Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0016053 (fibromyalgia)
 4,687 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The magnitude of placebo response and its predictors in fibromyalgia syndrome (FMS) and painful peripheral diabetic neuropathy (DPN) had not been studied. We performed a systematic review by searching MEDLINE, CENTRAL, SCOPUS, and the databases of the U.S. National Institutes of Health and the Pharmaceutical Research and Manufacturers of America until July 2010. We included randomised controlled trials of any pharmacological therapy compared with pharmacological placebo in patients with FMS and painful DPN. Pain values were converted to a 0 to 100 scale. We computed the pooled weighted mean difference (WMD) between pain baseline and end of treatment scores in placebo and active drug groups using a random effects model. A total of 72 studies (9827 patients) in FMS and of 70 studies in DPN (10,297 patients) were included. The pooled WMD in the FMS-placebo group was 7.69 (95% confidence interval [CI] 6.10 to 9.29) and 17.11 (95% CI 16.41 to 17.90) in painful DPN. The pooled WMD in the FMS-active drug group was 13.96 (95% CI 11.93 to 15.99) and in painful DPN was 22.54 (95% CI 20.49 to 24.58). The correlation between WMD in the placebo and active drug group in FMS was r=0.69 and painful DPN r=0.47. Placebo accounted for 45% of the response in the drug groups in FMS and for 62% in painful DPN. The placebo response was higher in painful DPN than in FMS (P<.001). The placebo response was not associated with age, sex, and race, but with year of study initiation, pain baseline, and effect size in active drug groups in both diseases.
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PMID:Systematic review: Placebo response in drug trials of fibromyalgia syndrome and painful peripheral diabetic neuropathy-magnitude and patient-related predictors. 2143 89

The definition of dual tryptophan pathways has increased the understanding of the mind-body, body-mind dichotomy. The serotonergic pathway highlights the primary (endogenous) psychiatric disorders. The up-regulation of the kynurenine pathway by physical illnesses can cause neuropathic and immunological disorders1 associated with secondary neuropsychiatric symptoms. Tryptophan and nicotinamide deficiencies fall within the protein energy malnutrition (PEM) spectrum. They can arise if the kynurenine pathway is stressed by primary or secondary inflammatory conditions and the consequent imbalance of available catabolic/anabolic substrates may adversely influence convalescent phase efficiency. The replacement of depleted or reduced NAD+ levels and other cofactors can perhaps improve the clinical management of these disorders. Chronic fatigue syndrome (CFS) and fibromyalgia (FM) appear to meet the criteria of a tryptophan-kynurenine pathway disorder with potential neuroimmunological sequelae. Aspects of some of the putative precipitating factors have been previously outlined.2,3 An analysis of the areas of metabolic dysfunction will focus on future directions for research and management.
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PMID:Kynurenine Pathway Pathologies: do Nicotinamide and Other Pathway Co-Factors have a Therapeutic Role in Reduction of Symptom Severity, Including Chronic Fatigue Syndrome (CFS) and Fibromyalgia (FM). 2392 1