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RESEARCH PRODUCT

Lack of genetic association of neutral endopeptidase (NEP) with complex regional pain syndrome (CRPS)

Arn M. J. M. Van Den MaagdenbergStefan LeisSteffen UebeChristian MaihöfnerFrank BirkleinBernd RautenstraussUte SchaalAndreas WinterpachtKathrin HuehneM. Florencia Gosso

subject

AdultMalemedicine.medical_specialtyLinkage disequilibrium5' Flanking RegionSubstance PHuman leukocyte antigenBiologyCalcitonin gene-related peptideLinkage Disequilibriumchemistry.chemical_compoundInternal medicinemedicineHumansGenetic Predisposition to DiseaseDinucleotide RepeatsPromoter Regions GeneticNeprilysinGenetic Association StudiesGenetic associationNeurogenic inflammationPolymorphism GeneticGeneral NeurosciencefungiMiddle Agedmedicine.diseaseCRPS Pain NEP Association reflex sympathetic dystrophy syndrome type-i facilitated neurogenic inflammation nociceptive abnormalities alzheimers-disease neprilysin gene rat model enkephalinase prevalence dystoniaEndocrinologyComplex regional pain syndromechemistryCase-Control StudiesFemaleNeprilysinComplex Regional Pain Syndromes

description

Complex regional pain syndrome (CRPS) is a condition that is characterized by severe pain and exaggerated neurogenic inflammation, which may develop after injury or surgery. Neurogenic inflammation is mediated by neuropeptides, such as calcitonin gene-related peptide (CGRP) and substance P (SP) that are released from nociceptors. Genetic factors may play a role in CRPS as was suggested by the occurrence of familial cases and several genetic association studies investigating mainly the human leukocyte antigen (HLA) system. Here we investigated the role of neutral endopeptidase (NEP), a key enzyme in neuropeptide catabolism. NEP dysfunction resulting in reduced inactivation of neuropeptides may be a possible pathomechanism in CRPS. To this end, we tested a GT-repeat polymorphism, in the NEP promoter region as well as 18 tag-SNPs in six linkage disequilibrium (LD) blocks in the NEP gene region in 320 CRPS patients and 376 controls. No significant genetic association was observed. Thus, we conclude that the NEP gene does not seem to be a major risk factor for CRPS. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

yearjournalcountryeditionlanguage
2010-03-12
10.1016/j.neulet.2010.01.044http://hdl.handle.net/1887/100781