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.