Department of Translational Research and Advanced Technologies in Medicine and Surgery, Regional Center of Nuclear Medicine, University of Pisa, Pisa, Italy
Endocrinology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
J Nucl Med. 2021 Mar;62(3):304-312. doi: 10.2967/jnumed.120.243170. Epub 2020 Oct 2.
Benign thyroid disorders, especially hyper- and hypothyroidism, are the most prevalent endocrine disorders. The most common etiologies of hyperthyroidism are autoimmune hyperthyroidism (Graves disease, GD), toxic multinodular goiter (TMNG), and toxic thyroid adenoma (TA). Less common etiologies include destructive thyroiditis (e.g., amiodarone-induced thyroid dysfunction) and factitious hyperthyroidism. GD is caused by autoantibodies against the thyroid-stimulating hormone (TSH) receptor. TMNG and TA are caused by a somatic activating gain-of-function mutation. Typical laboratory findings in patients with hyperthyroidism are low TSH, elevated free-thyroxine and free-triiodothyronine levels, and TSH-receptor autoantibodies in patients with GD. Ultrasound imaging is used to determine the size and vascularity of the thyroid gland and the location, size, number, and characteristics of thyroid nodules. Combined with lab tests, these features constitute the first-line diagnostic approach to distinguishing different forms of hyperthyroidism. Thyroid scintigraphy with either radioiodine or Tc-pertechnetate is useful to characterize different forms of hyperthyroidism and provides information for planning radioiodine therapy. There are specific scintigraphic patterns for GD, TMNG, TA, and destructive thyroiditis. Scintigraphy with Tc-sestamibi allows differentiation of type 1 from type 2 amiodarone-induced hyperthyroidism. The radioiodine uptake test provides information for planning radioiodine therapy of hyperthyroidism. Hyperthyroidism can be treated with oral antithyroid drugs, surgical thyroidectomy, or I-iodide. Radioiodine therapy is generally considered after failure of treatment with antithyroid drugs, or when surgery is contraindicated or refused by the patient. In patients with TA or TMNG, the goal of radioiodine therapy is to achieve euthyroid status. In GD, the goal of radioiodine therapy is to induce hypothyroidism, a status that is readily treatable with oral thyroid hormone replacement therapy. Dosimetric estimates based on the thyroid volume to be treated and on radioiodine uptake should guide selection of the I-activity to be administered. Early side effects of radioiodine therapy (typically mild pain in the thyroid) can be handled by nonsteroidal antiinflammatory drugs. Delayed side effects after radioiodine therapy for hyperthyroidism are hypothyroidism and a minimal risk of radiation-induced malignancies.
良性甲状腺疾病，尤其是甲状腺功能亢进和甲状腺功能减退，是最常见的内分泌疾病。甲状腺功能亢进的最常见病因是自身免疫性甲状腺功能亢进症（Graves 病，GD）、毒性多结节性甲状腺肿（TMNG）和毒性甲状腺腺瘤（TA）。较少见的病因包括破坏性甲状腺炎（如胺碘酮引起的甲状腺功能障碍）和人为性甲状腺功能亢进症。GD 是由针对促甲状腺激素（TSH）受体的自身抗体引起的。TMNG 和 TA 是由体细胞激活获得性功能突变引起的。甲状腺功能亢进症患者的典型实验室发现是 TSH 降低、游离甲状腺素和游离三碘甲状腺原氨酸水平升高以及 GD 患者的 TSH 受体自身抗体。超声成像用于确定甲状腺的大小和血管、甲状腺结节的位置、大小、数量和特征。结合实验室检查，这些特征构成了区分不同形式甲状腺功能亢进症的一线诊断方法。放射性碘或 Tc 高锝酸盐甲状腺闪烁显像有助于确定不同形式的甲状腺功能亢进症的特征，并为放射性碘治疗方案提供信息。GD、TMNG、TA 和破坏性甲状腺炎有特定的闪烁显像模式。Tc- sestamibi 闪烁显像可区分 1 型和 2 型胺碘酮引起的甲状腺功能亢进症。放射性碘摄取试验为甲状腺功能亢进症的放射性碘治疗方案提供信息。甲状腺功能亢进症可以用口服抗甲状腺药物、甲状腺切除术或碘-131 治疗。放射性碘治疗一般在抗甲状腺药物治疗失败后、或手术禁忌或患者拒绝手术时考虑。在 TA 或 TMNG 患者中，放射性碘治疗的目标是达到甲状腺功能正常状态。在 GD 患者中，放射性碘治疗的目标是诱导甲状腺功能减退，这种状态可以通过口服甲状腺激素替代治疗很容易控制。基于待治疗甲状腺体积和放射性碘摄取的剂量估计应指导所给予的 I-放射性活度的选择。放射性碘治疗的早期副作用（通常是甲状腺的轻度疼痛）可以用非甾体抗炎药处理。放射性碘治疗甲状腺功能亢进症后的迟发性副作用是甲状腺功能减退和辐射诱发恶性肿瘤的风险极小。
