title: Latex allergy and filaggrin null mutations.
abstract: OBJECTIVE
  Natural rubber latex (NRL) contains over 200 proteins of which 13 have been identified as allergens and the cause of type I latex allergy. Health care workers share a high occupational risk for developing latex allergy. Filaggrin null mutations increase the risk of type I sensitizations to aeroallergens and it is possible that filaggrin null mutations also increase the risk of latex allergy. The aim of this paper was to examine the association between filaggrin null mutations and type I latex allergy.
  
  
  METHODS
  Twenty latex allergic and 24 non-latex allergic dentists and dental assistants, occupationally exposed to latex, were genotyped for filaggrin null mutations R501X and 2282del4. Latex allergy was determined by a positive reaction or a historical positive reaction to a skin prick test with NRL.
  
  
  RESULTS
  41 individuals were successfully genotyped. Three individuals were filaggrin mutation carriers. One (2.4%) was a 2282del4 heterozygote and two (4.9%) were R501X heterozygote. No homozygote or compound heterozygote carriers were detected. No association between filaggrin null mutations and type I latex allergy was found (p=0.24). Patients with type I latex allergy more often reported contact dermatitis.
  
  
  CONCLUSIONS
  This is the first study to examine a highly plausible association between filaggrin null mutations and type I latex allergy. The study subjects were occupationally exposed to latex but no association between latex allergy and filaggrin mutations were detected. Sensitization to latex in the cases in this study may not have occurred through direct skin contact but through the respiratory organs via latex proteins that are absorbed in glove powder and aerosolized.
authors.affiliation: National Allergy Research Centre, Department of Dermato-Allergology, Copenhagen University Hospital Gentofte, 2900 Hellerup, Denmark. bccarlsen@dadlnet.dk
authors.forename: Berit C
authors.initials: BC
authors.lastname: Carlsen
authors.forename: Michael
authors.initials: M
authors.lastname: Meldgaard
authors.forename: Dathan
authors.initials: D
authors.lastname: Hamann
authors.forename: Quinlan
authors.initials: Q
authors.lastname: Hamann
authors.forename: Carsten
authors.initials: C
authors.lastname: Hamann
authors.forename: Jacob P
authors.initials: JP
authors.lastname: Thyssen
authors.forename: Daniel M
authors.initials: DM
authors.lastname: Meyer
authors.forename: Stephen E
authors.initials: SE
authors.lastname: Gruninger
authors.forename: Curt
authors.initials: C
authors.lastname: Hamann
mesh_terms: D000336:Aerosols; D000485:Allergens; D001120:Arginine / Q000235:genetics; D003726:Dental Assistants; D003815:Dentists; D017449:Dermatitis, Allergic Contact / Q000235:genetics; D005260:Female; D000091344:Filaggrin Proteins; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006579:Heterozygote; D006801:Humans; D006969:Hypersensitivity, Immediate / Q000235:genetics*; D007381:Intermediate Filament Proteins / Q000235:genetics*; D020315:Latex Hypersensitivity / Q000235:genetics*; D008297:Male; D009154:Mutation / Q000235:genetics*; D009784:Occupational Diseases / Q000235:genetics; D016273:Occupational Exposure; D011498:Protein Precursors / Q000235:genetics*; D017384:Sequence Deletion / Q000235:genetics
chemical_list: D000336:Aerosols; D000485:Allergens; C000717249:FLG protein, human; D000091344:Filaggrin Proteins; D007381:Intermediate Filament Proteins; D011498:Protein Precursors; D001120:Arginine