TSH suppression therapy after DTC refers to the application of thyroid hormones after surgery to suppress TSH at or below the low limit of normal, or even undetectable, to replenish the thyroid hormone deficiency in DTC patients on the one hand, and to inhibit the growth of DTC cells on the other. oral preparations of L-T4 are preferred for TSH suppression therapy. The dose of thyroid hormone and the T3/T4 ratio in dry thyroid tablets are unstable and may bring about TSH fluctuations, therefore they are not recommended as the first choice in long-term suppressive therapy. TSH suppression levels are strongly associated with recurrence, metastasis and cancer-related death in DTC, and this association is particularly clear for those with high-risk DTC. tsH >2
mU/L is associated with increased cancer-related death and recurrence. Postoperative TSH suppression in patients with high-risk DTC to <0.1
mU/L was associated with significantly lower tumor recurrence and metastasis. Postoperative TSH suppression at 0.1-0.5 mU/L in patients with low-risk DTC resulted in a significant improvement in overall prognosis, with no additional benefit when TSH was further suppressed to <0.1 mU/L. The growth and proliferation of some hypofractionated DTCs are not dependent on the action of TSH, and in such patients, even if TSH is
suppressed to very low levels, it is still difficult to slow down the progression of the disease. Long-term use of supraphysiologic doses of thyroid hormone can result in subclinical hyperthyroidism. In particular, TSH needs to be maintained at very low levels (<0.1 mU/L) for a long time, which may affect the QOL of patients with DTC, increase cardiac load and myocardial ischemia (especially in the elderly), trigger or aggravate cardiac rhythm disturbances (especially atrial fibrillation), cause resting tachycardia, increased myocardial weight, increased mean arterial pressure, diastolic and/or systolic dysfunction, and even lead to patients with cardiovascular disease-related The risk of hospitalization and death from cardiovascular events is increased. Another side effect of long-term TSH suppression is an increased incidence of osteoporosis (OP) in postmenopausal women and a possible increased risk of fracture.