Jod-Basedow syndrome refers to hyperthyroidism that develops as a result of administration of iodide, either as a dietary supplement or as IV contrast medium, or as an adverse effect of the antiarrhythmic drug amiodarone. This phenomenon is usually seen in a patient with endemic goiter.8-11 The relatively limited nature of the case patient's goiter and absence of a precipitating exposure to iodine made this diagnosis highly unlikely.
Subacute thyroiditis is a condition to which the patient's abnormal TFT results could reasonably be attributed. The patient had a substernal multinodular goiter that could not be palpated on physical examination, but it was visualized in the extended lower neck during thyroid scintigraphy.3 RAIU was minimal—a typical finding in this disorder,6 as TSH is suppressed by leakage of the excessive amounts of thyroid hormone. A tentative diagnosis of subacute thyroiditis was made.
As subacute thyroiditis is a self-limiting disorder, the patient was not started on any medications for hyperthyroidism but was advised to follow up with his primary care provider or an endocrinologist for repeat TFT and for fine-needle aspiration biopsy of the large thyroid nodule (a complex mass, containing cystic elements and calcifications, with a potential for malignancy) to rule out thyroid cancer.
Repeat ECG before discharge showed normal sinus rhythm with a ventricular rate of 74 beats/min. The patient was alert, awake, and oriented at discharge. He was continued on flecainide, metoprolol, and warfarin and advised to follow up with his primary care provider regarding his target INR.
DISCUSSION
The incidence of subacute thyroiditis, according to findings reported in 2003 from the Rochester Epidemiology Project in Olmsted County, Minnesota,12 is 12.1 cases per 100,000/year, with a higher incidence in women than men. It is most common in young adults and decreases with advancing age. Coxsackie virus, adenovirus, mumps, echovirus, influenza, and Epstein-Barr virus have been implicated in the disorder.12,13
Subacute thyroiditis is associated with a triphasic clinical course of hyperthyroidism, then hypothyroidism, then a return to normal thyroid function—as was seen in the case patient. Onset of subacute thyroiditis has been associated with recent viral infection, which may serve as a precipitant. The cause of this patient's high fever was never identified; thus, the etiology may have been viral.
The initial high thyroid hormone levels result from inflammation of thyroid tissue and release of preformed thyroid hormone into the circulation.6 At this point, TSH is suppressed and patients have very low RAIU, as was true in the case patient.
The condition is self-limiting and does not require treatment in the majority of patients, as TFT results return to normal levels within about two months.6 Patients can appear extremely ill due to thyrotoxicosis from subacute thyroiditis, but this usually lasts no longer than six to eight weeks.3 Subacute thyroiditis can be associated with atrial arrhythmia or heart failure.14,15
PATIENT OUTCOME
New-onset A-fib was attributed to the patient's thyrotoxicosis, which in turn was caused by subacute thyroiditis. He had a multinodular goiter, although he had not received any iodine supplements or IV contrast. As in most cases of subacute thyroiditis, no precipitating event was identified. However, given this patient's residence in a nursing facility and presentation with a high fever with no identifiable cause, a viral etiology for his subacute thyroiditis is possible.6
The patient's dementia may have been secondary to acute thyrotoxicosis, as his mental state improved during the hospital stay. His vitamin B12, folate, and A1C levels were within normal range. CT of the head showed multiple chronic infarcts and cerebral atrophy, and MRI of the brain indicated microvascular ischemic disease.
The patient was readmitted one month later for an episode of near-syncope (which, it was concluded, was a vasovagal episode). At that time, his TSH was found normal at 1.350 µIU/mL. Flecainide and metoprolol were discontinued; he was started on diltiazem for continued rate and rhythm control (as recommended by cardiology) and continued on warfarin.
CONCLUSION
In this case, subacute thyroiditis was most likely caused by a viral infection that led to destruction of the normal thyroid follicles and release of their preformed thyroid hormone into the circulation; this in turn led to sudden-onset A-fib. The diagnosis of subacute thyroiditis was suggested based on the abnormalities seen in this patient's TFT results, coupled with the suppressed RAIU—a typical finding in this disease.
Because subacute thyroiditis is a self-limiting condition, there is no role for antithyroid medication. Instead, treatment should be focused on relieving the patient's symptoms, such as ß-blockade or calcium channel blockers for tachycardia and corticosteroids or NSAIDs for neck pain.