Can heterogeneity of chronic sickle-cell disease pain be explained by genomics? A literature review.
This literature review explores the potential of genomics to explain, or at least contribute to the discussion about, heterogeneity in chronic pain in sickle-cell disease (SCD).


BACKGROUND
Adults with SCD, a single-gene disorder, are living longer than in years past, yet report being burdened by chronic pain. With only a few studies on chronic pain in this population, the epidemiology is unclear. However, research in the area of pain genetics continues to advance since the conclusion of the Human Genome Project. Two pain susceptibility genes, catechol-O-methyltransferase (COMT) and cytochrome P450, have, to date, been discovered that can increase individual susceptibility to the development of chronic pain.


METHODS
A search was conducted in PubMed, CINAHL, and EBSCO using the terms "sickle cell,'' "chronic pain,'' "polymorphism,'' "genetics,'' "pain genetics,'' "human,'' "adult,'' "association studies,'' and "pain susceptibility genes'' to search for articles published between 1970 and 2008.


RESULTS
Chronic pain generally is more prevalent and severe than previously reported, and individuals with SCD report daily pain. The genomic era has made it possible for scientists to identify pain susceptibility genes that contribute to variability in the interindividual experience of chronic pain.


CONCLUSIONS
Nurses are well positioned to generate and translate genomic research, thus improving care delivery. Such research may lead to the identification of polymorphisms associated with pain sensitivity in individuals with SCD.
Adegbola
Maxine A
MA
School of Nursing, The University of Texas at Arlington, Arlington, Texas 76019, USA. adegbola@uta.edu
D000328:Adult; D000701:Analgesics, Opioid / Q000378:metabolism / Q000627:therapeutic use; D000755:Anemia, Sickle Cell / Q000235:genetics*; D002394:Catechol O-Methyltransferase / Q000235:genetics; D002908:Chronic Disease; D003577:Cytochrome P-450 Enzyme System / Q000235:genetics; D005260:Female; D018740:Genetic Heterogeneity; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D023281:Genomics / Q000379:methods; D014453:Glucuronosyltransferase / Q000235:genetics; D006801:Humans; D008297:Male; D009020:Morphine / Q000378:metabolism / Q000627:therapeutic use; D024802:Nurse's Role; D010146:Pain / Q000188:drug therapy / Q000208:ethnology / Q000235:genetics*; D010597:Pharmacogenetics; D010641:Phenotype; D017450:Receptors, Opioid, mu / Q000235:genetics; D012307:Risk Factors; D012727:Sex Characteristics
D000701:Analgesics, Opioid; D017450:Receptors, Opioid, mu; D009020:Morphine; D003577:Cytochrome P-450 Enzyme System; D002394:Catechol O-Methyltransferase; C491474:UGT2B7 protein, human; D014453:Glucuronosyltransferase