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Adipose Tissue_Appetite_and Obesity

SAT-696 - The Impact of Adjuvant Tamoxifen Therapy on the Development and Progression of Hepatic Steatosis in Women with Early-Stage Breast Cancer: A Pilot Study

Saturday, June 13, 2026
9:30 AM - 4:30 PM CT
Location: ENDOExpo; Poster Floor
Disclosure(s):
Karen K. Miller, MD: No relevant disclosure to display


Background:
Tamoxifen, a selective estrogen receptor modulator prescribed for hormone receptor-positive breast cancer, has been associated with the development of drug-induced hepatic steatosis. However, prior studies have been limited by lack of gold-standard measurement of intrahepatic lipid content (IHL) and inclusion of heterogenous populations, including women receiving hepatotoxic systemic chemotherapy. We hypothesized that women with early stage breast cancer would be at risk of development and/or progression of hepatic steatosis over 6 months of tamoxifen monotherapy.

Methods:
Women with breast cancer who were not candidates for systemic chemotherapy were studied before initiation and after 6 months of tamoxifen. The primary endpoint was change in IHL (absolute %) by proton magnetic resonance spectroscopy (steatosis defined by IHL ≥5%). Paired t-tests were performed to compare pre and post tamoxifen measures. Data are reported as mean ± standard deviation (SD).

Results:
Baseline characteristics of all 13 included age 53±5 years, 62% premenopausal (n=8/13), BMI 26.7±5.2 kg/m² (range 21.4-38.3 kg/m²), ALT 15±5 IU/L, HbA1c 5.5±0.2% and IHL 5.4±6.0%. After 6 months of tamoxifen therapy, no significant changes (all p >0.05) were observed in mean weight (-0.2±2.3 kg), IHL (-0.2±3.1%, p=0.9), ALT (-0.1±4.3 IU/L) or HbA1c (0.1±0.2%).

Four women (31%) had preexisting MASLD at baseline, with mean IHL 12.4±6.8% (range 6.0-19.4%), age 54±5 years, 75% premenopausal (n=3/4), BMI 28.2±7.2 kg/m², ALT 18±7 IU/L, HbA1c (5.5±0.1%), 1/4 had type 2 diabetes and 1/4 had prediabetes. One had resolution of IHL to < 5%, two had stable IHL and one had a decrease in IHL (19% to 11%) with tamoxifen.

Nine women (69%) did not have MASLD at baseline, with mean IHL 2.3±0.9%, age 52±6 years, 56% premenopausal (n=5/9), BMI 26.0±4.5 kg/m², ALT 14±4 IU/L, HbA1c 5.5±0.3% and 44% (n=4/9) had prediabetes. In this group, 2/9 (22%) developed new mild steatosis (increase to ≥5%), with IHL measures of 5.3% and 6.7% after tamoxifen. These two subjects both had prediabetes and BMI >25 kg/m² at baseline. Overall, 50% (2/4) of women with prediabetes/diabetes, 40% (2/5) of women with BMI >25 kg/m² and 2/6 (33%) of women developed new IHL with tamoxifen treatment.

Conclusion:
In a small group of women with and without preexisting MASLD, treatment with tamoxifen monotherapy did not induce clinically significant hepatic fat accumulation or transaminase elevation over 6 months. These findings are reassuring for the large proportion of breast cancer patients for whom tamoxifen therapy is recommended. Because the group of patients we studied with MASLD was small and the overall cohort had low baseline hepatic fat, further research is needed in women with more severe forms of MASLD and/or at higher metabolic risk to better define tamoxifen’s hepatic safety across the full metabolic spectrum.

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