
<ArticleTitle>The effect of human platelet alloantigen polymorphisms on the in vitro responsiveness to adrenaline and <prot>collagen</prot>.</ArticleTitle>
<AbstractText>A number of clinical studies have suggested that carriage of the low frequency allele (b) of the <prot>human platelet antigen 1</prot> (<prot>HPA-1</prot>) system is a risk factor for coronary thrombosis. We have examined the effect of a series of HPA biallelic polymorphisms (systems -1, -2, -3 and -5) on the in vitro platelet aggregation in response to adrenaline and <prot>collagen</prot> in 30 healthy volunteers. There was a significantly higher prevalence (10 out of 18) of carriers of the <prot>HPA-1b</prot> polymorphism among subjects showing a  50% aggregation response to adrenaline ('responders') than the prevalence (1/12) in 'non-responders' (P &#60; 0.05). Platelets heterozygous for the <prot>HPA-1b</prot> polymorphism showed a significantly higher rate (slope) and greater extent (%) of adrenaline-induced aggregation than platelets not carrying the <prot>HPA-1b</prot> allele (P &#60; 0.05). A greater extent of <prot>collagen</prot>-induced aggregation was also demonstrated in <prot>HPA-1ab</prot> platelets (P &#60; 0.05). Inhibition of adrenaline-induced aggregation following incubation with aspirin was greater (P &#60; 0.01) in <prot>HPA-1ab</prot> than in <prot>HPA-1aa</prot> platelets. <prot>Collagen</prot>-induced aggregation was slower in carriers of the <prot>HPA-5b</prot> allele than in <prot>HPA-5aa</prot> subjects (P &#60; 0.05). Polymorphisms of the <prot>HPA-2</prot> and <prot>HPA-3</prot> systems were not associated with different aggregation responses to either adrenaline or <prot>collagen</prot>. These results support the clinical observation that polymorphism <prot>HPA-1b</prot> may predispose to increased platelet thrombogenicity and suggest that the presence of polymorphism <prot>HPA-5b</prot> might render the platelet less reactive to <prot>collagen</prot>.</AbstractText>
