6533b833fe1ef96bd129b78a

RESEARCH PRODUCT

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).

Martin SchmelzFrank BirkleinBernd RautenstraussK. HühneS. Leis

subject

MaleCandidate geneGenotypeDNA Mutational AnalysisPeptidyl-Dipeptidase Amedicine.disease_causeGene FrequencyPolymorphism (computer science)GenotypemedicineHumansGenetic Predisposition to DiseaseGenetic TestingAlleleAllele frequencyGeneticsMutationPolymorphism GeneticbiologyNeuropeptidesAngiotensin-converting enzymemedicine.diseaseIntronsPedigreeReflex Sympathetic DystrophyAnesthesiology and Pain MedicineComplex regional pain syndromePhenotypeImmunologyMutationbiology.proteinFemale

description

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.

yearjournalcountryeditionlanguage
2004-06-01European journal of pain (London, England)
10.1016/j.ejpain.2003.08.004https://pubmed.ncbi.nlm.nih.gov/15109972