.021http://hdl.handle.net/10447/73586