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The influence of tumor necrosis factor gene polymorphisms on experimental and clinical pain responses in humans
Author(s) -
Kim H.,
Picco C.,
Rowan J.,
Brahim J.,
Dionne R.
Publication year - 2004
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/j.clpt.2003.11.262
Subject(s) - single nucleotide polymorphism , medicine , analgesic , tumor necrosis factor alpha , cohort , pharmacogenetics , genotype , chronic pain , oncology , anesthesia , pharmacology , gene , biology , genetics , physical therapy
Acute inflammation following tissue injury is characterized by the synthesis, release, and expression of inflammatory mediators and their activation of pain receptors. Tumor necrosis factor (TNF) family is associated with many chronic inflammatory conditions; however, its role in acute inflammation and pain has not been clearly elucidated. In this study, we examined the influence of common genetic polymorphisms of TNF‐α and β genes on the modulation of clinically and experimentally induced acute pain in humans. Subjects (N=560) rated sensory intensity and unpleasantness for heat stimuli and 3 min cold pressor test. From the total sample, 146 patients underwent standardized oral surgery; maximum postoperative pain was recorded after local anesthetic offset by visual analog scale; the response to a fixed dose of NSAID analgesic (ketorolac 15 mg I.V.) was evaluated. For genotyping of genomic DNA, 5′ exonuclease allelic discrimination assay was used. In the present human cohort, 4 TNF‐α single nucleotide polymorphisms (SNPs) in promoter region and one mis‐sense and 5′ untranslated region SNPs from TNF‐β gene did not demonstrate any significant association with clinically or experimentally induced pain responses or on NSAID analgesia. Although none of the SNPs evaluated showed an association with pain responses for this cohort, this may not be representative of individual responses, the effect of other TNF polymorphisms, or other acute pain conditions. Clinical Pharmacology & Therapeutics (2004) 75 , P70–P70; doi: 10.1016/j.clpt.2003.11.262