Lack of genetic association of neutral endopeptidase (NEP) with complex regional pain syndrome (CRPS) |
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| Authors: | Kathrin Huehne,Ute Schaal,Stefan Leis,Steffen Uebe,M. Florencia Gosso,Arn M.J.M. van den Maagdenberg,Christian Maihö fner,Frank Birklein,Bernd Rautenstrauss,Andreas Winterpacht |
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| Affiliation: | 1. Institute of Human Genetics, University Hospital Erlangen-Nuremberg, Schwabachanlage 10, 91054 Erlangen, Germany;2. Division of Molecular and Experimental Surgery, University Clinical Center Erlangen, Schwabachanlage 10, 91054 Erlangen, Germany;3. Department of Neurology, University Hospital Erlangen-Nuremberg, Erlangen, Schwabachanlage 6, 91054 Erlangen, Germany;4. Department of Neurology, Christian-Doppler-Clinic, University Hospital, Paracelsus Private Medical University, Ignaz Harrer Straße 79, 5020 Salzburg, Austria;5. Department of Human Genetics, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands;6. Department of Neurology, Leiden University Medical Center, PO Box 9600, 2300 RC Leiden, The Netherlands;g Department of Neurology, Pain Research Unit, University of Mainz, Langenbeckstr. 1, 55101 Mainz, Germany;h MGZ, Medical Genetics Center, Bayerstraße 3-5, 80335 Munich, Germany |
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| Abstract: | 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. |
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| Keywords: | CRPS Pain NEP Association |
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