Personalized Medicine for HLA-associated Drug-hypersensitivity Reactions

Mandvi Bharadwaj; Patricia Illing; Lyudmila Kostenko

Disclosures

Personalized Medicine. 2010;7(5):495-516. 

In This Article

FDE in Response to Trimethoprim–Sulfamethoxazole Treatment & HLA-A30

The observation of HLA-associated FDE in response to feprazone, inspired another study investigating correlations between HLA class I and drug-induced FDE in a Turkish population. An association between HLA-A30 and FDE was detected in response to the combined antibiotic treatment with trimethoprim and sulfamethoxazole, wherein, 23.8% of patients suffering from trimethoprim-sulfamethoxazole-induced FDE possessed the HLA-A30 allele compared with 0% of naproxen-induced FDE patients and 4.8% of healthy controls.[55] This association is much weaker than those previously cited making it plausible that either HLA-A30 is mechanistically involved in FDE, but other alleles or unassociated factors may also cause the reaction, or that a polymorphism in LD with HLA-A30 is responsible for the observed association. In vitro investigation of the activation of T cells in this reaction may elucidate the nature of HLA-A30 in the development of this FDE. As with feprazone–FDE there is no indication of the prevalence of HLA-A30 in trimethoprim-sulfamethoxazole-tolerant individuals so its positive predictive value for this ADR is not easily assessed, nor is it known if this association persists in other ethnicities. So whilst screening for HLA-A30 may currently help aid diagnosis in a subset of individuals in the Turkish population, it is unknown whether prescreening would inappropriately preclude many patients from drug treatment.

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