Polymorphisms in the GTP cyclohydrolase gene ( GCH1 ) are associated with ratings of capsaicin pain

Campbell, Claudia M.; Edwards, Robert R.; Carmona, Cheryl; Uhart, Magdalena; Wand, Gary S.; Carteret, Alene F.; Kim, Yu Kyeong; Frost, J. James; Campbell, James N.

doi:10.1016/j.pain.2008.10.023

Cited by 91 publications

(81 citation statements)

References 20 publications

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“…1). Similar correlations with pain hypersensitivity have since been found in three independent studies of different populations [11,12]. This shows the utility of validating a putative target with human polymorphisms in its gene.…”

Section: Choice Of Targetsupporting

confidence: 81%

Future Directions in Neuropathic Pain Therapy: Closing the Translational Loop

Bačkonja

Woolf

2010

The Oncologist

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In the majority of patients, existing therapies for neuropathic pain are far from effective. Furthermore, all current treatments are symptomatic rather than disease-modifying or curative. A range of therapeutic modalities is emerging, targeting a variety of mechanisms, but choosing the best target and evaluating the resulting therapies against the many types of neuropathic pain disorders is not an easy task. In this article, we suggest a shift in emphasis of the drug discovery paradigm toward unbiased evaluation of the particular neurobiological mechanisms contributing to neuropathic pain in individual patients. Genomewide association studies and other discovery science approaches to identify significant novel targets should be given priority as should the development of increasingly sophisticated tools for measuring and categorizing neuropathic pain. The Oncologist 2010; 15(suppl 2):24 -29

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Section: Choice Of Targetsupporting

confidence: 81%

Future Directions in Neuropathic Pain Therapy: Closing the Translational Loop

Bačkonja

Woolf

2010

The Oncologist

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“…Some of these gene products are implicated in a predisposition toward pain hypersensitivity, including catechol-O-methyltransferase (gene designation: COMT) [450], the opioid receptor μ1 (OPRM1) [451,452], and GTP cyclohydrolase (GCH1), which may also influence the extent and duration of clinical pain [453][454][455]. However, in several large European cohorts, COMT SNPs and haplotypes did not show any associations with CWP or other chronic musculoskeletal complaints [456,457] and GCH1 did not confer any risk of CWP [458].…”

Section: Potential Pathogenetic Mechanisms Genetics and Epigeneticsmentioning

confidence: 99%

Fibromyalgia: A Critical and Comprehensive Review

Borchers

Gershwin

2015

Clinic Rev Allerg Immunol

225

217

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Fibromyalgia is a disorder that is part of a spectrum of syndromes that lack precise classification. It is often considered as part of the global overview of functional somatic syndromes that are otherwise medically unexplained or part of a somatization disorder. Patients with fibromyalgia share symptoms with other functional somatic problems, including issues of myalgias, arthralgias, fatigue and sleep disturbances. Indeed, there is often diagnostic and classification overlap for the case definitions of a variety of somatization disorders. Fibromyalgia, however, is a critically important syndrome for physicians and scientists to be aware of. Patients should be taken very seriously and provided optimal care. Although inflammatory, infectious, and autoimmune disorders have all been ascribed to be etiological events in the development of fibromyalgia, there is very little data to support such a thesis. Many of these disorders are associated with depression and anxiety and may even be part of what has been sometimes called affected spectrum disorders. There is no evidence that physical trauma, i.e., automobile accidents, is associated with the development or exacerbation of fibromyalgia. Treatment should be placed on education, patient support, physical therapy, nutrition, and exercise, including the use of drugs that are approved for the treatment of fibromyalgia. Treatment should not include opiates and patients should not become poly pharmacies in which the treatment itself can lead to significant morbidities. Patients with fibromyalgia are living and not dying of this disorder and positive outlooks and family support are key elements in the management of patients.

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“…Variations in the GCH1 gene are closely associated with pain sensitivity. Changes in GCH1 enzyme activity can lead to higher BH4 levels and increased NO production, which enhances pain sensitivity, while specific GCH1 gene polymorphisms have a pain-protective role [51,52]. With this in the background, Kim et al have studied specific SNPs and haplotypes of the GCH1 gene among FMS patients [53].…”

Section: Role Of the Catechol-o-methyltransferase Gene Polymorphism Imentioning

confidence: 99%