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Polymorphisms of GSTT1, GSTM1 and EPHX genotypes in patients with cryptogenic polyneuropathy: a case control study

Lindh, Jonas, 1967- (author)
Linköpings universitet,Neurologi,Hälsouniversitetet,Polyneuropatigruppen, Neurofys, Linköping
Söderkvist, Peter (author)
Linköpings universitet,Cellbiologi,Hälsouniversitetet
Fredrikson, Mats (author)
Linköpings universitet,Yrkes- och miljömedicin,Hälsouniversitetet
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Hosseininia, Shahzad (author)
Yrkes och miljömedicin, Medicinska fakulteten, Teherans universitet, Teheran, Iran
Tondel, Martin, 1962 (author)
Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för samhällsmedicin och folkhälsa,Institute of Medicine, School of Public Health and Community Medicine,Arbets- och miljömedicin, Sahlgrenska Universitetssjukhuset, Göteborg
Persson, Bodil (author)
Östergötlands Läns Landsting,Linköpings universitet,Yrkes- och miljömedicin,Hälsouniversitetet,Arbets- och miljömedicin
Vrethem, Magnus (author)
Östergötlands Läns Landsting,Linköpings universitet,Klinisk neurofysiologi,Hälsouniversitetet,Neurologiska kliniken
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 (creator_code:org_t)
2012-07-31
2011
English.
In: Brain and Behavior. - Hoboken, New Jersey, USA : John Wiley & Sons, Inc. - 2162-3279. ; 1:2, s. 135-141
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • The aim of this study was to analyze whether polymorphisms for the null alleles of Glutathione S-Transferase Mu-1 (GSTM1) and 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. 79 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 (OR) 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 odds ratio 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.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Neurologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Neurology (hsv//eng)

Keyword

Polyneuropathy
Neurology
Neurologi

Publication and Content Type

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