We excluded 20 patients with anti-Tg antibody (TgAb) concentrations >60 U/mL because this high titer may interfere with reliable measurements of serum Tg, and also 28 patients with uptake on DxWBS 1 year after remnant ablation. Of these remaining patients, 337 were found to have sTg concentrations 1 year after remnant ablation (sTg1) of ≥2 ng/mL. RRA, radioactive iodine remnant ablation sTg, stimulated thyroglobulin RxWBs, post-treatment whole-body scan TgAb, anti-thyroglobulin antibody sTg1, sTg measured 1 year after total thyroidectomy and remnant ablation sTg2, sTg measured 1–2 years after sTg1 US, ultrasonography FDG-PET, fluorodeoxyglucose positron emission tomography CT, computed tomogram RAI, radioactive iodine BR, biochemical remission NSED, no structural evidence of disease. Patients were classified into three groups according to sTg1 concentrations: (A) 2–4.9 ng/mL, (B) 5–19.9 ng/mL, (C) ≥20 ng/mL. Seventy-six patients with structural recurrences detected on neck US or CT scan and any other imaging performed as part of the clinical evaluation 1 year after remnant ablation, 6 who received empirical RAI therapy and 21 without available follow-up sTg were excluded. This algorithm demonstrates how the final inclusion of patients was determined. We sought to determine if, in patients with DTC who had been treated with bilateral thyroidectomy and remnant ablation with RAI, sTg1 after initial treatment, and repeated sTg measurements 1–2 years after sTg1, would help predict the long-term outcome with respect to structural recurrence and biochemical remission (BR), defined as sTg<1 ng/mL.ĭescription of the study cohort. We therefore assessed the changing pattern of stimulated Tg (sTg) and the clinical course of patients with no structural evidence of disease (NSED), based on imaging studies such as neck ultrasonography (US), fluorodeoxyglucose positron emission tomography (FDG-PET), and/or chest computed tomogram (CT). Those studies, however, only included small numbers of patients, and did not show natural courses that change in clinical state and patterns of spontaneous reduction in the sTg level specifically in patients who did not receive additional treatment. However, other studies have found that sTg can decrease even in the absence of further treatment ( 12, 16– 18).Ībout 30%–68% of patients with elevated sTg 1 year after RRA have a subsequent decline in sTg concentration or an undetectable sTg ( 11, 12, 16). Empirical radioactive iodine (RAI) therapy in some patients with elevated sTg and a negative DxWBS reduced the serum Tg concentration ( 11– 13), but did not improve survival ( 12, 14, 15). Some patients with detectable sTg have no structurally evident disease. Recently, new methods for serum Tg measurement with functional sensitivities 2 ng/mL undergo diagnostic whole-body scans (DxWBSs) and further testing to localize the source of Tg ( 7– 10). Serum Tg concentrations after thyroid hormone withdrawal during the first year after surgery and RRA is a highly sensitive and specific indicator of future recurrence ( 1, 3).
This is because the only possible source of Tg is thyroid tissue, which may be normal or neoplastic ( 1, 2). Serum thyroglobulin (Tg) is the most sensitive and established biomarker for DTC recurrence/persistence, especially in patients who have undergone thyroid surgery and radioactive iodine remnant ablation (RRA). Therefore, evaluation of strategies for the detection and monitoring of recurrent and/or persistent disease are needed to reduce progression and mortality, while minimizing unnecessary procedures for patients with low risk of recurrence. Although DTC is generally an indolent tumor and cancer-specific mortality is low, persistent/recurrent disease is common and is associated with significant morbidity and long-term mortality. D ifferentiated thyroid cancer (DTC) is the most common endocrine malignancy with a rapidly increasing incidence worldwide.
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