Funded by grants from FORSS (Medical Research Council of Southeast Sweden) and Futurum—the academy for healthcare, Jönköping County council.
Polymorphisms of GSTT1, GSTM1, and EPHX genotypes in patients with cryptogenic polyneuropathy: a case–control study
Article first published online: 31 JUL 2012
©2011 The Authors. Brain and Behavior published by Blackwell Publishing Ltd.
This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
Brain and Behavior
Volume 1, Issue 2, pages 135–141, November 2011
How to Cite
Lindh, J., Söderkvist, P., Fredrikson, M., Hosseininia, S., Tondel, M., Persson, B. and Vrethem, M. (2011), Polymorphisms of GSTT1, GSTM1, and EPHX genotypes in patients with cryptogenic polyneuropathy: a case–control study. Brain and Behavior, 1: 135–141. doi: 10.1002/brb3.26
- Issue published online: 31 JUL 2012
- Article first published online: 31 JUL 2012
- Received: 14 June 2011; Revised: 02 September 2011; Accepted: 12 September 2011
- Chronic idiopathic axonal neuropathy;
- Glutathione S-Transferase;
- epoxide hydrolase;
The aim of this study was to analyze whether polymorphisms for the null alleles of Glutathione S-Transferase Mu-1 (GSTM1), Glutathione S-Transferase Theta-1 (GSTT1), and a low-activity genetic variation of epoxide hydrolase exon three (EPHX*3) affect the risk of developing polyneuropathy. The enzymes of these genes are important in the metabolism of toxic compounds. Seventy-nine patients with cryptogenic polyneuropathy (equivalent to chronic idiopathic axonal neuropathy) and 398 controls were tested for the genetic polymorphism. Medical records were reviewed to collect data regarding clinical findings at diagnosis, and exposure data was collected via questionnaires. The odds ratios (ORs) for the null forms of GSTM1 and GSTT1 and the normal activity YY form of EPHX*3 were close to one except GSTT1, which reached 1.86. The highest risk of polyneuropathy was found in smokers with GSTT1 null, who had a 3.7 times increased risk. Interactions between genes were analyzed and confirmed the increased OR for GSTT1, which was strongest if the patients had the low-activity HH form of EPHX*3 (OR 2.37). Our hypothesis is that the GSTT1 null polymorphism may be related to an impaired metabolism of toxic substances that could lead to nerve damage in the peripheral nervous system.