Abstract

An association between ADA1 and Coronary Artery Disease (CAD) has been observed in Polish and in Italian populations but in Italian population the association was present in males only. In order to enlighten these differences we have carried out a collaborative study in the two populations. In Italy 215 subjects admitted to the Hospital for CAD, 275 subjects with Type 2 Diabetes (T2D) without CAD and 398 healthy new-borns were studied. In Poland 173 subjects with CAD and 200 healthy newborns were studied. Written informed consent was obtained from all subjects or from their mothers to participate to the study that was approved by the I.R.B. ADA1 polymorphism was determined by DNA analysis. Three way contingency table analysis was performed by a log linear model. The association between CAD and ADA1 is present in non diabetic male subjects only: OR = 0.195, p = 0.007 in the Italian population and OR = 0.163, p = 0.004 in the Polish population. The data suggest a significant role of immunological mechanisms in the pathogenesis of CAD without diabetes. Gender differences in immune diseases could explain the lack of association in females.

Highlights

  • An association between Adenosine Deaminase locus 1 (ADA1) and Coronary Artery Disease (CAD) has been described in the Polish population [1] and confirmed in the Italian population [2]

  • The relationship among the variables considered i.e. ADA1 genotype, CAD, diabetes, gender and population have been examined by log linear models

  • The analysis of interaction among ADA1, diabetes and gender (a) within CAD subjects shows a significant interaction among the three variables with a pattern similar in Italian and Polish samples

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Summary

Introduction

An association between Adenosine Deaminase locus 1 (ADA1) and Coronary Artery Disease (CAD) has been described in the Polish population [1] and confirmed in the Italian population [2]. ADA1 is a polymorphic enzyme present in all mammalian tissue that catalyzes the irreversible deamination of adenosine to inosine [3]. It is controlled by a locus with 2 codominant alleles ADA1*1 and ADA1*2 located in the long arm of chromosome 20 [4]: the activity associated to ADA1*2 is lower than that associated to ADA1*1. ADA1 and CD26 are colocalized on T cell surface and these cells are much more resistant to the inhibitory effects of adenosine

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