Discussion
Thyrotoxicosis is a common problem of endocrine disorder [2]. The common cause of hyperthyroidism is Graves’ disease that commonly occurs among female, aged 20-40 years. Prevalence of hyperthyroidism is 0.8% in Europe, and 1.3% in the USA. Thyrotoxicosis has many different causes both endogenous and exogenous [1]. Exogenous thyrotoxicosis is factitious or iatrogenic, develops after ingestion of excessive amounts of thyroid hormone, and is associated with low serum thyroglobulin concentrations. In this case report, she had many clinical conditions of thyrotoxicosis [1]. She received a diagnosis of Graves’ disease due to high TgAb level. It could explain that she had subclinical Graves’ disease. When she underwent CT of the abdomen with contrast-injection that excessed contrast-induced thyrotoxicosis, she showed clinical conditions of hyperthyroidism. It revealed that this event was very dangerous because it might lead to the thyroid storm at any moment since the preoperative until the postoperative period. Clinical features are similar to hyperthyroid symptoms such as palpitations, dyspnea, and weight loss [3].
The mechanism of iodine- or contrast-induced thyrotoxicosis can be explained in massive iodine exposure to the thyroid gland. Patients suspected of iodine-induced thyrotoxicosis need to receive iodine-contrast injection not exceeding 24 hours [4]. Iodine is used to synthesize thyroid hormones using sodium-iodine symporters at the thyroid follicles [5]. Large amounts of iodine can affect thyroid dysfunction. Diet, medications, or radiographic iodine-contrast media (ICM) are iodine excess sources [6]. Iodine-induced hyperthyroidism has been reported with as little as 300–500 μg of iodide. A typical dose of iodinated contrast medium contains about 13500 μg of free iodide and 15–60 g of bound iodine that may be liberated as free iodide in the body [4]. Exogenous iodine decreases thyroidal radio-iodine uptake both by dilution of the total body iodine pool, and by inhibiting the thyroid hormone synthesis via the Wolff- Chaikoff effect. Among patients with euthyroidism, exogenous iodine in large doses inhibits organification of iodide and thyroid hormone synthesis and may lead to hypersecretion of thyroid hormones, a phenomenon known as the Jod–Basedow effect [7,8].
Risk factors include nontoxic diffuse or nodular goiter, latent Graves’ disease, and long-standing iodine deficiency [9]. Generally, for patients suspected of ICM-induced thyrotoxicosis, their serum TSH concentrations will be suppressed, and T4, FT4 and/or total T3 concentrations may be elevated. Once contrast-induced hyperthyroidism is diagnosed, further excess iodine exposure should be avoided. In this case, we suspected iodine-induced thyrotoxicosis with undiagnosed Graves’ disease that was confirmed by TgAb. When a patient develops amiodarone or iodine-induced thyrotoxicosis, distinguishing between the two forms of thyrotoxicosis would be extremely important. Type I usually occurs when patients with an underlying euthyroid nodular goitre or latent Graves’ disease are exposed to the high iodine content of amiodarone. This exposure leads to excess thyroid hormone synthesis and release, similar to iodine-induced hyperthyroidism among patients receiving excess iodine from other sources. It can be treated with antithyroid drugs but type II constitutes a destructive thyroiditis caused by a direct toxic effect of amiodarone on thyrocytes. This form is usually self-limiting and, when necessary, amiodarone can be continued [1]. However, the Contrast Media Safety Committee of the European Society of Urogenital Radiology has concluded that routine monitoring of thyroid function before contrast-injection among patients with a normal thyroid is not indicated. However, high risk patients, i.e., those with a history of Graves’ disease or nodular goiter, especially the elderly or those residing in areas of dietary iodine deficiency, should be carefully monitored after iodinated contrast studies [10]. This includes patients, particularly unable to tolerate thyroid dysfunction, such as those with underlying unstable cardiovascular disease. CT scanning is being used much more frequently in the acute care setting. A study in one emergency department revealed that from 2000 to 2005, CT scanning of the chest increased by 226%, and of the abdomen by 72% [11]. Prompt diagnosis of thyrotoxicosis, along with awareness of the interference of intravenous contrast with use of radioactive iodine and the frequency with which this occurs, may prevent unnecessary CT scans among some patients. Therefore, it might lead to increased incidence of ICM-induced thyrotoxicosis and produce severe thyrotoxicosis or the thyroid storm. However, thyroid storm is a rare disorder. The incidence is 0.2 per 100,000 person-years in Japan and occurs in 1-5% of patients admitted to a hospital for thyrotoxicosis. It constitutes an emergency with a high mortality rate of 8–25% [12]. The pathogenesis of the thyroid storm is still poorly understood. Diagnosis is clinical and based on the presence of hyperthyroidism in a patient with severe and life-threatening manifestations [1]. To make the diagnosis, Burch and Wartofsky proposed a scoring system, modified by Akamizu and colleagues [12]. A multidisciplinary treatment approach should be used. Goals of treatment are lowering thyroid hormone synthesis and secretion, reducing circulating thyroid hormones, controlling peripheral effects of thyroid hormones, and treating any precipitating illness [1].
In conclusion, the clinical clues of thyrotoxicosis remain very crucial. To prevent the thyroid storm is the goal of treatment of patients with thyrotoxicosis especially patients undergoing surgery. Widespread use of radiologic investigations and interventional procedures is important and can increase the incidence of contrast-induced thyrotoxicosis especially among high-risk patients. Clinicians need to prompt manage thyrotoxicosis and prevention the thyroid storm using a multidisciplinary team.
Funding: None.
Conflicts of Interest: All authors declare they have no conflict of interest.