Addiction Rehab: Erratum To: Validation of the PHQ-15 for Somatoform Disorder in the Occupational Health Care Setting.
Erratum to: Validation of the PHQ-15 for Somatoform Disorder in the Occupational Health Care Setting.
Filed under: Addiction Rehab
J Occup Rehabil. 2012 Aug 21;
de Vroege L, Hoedeman R, Nuyen J, Sijtsma K, van der Feltz-Cornelis CM
General mechanisms of nicotine-induced fibrogenesis.
Filed under: Addiction Rehab
FASEB J. 2012 Aug 20;
Jensen K, Nizamutdinov D, Guerrier M, Afroze S, Dostal D, Glaser S
Cigarette smoking contributes to the development of cancer, and pathogenesis of other diseases. Many chemicals have been identified in cigarettes that have potent biological properties. Nicotine is especially known for its role in addiction and plays a role in other physiological effects of smoking and tobacco use. Recent studies have provided compelling evidence that, in addition to promoting cancer, nicotine also plays a pathogenic role in systems, such as the lung, kidney, heart, and liver. In many organ systems, nicotine modulates fibrosis by altering the functions of fibroblasts. Understanding the processes modulated by nicotine holds therapeutic potential and may guide future clinical and research decisions. This review discusses the role of nicotine in the general fibrogenic process that governs fibrosis and fibrosis-related diseases, focusing on the cellular mechanisms that have implications in multiple organ systems. Potential research directions for the management of nicotine-induced fibrosis, and potential clinical considerations with regard to nicotine-replacement therapy (NRT) are presented.-Jensen, K., Nizamutdinov, D., Guerrier, M., Afroze, S., Dostal, D., Glaser, S. General mechanisms of nicotine-induced fibrogenesis.
HubMed – addiction
Pharmacogenetic Randomized Trial for Cocaine Abuse: Disulfiram and Dopamine ?-Hydroxylase.
Filed under: Addiction Rehab
Biol Psychiatry. 2012 Aug 17;
Kosten TR, Wu G, Huang W, Harding MJ, Hamon SC, Lappalainen J, Nielsen DA
BACKGROUND: Disulfiram has been an effective cocaine addiction pharmacotherapy, and one of its possible mechanisms of efficacy is through copper chelation and inhibition of an enzyme involved in catecholamine metabolism, dopamine ?-hydroxylase (D?H), which converts dopamine to norepinephrine. A variant in the gene encoding D?H leads to reduced D?H activity, and as such, disulfiram might not be an effective treatment of cocaine dependence for individuals with this variant. This study explored that potential matching. METHODS: Seventy-four cocaine- and opioid-codependent (DSM-V) subjects were stabilized on methadone for 2 weeks and subsequently randomized into disulfiram (250 mg/day, n = 34) and placebo groups (n = 40) for 10 weeks. We genotyped the DBH gene polymorphism, -1021C/T (rs1611115), that reduces D?H enzyme levels and evaluated its role for increasing cocaine free urines with disulfiram. RESULTS: With repeated measures analysis of variance, corrected for population structure, disulfiram pharmacotherapy reduced cocaine-positive urines from 80% to 62% (p = .0001), and this disulfiram efficacy differed by DBH genotype group. Patients with the normal D?H level genotype dropped from 84% to 56% on disulfiram (p = .0001), whereas those with the low DBH level genotype showed no disulfiram effect. CONCLUSIONS: This study indicates that the DBH genotype of a patient could be used to identify a subset of individuals for which disulfiram treatment might be an effective pharmacotherapy for cocaine dependence.
HubMed – addiction
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