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A polymorphic locus in the intron 16 of the human angiotensin‐converting enzyme (ACE) gene is not correlated with complex regional pain syndrome I (CRPS I)
Author(s) -
Hühne K.,
Leis S.,
Schmelz M.,
Rautenstrauss B.,
Birklein F.
Publication year - 2004
Publication title -
european journal of pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.305
H-Index - 109
eISSN - 1532-2149
pISSN - 1090-3801
DOI - 10.1016/j.ejpain.2003.08.004
Subject(s) - complex regional pain syndrome , allele , locus (genetics) , genotype , medicine , angiotensin converting enzyme , gene , genetics , endocrinology , biology , anesthesia , blood pressure
Exaggerated neurogenic inflammation has been recognized to be one reason for many CRPS symptoms. Since angiotensin‐converting enzyme (ACE) is a key enzyme for the termination of neurogenic inflammation, it has been selected as a candidate gene for CRPS predisposition. A previous report of an insertion/deletion (I/D) polymorphism in intron 16 within the ACE gene implicated an increased risk to develop CRPS I associated with the D allele. However, in the present study the D allele frequency was not increased in CRPS I cases (0.51 for D allele, 0.49 for I allele). Furthermore, there was no co‐segregation of any genotype ( DD , ID , II ) with the CRPS phenotype in 12 selected familial CRPS I cases from six CRPS I families. In conclusion, the results presented herein render this particular ACE gene polymorphism unlikely to be a predisposing factor for CRPS I.