Relationship between acetylation polymorphism and risk of atopic diseases

Clin Pharmacol Ther. 1999 May;65(5):562-9. doi: 10.1016/S0009-9236(99)70076-7.

Abstract

It has been shown that slow acetylation rate may be a factor that influences the development of allergic diseases. The influence of NAT2 genetic polymorphism on the risk of development of atopic diseases was evaluated among the white Polish population of 85 patients with atopy (62 children and 23 parents) and 181 healthy individuals (127 children and 54 adults). The NAT2 alleles (*4, *5, *6, and *7) were identified by polymerase chain reaction-restriction fragment length polymorphism methods with DNA extracted from peripheral blood. A significant predominance of homozygous slow acetylators (85%) among patients with atopic diseases was observed. There were no homozygous fast acetylators within this group of individuals. Comparison of the frequency of slow acetylators between the above group of patients and healthy subjects (54%) showed that the significant predominance of slow acetylators was observed in the first group (P < .001). The risk of development of atopic diseases was 5-fold greater for homozygous slow acetylators (odds ratio, 4.69; 95% confidence interval, 2.33-9.59) compared with healthy subjects. We therefore concluded that slow acetylation genotype may be an important factor of individual susceptibility to atopic diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation
  • Adolescent
  • Adult
  • Alleles
  • Arylamine N-Acetyltransferase / genetics*
  • Asthma / metabolism
  • Child
  • Child, Preschool
  • Dermatitis, Atopic / metabolism
  • Female
  • Genotype
  • Humans
  • Hypersensitivity / enzymology
  • Hypersensitivity / genetics
  • Hypersensitivity / metabolism*
  • Male
  • Middle Aged
  • Mutation
  • Poland
  • Polymorphism, Genetic*
  • Polymorphism, Restriction Fragment Length
  • Rhinitis, Allergic, Perennial / metabolism
  • White People / genetics

Substances

  • Arylamine N-Acetyltransferase
  • NAT2 protein, human