I. Theodoropoulos et al., The effect of human platelet alloantigen polymorphisms on the in vitro responsiveness to adrenaline and collagen, BR J HAEM, 114(2), 2001, pp. 387-393
A number of clinical studies have suggested that carriage of the low freque
ncy allele (b) of the human platelet antigen 1 (HPA-1) system is a risk fac
tor 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 platel
et aggregation in response to adrenaline and collagen in 30 healthy volunte
ers. There was a significantly higher prevalence (10 out of 18) of carriers
of the HPA-1b polymorphism among subjects showing a >50% aggregation respo
nse to adrenaline ('responders') than the prevalence (1/12) in 'non-respond
ers' (P<0.05). Platelets heterozygous for the HPA-1b polymorphism showed a
significantly higher rate (slope) and greater extent (%) of adrenaline-indu
ced aggregation than platelets not carrying the HPA-1b allele (P<0.05). A g
reater extent of collagen-induced aggregation was also demonstrated in HPA-
1ab platelets (P<0.05). Inhibition of adrenaline-induced aggregation follow
ing incubation with aspirin was greater (P<0.01) in HPA-1ab than in HPA-1aa
platelets. Collagen-induced aggregation was slower in carriers of the HPA-
5b allele than in HPA-5aa subjects (P<0.05). Polymorphisms of the HPA-2 and
HPA-3 systems were not associated with different aggregation responses to
either adrenaline or collagen. These results support the clinical observati
on that polymorphism HPA-1b may predispose to increased platelet thrombogen
icity and suggest that the presence of polymorphism HPA-5b might render the
platelet less reactive to collagen.