Fujiwara Y, Chayahara N, Mukohara T, Kiyota N, Tomioka H, Funakoshi Y, Minami H – “Hypothyroidism in patients with colorectal carcinoma treated with fluoropyrimidines” Oncol Rep 30(4):1802-1806 (2013)
https://doi.org/10.3892/or.2013.2644
This clinical study examined thyroid function in colorectal cancer patients receiving fluoropyrimidine chemotherapy (5-FU or its derivatives). It found that a subset developed biochemical hypothyroidism during treatment, likely due to direct fluoropyrimidine effects on thyroid hormone metabolism or synthesis. The authors emphasized that thyroid function should be monitored in patients under prolonged fluoropyrimidine therapy.
Thyroid function in colorectal cancer patients receiving fluoropyrimidine-based chemotherapy with or without bevacizumab was evaluated at baseline and monthly. In the present study, 3 of 27 (11.1%) patients who received fluoropyrimidine-based chemotherapy developed a thyroid-stimulating hormone (TSH) level >10 µU/ml, and 13 (48.1%) developed an elevation above the upper limit of the normal range. No difference in TSH elevation was noted between the bevacizumab and chemotherapy-alone group (50 vs. 45%; P=1.00, respectively). Three (11.1%) patients developed a TSH level >10 µU/ml and 2 with hypothyroidism were treated with thyroid hormone replacement therapy. We demonstrated that bevacizumab does not affect thyroid function but fluoropyrimidines may induce thyroid dysfunction in patients with colorectal cancer. Further investigation is required to clarify the mechanism of fluoropyrimidine-induced thyroid dysfunction.