title: Absence of association between angiotensin converting enzyme polymorphism and development of adult respiratory distress syndrome in patients with severe acute respiratory syndrome: a case control study.
abstract: BACKGROUND
  It has been postulated that genetic predisposition may influence the susceptibility to SARS-coronavirus infection and disease outcomes. A recent study has suggested that the deletion allele (D allele) of the angiotensin converting enzyme (ACE) gene is associated with hypoxemia in SARS patients. Moreover, the ACE D allele has been shown to be more prevalent in patients suffering from adult respiratory distress syndrome (ARDS) in a previous study. Thus, we have investigated the association between ACE insertion/deletion (I/D) polymorphism and the progression to ARDS or requirement of intensive care in SARS patients.
  
  
  METHODS
  One hundred and forty genetically unrelated Chinese SARS patients and 326 healthy volunteers were recruited. The ACE I/D genotypes were determined by polymerase chain reaction and agarose gel electrophoresis.
  
  
  RESULTS
  There is no significant difference in the genotypic distributions and the allelic frequencies of the ACE I/D polymorphism between the SARS patients and the healthy control subjects. Moreover, there is also no evidence that ACE I/D polymorphism is associated with the progression to ARDS or the requirement of intensive care in the SARS patients. In multivariate logistic analysis, age is the only factor associated with the development of ARDS while age and male sex are independent factors associated with the requirement of intensive care.
  
  
  CONCLUSIONS
  The ACE I/D polymorphism is not directly related to increased susceptibility to SARS-coronavirus infection and is not associated with poor outcomes after SARS-coronavirus infection.
authors.affiliation: The Centre for Emerging Infectious Diseases, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong. allen@cuhk.edu.hk
authors.forename: K C Allen
authors.initials: KC
authors.lastname: Chan
authors.forename: Nelson L S
authors.initials: NL
authors.lastname: Tang
authors.forename: David S C
authors.initials: DS
authors.lastname: Hui
authors.forename: Grace T Y
authors.initials: GT
authors.lastname: Chung
authors.forename: Alan K L
authors.initials: AK
authors.lastname: Wu
authors.forename: Stephen S C
authors.initials: SS
authors.lastname: Chim
authors.forename: Rossa W K
authors.initials: RW
authors.lastname: Chiu
authors.forename: Nelson
authors.initials: N
authors.lastname: Lee
authors.forename: K W
authors.initials: KW
authors.lastname: Choi
authors.forename: Y M
authors.initials: YM
authors.lastname: Sung
authors.forename: Paul K S
authors.initials: PK
authors.lastname: Chan
authors.forename: Y K
authors.initials: YK
authors.lastname: Tong
authors.forename: S T
authors.initials: ST
authors.lastname: Lai
authors.forename: W C
authors.initials: WC
authors.lastname: Yu
authors.forename: Owen
authors.initials: O
authors.lastname: Tsang
authors.forename: Y M Dennis
authors.initials: YM
authors.lastname: Lo
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000483:Alleles; D016022:Case-Control Studies; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism; D011110:Polymorphism, Genetic / Q000235:genetics*; D012128:Respiratory Distress Syndrome / Q000150:complications* / Q000235:genetics*; D045169:Severe Acute Respiratory Syndrome / Q000150:complications*
chemical_list: D007703:Peptidyl-Dipeptidase A