Deficit of circulating stem – progenitor cells in opiate addiction: a pilot study

<p>Abstract</p> <p>A substantial literature describes the capacity of all addictive drugs to slow cell growth and potentiate apoptosis. Flow cytometry was used as a means to compare two lineages of circulating progenitor cells in addicted patients. Buprenorphine treated opiate addi...

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Bibliographic Details
Main Authors: Davidson Peter, Reece Albert S
Format: Article
Language:English
Published: BMC 2007-07-01
Series:Substance Abuse Treatment, Prevention, and Policy
Online Access:http://www.substanceabusepolicy.com/content/2/1/19
Description
Summary:<p>Abstract</p> <p>A substantial literature describes the capacity of all addictive drugs to slow cell growth and potentiate apoptosis. Flow cytometry was used as a means to compare two lineages of circulating progenitor cells in addicted patients. Buprenorphine treated opiate addicts were compared with medical patients. Peripheral venous blood CD34<sup>+ </sup>CD45<sup>+ </sup>double positive cells were counted as haemopoietic stem cells (HSC's), and CD34<sup>+ </sup>KDR<sup>+ </sup>(VEGFR2<sup>+</sup>) cells were taken as endothelial progenitor cells (EPC's). 10 opiate dependent patients with substance use disorder (SUD) and 11 non-addicted (N-SUD) were studied. The ages were (mean + S.D.) 36.2 + 8.6 and 56.4 + 18.6 respectively (P <0.01). HSC's were not different in the SUD (2.38 + 1.09 Vs. 3.40 + 4.56 cells/mcl). EPC's were however significantly lower in the SUD (0.09 + 0.14 Vs. 0.26 + 0.20 cells/mcl; No. > 0.15, OR = 0.09, 95% C.I. 0.01–0.97), a finding of some interest given the substantially older age of the N-SUD group. These laboratory data are thus consistent with clinical data suggesting accelerated ageing in addicted humans and implicate the important stem cell pool in both addiction toxicology and ageing. They carry important policy implications for understanding the fundamental toxicology of addiction, and suggest that the toxicity both of addiction itself and of indefinite agonist maintenance therapies may have been seriously underestimated.</p>
ISSN:1747-597X