title: Glucose-6-phosphate-dehydrogenase deficiency as a risk factor for pterygium.
abstract: OBJECTIVE
  Glucose-6-phosphate dehydrogenase (G6PD) is an important site of metabolic control in the pentose phosphate pathway (PPP), providing reducing power (NADPH) and pentose phosphates. The purpose of this study was to investigate the possible involvement of G6PD deficiency (G6PD-) in the pathogenesis of pterygium.
  
  
  METHODS
  Erythrocyte G6PD activity was evaluated in 123 pterygium patients and in 112 age-matched control patients. Enzyme activity, mRNA, rate of growth, green autofluorescence, response to oxidative stress, and cholesterol metabolism were determined in pterygium fibroblasts (PFs) and in normal conjunctival fibroblasts (NCFs) isolated from G6PD normal (NCFs+ and PFs+) and G6PD- (NCFs- and PFs-) patients.
  
  
  RESULTS
  Higher prevalence of G6PD- was found in patients affected by primary pterygium than in control subjects, both men and women, suggesting that this enzymatic defect may be a predisposing factor for pterygium. G6PD activity was significantly lower in NCFs- than in NCFs+, but not in PFs- than in PFs+. In PFs-, G6PD mRNA levels were significantly higher than in PFs+. Growth-stimulated NCFs- grew at half the rate of NCFs+, although PFs- and PFs+ grew at the same rate. Increased green autofluorescence and susceptibility to oxidative stress were observed in PFs (+/-) and in NCFs-, but not in NCFs+. Moreover, ex vivo PFs (+/-) accumulated more lipids than corresponding NCFs.
  
  
  CONCLUSIONS
  The results of this study, although restricted to a limited group of subjects (i.e., those of Sardinian ancestry), suggest that G6PD- not only does not protect against pterygium, but may even be considered a risk factor for the development of this disorder.
authors.affiliation: Department of Surgical Sciences and Odontoiatry, Eye Clinic, University of Cagliari, Cagliari, Italy.
authors.forename: Enrico
authors.initials: E
authors.lastname: Peiretti
authors.forename: Antonella
authors.initials: A
authors.lastname: Mandas
authors.forename: Pierluigi
authors.initials: P
authors.lastname: Cocco
authors.forename: Claudia
authors.initials: C
authors.lastname: Norfo
authors.forename: Claudia
authors.initials: C
authors.lastname: Abete
authors.forename: Fabrizio
authors.initials: F
authors.lastname: Angius
authors.forename: Alessandra
authors.initials: A
authors.lastname: Pani
authors.forename: Sarah
authors.initials: S
authors.lastname: Vascellari
authors.forename: Guido
authors.initials: G
authors.lastname: Del Fiacco
authors.forename: Dolores
authors.initials: D
authors.lastname: Cannas
authors.forename: Giacomo
authors.initials: G
authors.lastname: Diaz
authors.forename: Sandra
authors.initials: S
authors.lastname: Dessì
authors.forename: Maurizio
authors.initials: M
authors.lastname: Fossarello
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D002470:Cell Survival; D002784:Cholesterol / Q000378:metabolism; D003228:Conjunctiva / Q000166:cytology; D004910:Erythrocyte Membrane / Q000201:enzymology; D005260:Female; D005347:Fibroblasts / Q000201:enzymology; D005954:Glucosephosphate Dehydrogenase / Q000235:genetics / Q000378:metabolism; D005955:Glucosephosphate Dehydrogenase Deficiency / Q000150:complications* / Q000201:enzymology; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress; D011625:Pterygium / Q000175:diagnosis / Q000209:etiology* / Q000601:surgery; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012307:Risk Factors
chemical_list: D012333:RNA, Messenger; D002784:Cholesterol; D006861:Hydrogen Peroxide; D005954:Glucosephosphate Dehydrogenase