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Association of insertion/deletion polymorphism of the angiotensin‐converting enzyme gene with psoriasis
Author(s) -
Ozkur M.,
Erbagci Z.,
Nacak M.,
Tuncel A.A.,
Alasehirli B.,
Aynacioglu A.S.
Publication year - 2004
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2004.06148.x
Subject(s) - psoriasis , gene , angiotensin converting enzyme , genetics , polymorphism (computer science) , medicine , biology , genotype , dermatology , blood pressure
Summary Background Genetic factors are likely to be of fundamental importance in the pathogenesis of psoriasis. There are reports concerning the induction or/and exacerbation of psoriasis by angiotensin‐converting enzyme (ACE) inhibitors, which have been attributed to the ACE inhibitor‐induced augmentation of kinin levels in skin. However, to the best of our knowledge there has been no molecular genetic study investigating whether ACE insertion/deletion (I/D) polymorphism may contribute to the genetic background in psoriasis. Objectives To assess the role of ACE I/D polymorphism in psoriasis. Methods A group of 86 patients with psoriasis and 154 control subjects were analysed for ACE I/D polymorphism by polymerase chain reaction. Results The distribution of ACE I/D polymorphism and allele frequencies in psoriatic patients was not significantly different from controls. Further analyses of psoriasis patients showed that ACE I/D polymorphism was not associated with age at onset of disease, clinical type of psoriasis or gender. However, the frequency of the I allele was significantly higher in patients with a positive family history of psoriasis than in those with no family history (sporadic psoriasis) (48% vs. 32%; P =0·03). In addition, the I allele was found significantly more frequently in type I psoriasis patients (onset < 40 years and positive family history) than in type II psoriasis patients (onset ≥ 40 years, no family history) (48% vs. 27%; P = 0·04). Conclusions Our results suggest that the presence of the I allele may confer susceptibility to development of psoriasis in individuals from psoriatic families.