Methylphenidate and amphetamine do not induce cytogenetic damage in lymphocytes of children with ADHD.

Published

Journal Article

OBJECTIVE: In response to previously published findings of methylphenidate-induced chromosomal changes in children, this study was designed to determine whether methylphenidate- or amphetamine-based drugs induce chromosomal damage (structural aberrations, micronuclei, and sister chromatid exchanges) in peripheral blood lymphocytes of children with attention-deficit/hyperactivity disorder after 3 months of continuous treatment. METHOD: Stimulant drug-naïve subjects, 6 to 12 years of age, in good overall health, and judged to be appropriate candidates for stimulant therapy based on rigorously diagnosed ADHD using DSM-IV criteria, were randomized into two open-label treatment groups (methylphenidate or mixed amphetamine salts). Each subject provided a blood sample before initiation of treatment and after 3 months of treatment. Pretreatment and posttreatment frequencies of chromosomal aberrations, micronuclei, and sister chromatid exchanges were determined for each subject. RESULTS: Sixty-three subjects enrolled in the study; 47 subjects completed the full 3 months of treatment, 25 in the methylphenidate group and 22 in the amphetamine group. No significant treatment-related increases were observed in any of the three measures of cytogenetic damage in the 47 subjects who completed treatment or the 16 subjects who did not. CONCLUSIONS: Earlier findings of methylphenidate-induced chromosomal changes in children were not replicated in this study. These results add to the accumulating evidence that therapeutic levels of methylphenidate do not induce cytogenetic damage in humans. Furthermore, our results indicate that amphetamine-based products do not pose a risk for cytogenetic damage in children.

Full Text

Duke Authors

Cited Authors

  • Witt, KL; Shelby, MD; Itchon-Ramos, N; Faircloth, M; Kissling, GE; Chrisman, AK; Ravi, H; Murli, H; Mattison, DR; Kollins, SH

Published Date

  • December 2008

Published In

Volume / Issue

  • 47 / 12

Start / End Page

  • 1375 - 1383

PubMed ID

  • 18978633

Pubmed Central ID

  • 18978633

Electronic International Standard Serial Number (EISSN)

  • 1527-5418

Digital Object Identifier (DOI)

  • 10.1097/CHI.0b013e3181893620

Language

  • eng

Conference Location

  • United States