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Forschungsdatenbank PMU-SQQUID

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).
Hühne, K; Leis, S; Schmelz, M; Rautenstrauss, B; Birklein, F;
Eur J Pain. 2004; 8(3):221-225
Originalarbeiten (Zeitschrift)

PMU-Autor/inn/en

Leis Stefan

Abstract

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.


Useful keywords (using NLM MeSH Indexing)

DNA Mutational Analysis

Female

Gene Frequency

Genetic Predisposition to Disease/genetics*

Genetic Testing

Genotype

Humans

Introns/genetics

Male

Mutation/genetics

Neuropeptides

Pedigree

Peptidyl-Dipeptidase A/genetics*

Phenotype

Polymorphism, Genetic/genetics*

Reflex Sympathetic Dystrophy/diagnosis

Reflex Sympathetic Dystrophy/enzymology*

Reflex Sympathetic Dystrophy/genetics*


Find related publications in this database (Keywords)

complex regional pain syndrome
neurogenic inflammation
angiotensin converting enzyme
polymorphism