Blick Carly, Nguyen Minhthao, Jialal Ishwarlal
Temple University Hospital
University Hospitals Richmond and Bedford Medical Center
Thyrotoxicosis is a clinical condition characterized by excessive thyroid hormone activity, primarily T and T, regardless of the underlying cause. While often confused with hyperthyroidism, the latter specifically refers to a form of thyrotoxicosis, involving excessive hormone production by the thyroid gland. Other causes of thyrotoxicosis include but are not limited to, Graves disease (where autoantibodies bind to and stimulate the thyroid-stimulating hormone [TSH] receptor), thyroiditis (which releases hormones from damaged thyroid tissue), toxic nodules and multinodular goiter (where autonomous nodules produce hormones), and iatrogenic or factitious thyrotoxicosis due to exogenous hormone intake. If left untreated, thyrotoxicosis can result in serious complications such as cardiovascular dysfunction, osteoporosis, and, in severe cases, thyroid storm—a life-threatening emergency. The clinical presentation of thyrotoxicosis ranges from asymptomatic cases to the life-threatening condition of thyroid storm. Common symptoms stem from the hypermetabolic state caused by excess thyroid hormones and include weight loss, heat intolerance, and palpitations. A comprehensive medical history, thorough physical examination, and appropriate laboratory and imaging studies are essential to establish the differential diagnosis and determine the underlying cause for effective treatment.[2] The thyroid gland is a butterfly-shaped organ located in the lower front of the neck. The thyroid gland regulates metabolism by producing and releasing thyroid hormones. The thyroid consists of 2 lobes connected by an isthmus and primarily produces T and T, which regulate metabolic processes in nearly all body tissues. Thyroid-stimulating hormone (TSH), released by the anterior pituitary gland, stimulates the release of triiodothyronine (T) and thyroxine (T). In thyrotoxicosis, the balance of hormone production and release is disrupted, causing elevated circulating levels of T and T and triggering a hypermetabolic state.[3] The natural course of thyrotoxicosis varies depending on the underlying cause. In cases of hyperthyroidism, such as in Graves disease, the condition typically progresses with persistent overproduction of thyroid hormones if left untreated. In other cases, such as thyroiditis, the condition may be self-limiting, with an acute phase followed by recovery as inflammation resolves. However, without intervention, thyrotoxicosis can lead to significant systemic complications, including neuropsychiatric symptoms such as anxiety and cognitive impairment. Thyrotoxicosis can have widespread systemic effects due to the extensive influence of thyroid hormones on various organs. The cardiovascular system is especially vulnerable, with an increased risk of tachycardia, atrial fibrillation, heart failure, thromboembolic events, and cardiovascular collapse.[2] Additionally, excessive thyroid hormones can also impact bone metabolism, leading to accelerated bone loss and osteoporosis, as well as the nervous system, causing symptoms such as tremors, anxiety, and, in severe cases, delirium during thyroid storm. Recent studies have also identified thyrotoxicosis as a risk factor for cognitive disorders in patients aged 65 or older. Identifying and addressing the underlying cause of thyrotoxicosis is essential for effectively managing its systemic effects.
甲状腺毒症是一种临床病症,其特征为甲状腺激素活性过高,主要是T3和T4,无论其潜在病因是什么。虽然甲状腺毒症常与甲状腺功能亢进相混淆,但后者具体指的是甲状腺毒症的一种形式,涉及甲状腺过度产生激素。甲状腺毒症的其他病因包括但不限于格雷夫斯病(自身抗体结合并刺激促甲状腺激素[TSH]受体)、甲状腺炎(从受损的甲状腺组织释放激素)、毒性结节和多结节性甲状腺肿(自主结节产生激素),以及因外源性激素摄入导致的医源性或人为性甲状腺毒症。如果不进行治疗,甲状腺毒症可导致严重并发症,如心血管功能障碍、骨质疏松症,在严重情况下还会引发甲状腺危象——一种危及生命的紧急情况。甲状腺毒症的临床表现范围从无症状病例到危及生命的甲状腺危象状态。常见症状源于甲状腺激素过多引起的高代谢状态,包括体重减轻、不耐热和心悸。全面的病史、彻底的体格检查以及适当的实验室和影像学检查对于建立鉴别诊断和确定有效治疗的潜在病因至关重要。甲状腺是一个位于颈部前下方的蝴蝶形器官。甲状腺通过产生和释放甲状腺激素来调节新陈代谢。甲状腺由通过峡部相连的两个叶组成,主要产生T3和T4,它们调节几乎所有身体组织中的代谢过程。垂体前叶释放的促甲状腺激素(TSH)刺激三碘甲状腺原氨酸(T3)和甲状腺素(T4)的释放。在甲状腺毒症中,激素产生和释放的平衡被打破,导致循环中的T3和T4水平升高,并引发高代谢状态。甲状腺毒症的自然病程因潜在病因而异。在甲状腺功能亢进的情况下,如格雷夫斯病,如果不进行治疗,病情通常会随着甲状腺激素持续过度产生而进展。在其他情况下,如甲状腺炎,病情可能是自限性的,急性期过后随着炎症消退而恢复。然而,如果不进行干预,甲状腺毒症可导致严重的全身并发症,包括焦虑和认知障碍等神经精神症状。由于甲状腺激素对各个器官有广泛影响,甲状腺毒症可产生广泛的全身效应。心血管系统尤其脆弱,患心动过速、心房颤动、心力衰竭、血栓栓塞事件和心血管衰竭的风险增加。此外,过多的甲状腺激素还会影响骨代谢,导致骨质流失加速和骨质疏松症,以及影响神经系统,引起震颤、焦虑等症状,在严重情况下,甲状腺危象期间还会出现谵妄。最近的研究还将甲状腺毒症确定为65岁及以上患者认知障碍的一个危险因素。识别并解决甲状腺毒症的潜在病因对于有效管理其全身效应至关重要。