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Menopausal status and estrogen receptor genotypes influenced the severity of hot flashes after tamoxifen treatment
Author(s) -
Jin Y.,
Skaar T.,
Storniolo A.,
Desta Z.,
Nguyen A.,
Li L.,
Hayes D.,
Flockhart D. A.,
Stearns V.
Publication year - 2005
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1016/j.clpt.2004.11.017
Subject(s) - tamoxifen , hot flash , medicine , postmenopausal women , observational study , menopause , oncology , estrogen receptor , genotype , prospective cohort study , post menopausal , estrogen , selective estrogen receptor modulator , genotyping , gynecology , endocrinology , breast cancer , cancer , biology , biochemistry , gene
Background/Aims Hot flashes are the most common side effect of tamoxifen treatment. We conducted a prospective observational trial to evaluate factors that influenced hot flash severity after tamoxifen treatment. Methods Hot flashes frequency and severity were recorded in 7‐day hot flashes diaries before, and 1, 4, 8, 12 months after tamoxifen treatment in 122 subjects. Hot flashes composit scores were calculated. Demographic information was collected at baseline, and estrogen receptor (ESR1 & 2) genotyping was also performed. Results Pre‐menopausal women showed the biggest increase in hot flashes severity, from 5.2±10.5 at baseline to 28.5±51.6 at 4 month (P<0.0001), whereas there was no significant change in peri‐ or postmenopausal women. Twenty‐two of the 122 women did not develop hot flashes. G allele carriers of the ESR2‐02 SNP were 4.2 times more likely to develop hot flashes than homozygotes with AA genotype (P=0.008). Conclusion Pre‐menopausal women were most likely to develop hot flashes after tamoxifen treatment. ESR2‐02 genotype may also influence the risk of developing hot flashes after tamoxifen treatment. Clinical Pharmacology & Therapeutics (2005) 77 , P4–P4; doi: 10.1016/j.clpt.2004.11.017