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. 2013 Feb 22;110(8):133. doi: 10.3238/arztebl.2013.0133b

Correspondence (reply): In Reply

Ingolf Cascorbi *
PMCID: PMC3594711  PMID: 23505402

The considerations of the article on drug interactions apply not only to patients with multimorbidities but also in general.

I agree that the consequences of pharmacokinetic interactions are more pronounced especially among drugs with a narrow therapeutic range. Lithium is a further typical example in this context.

The correspondent’s statement that dexamethasone “seals” the blood-brain barrier and thus inhibits the penetration of the alkylant temozolomide, which is indicated for glioblastoma tumors, lacks evidence. Möhnle et al. discuss non-genomic effects of high-dose dexamethasone on plasma membranes, which would lead to inhibition of the Na+- and K+-fluxes, rather than pharmacokinetic interactions with temozolomide (1). A reduction of the bioavailability of temozolomide in the central nervous system in presence of glucocorticoids has not been described. However, there are in-vitro indications of a pharmacodynamic interaction, albeit one whose effects are negative: it seems that dexamethasone protects human glioblastoma cells from temozolomide induced apoptosis (2, 3).

There are certainly many specific examples that provide an impetus for further discussion; however, our CME article aimed to provide a systematic overview of pharmacokinetic interactions in principle and, in addition, to draw attention to some examples of typical pharmacodynamic interactions that should be considered during therapy.

Footnotes

Conflict of interest statement

The authors of all contributions declare that no conflict of interest exists.

References

  • 1.Möhnle P, Uhl E, Briegel J. Glukokortikoide in der Neurointensivmedizin - welche Indikationen sind gesichert? J Neurol Neurochir Psychiatr. 2008;9:7–12. [Google Scholar]
  • 2.Das A, Banik NL, Patel SJ, Ray SK. Dexamethasone protected human glioblastoma U87MG cells from temozolomide induced apoptosis by maintaining Bax: Bcl-2 ratio and preventing proteolytic activities. Mol Cancer. 2004;3 doi: 10.1186/1476-4598-3-36. [DOI] [PMC free article] [PubMed] [Google Scholar]
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  • 4.Cascorbi I. Drug interactions—principles, examples and clinical consequences. Dtsch Arztebl Int. 2012;109(33-34):546–556. doi: 10.3238/arztebl.2012.0546. [DOI] [PMC free article] [PubMed] [Google Scholar]

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