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TRPM8 polymorphisms associated with increased risk of IBS-C and IBS-M
  1. Maria Henström1,
  2. Fatemeh Hadizadeh1,2,
  3. Arthur Beyder3,
  4. Ferdinando Bonfiglio1,4,
  5. Tenghao Zheng1,
  6. Ghazaleh Assadi1,
  7. Joseph Rafter1,
  8. Luis Bujanda4,
  9. Lars Agreus5,
  10. Anna Andreasson5,6,
  11. Aldona Dlugosz7,
  12. Greger Lindberg7,
  13. Peter T Schmidt7,
  14. Pontus Karling8,
  15. Bodil Ohlsson9,
  16. Nicholas J Talley10,
  17. Magnus Simren11,
  18. Susanna Walter12,
  19. Mira Wouters13,
  20. Gianrico Farrugia3,
  21. Mauro D'Amato4,14,15,16
  1. 1Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden
  2. 2School of Nutrition, Isfahan University of Medical Sciences, Isfahan, Iran
  3. 3Enteric Neuroscience Program, Division of Gastroenterology and Hepatology, Department of Physiology and Biomedical Engineering, Mayo Clinic, Rochester, Minnesota, USA
  4. 4Department of Gastrointestinal and Liver Diseases, BioDonostia Health Research Institute, San Sebastian, Spain
  5. 5Division for Family Medicine, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
  6. 6Stress Research Institute, Stockholm University, Stockholm, Sweden
  7. 7Department of Medicine, Karolinska Institutet, Center for Digestive Diseases, Karolinska University Hospital Huddinge, Stockholm, Sweden
  8. 8Division of Medicine, Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden
  9. 9Department of Internal Medicine, Lund University, Skåne University Hospital, Sweden
  10. 10Faculty of Health and Medicine, University of Newcastle, Newcastle, New South Wales, Australia
  11. 11Department of Internal Medicine and Clinical Nutrition, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
  12. 12Division of Neuro and Inflammation Science, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden
  13. 13Translational Research Center for Gastrointestinal Disorders (TARGID), Leuven University, Leuven, Belgium
  14. 14BioCruces Health Research Institute, Bilbao, Spain
  15. 15IKERBASQUE, Basque Foundation for Science, Bilbao, Spain
  16. 16Clinical Epidemiology Unit, Department of Medicine Solna, Karolinska Institutet, Stockholm, Sweden
  1. Correspondence to Professor Mauro D'Amato, BioDonostia Health Research Institute, Donostia University Hospital, Paseo Dr Begiristain s/n, San Sebastian E-200014, Spain; mauro.damato{at}biodonostia.org

https://doi.org/10.1136/gutjnl-2016-313346

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    Recently in Gut, genetic variation affecting ion channels activity has been highlighted in relation to bowel function and the biology of stool frequency.1 It is also known that 2% of patients with IBS carry functional missense mutations in the voltage-gated channel NaV1.5 (SCN5A gene).2 Hence, channelopathies represent potential abnormalities underlying GI dysfunction and IBS. We inspected data from our previous genome-wide association study (GWAS) of IBS,3 in relation to 27 genes whose ion channel products contribute to GI sensorimotor development and function, visceral sensation and GI motility (see online supplementary table S1). Significant (uncorrected) results were detected for four genes (calcium voltage-gated channels CACNA1A and CACNA1E, and transient receptor potential channels TRPV3 and TRPM8; see online supplementary figure S1), which were selected for replication analyses in an independent set of IBS cases (N=386) and controls (N=357) (see online supplementary material methods). A sex-adjusted logistic regression analysis of genotype data from this cohort (see online supplementary material methods) detected significant associations for …

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