Cancer patients who smoke have significantly lower levels of irinotecan and its active metabolite than non-smokers. They also had much less toxicity leading researchers to question whether or not they are at risk for treatment failure.
Analyzing the available dose of irinotecan in the blood of both smokers and non-smokers, scientists found less drug for smokers. In addition, smokers had an almost 40 percent reduction in the level of SN-38. Irinotecan is converted to SN-38 by body enzymes, and SN-38 attacks cancer cells.
Only 6 percent of smokers being treated with irinotecan developed serious low white cell counts (neutropenia) compared to 38 percent of non-smokers in the study. There was no significant difference in diarrhea.
Jessica M. van der Bol and her colleagues in the Netherlands, Sweden, and the United States speculated that cigarette smoke interferes with the enzymes that metabolize irinotecan. They concluded,
This study indicates that smoking significantly lowers both the exposure to irinotecan and treatment-induced neutropenia, indicating a potential risk of treatment failure. Although the underlying mechanism is not entirely clear, modulation of CYP3A and uridine diphosphate glucuronosyltransferase isoform 1A1 may be part of the explanation. The data suggest that additional investigation is warranted to determine whether smokers are at increased risk for treatment failure.
SOURCE: van der Bol et.al. Journal of Clinical Oncology, Volume 25, Number 19, July 1, 2007.
WHAT THIS MEANS FOR PATIENTS
If you are receiving Camptosar® (irinotecan or CPT-11) chemotherapy and smoke, talk to your doctor about dosage. Stopping smoking might make the treatment more effective for you.



