A 42-year-old female, with a past medical history of IgA deficiency and recurrent sinopulmonary infections, underwent total thyroidectomy for a 1.1-cm follicular variant PTC. Preoperative ultrasound (US) found no abnormal lymph nodes, and pathology demonstrated a well-differentiated unifocal cancer with no capsular or lymphovascular invasion. At 3-month follow-up, the rhTSH-stimulated Tg level was low at 1.7 ng/ml with negative Tg antibodies. However, the 123I whole-body scan demonstrated focal increased uptake in the left thyroid bed and diffuse uptake in both lungs, suggestive of metastatic disease (Fig. 1a). At the time of testing, the patient was taking oral prednisone, inhaled mometasone/formoterol, and oral amoxicillin/clavulanate for a bronchitis flare. Given her conflicting results, the possibility of a false-positive radioiodine uptake result in the setting of active pulmonary inflammation was raised. In view of these findings, the patient was scheduled for 131I dosimetry after levothyroxine withdrawal. Imaging at 48 h confirmed the thyroid bed findings, but the lungs had only minimal uptake (Fig. 1b). Labwork demonstrated an appropriately elevated TSH of 67.3 mcIU/ml, with a low Tg of 4.6 ng/ml, and negative Tg antibodies. These results suggested that the initial pulmonary uptake was a false positive. The patient was subsequently treated with 100 mCi of 131I. The post-treatment scan (Fig. 1c) confirmed the pretreatment findings.

Fig. 1
figure 1

Serial radioactive iodine whole-body scans (WBS) from the anterior and poster views, respectively, of the: a initial diagnostic 123I WBS, b diagnostic 5 mCi 131I WBS used for dosimetry, c post-treatment 131I WBS, and d 1-year follow-up 123I WBS

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At 1-year follow-up, the rhTSH-stimulated 123I scan again showed faint diffuse uptake in both lungs. Stimulated Tg and Tg antibody levels were undetectable, neck US was negative for residual or recurrent disease, and CT of the lungs demonstrated bilateral bronchiectasis with no obvious metastatic lesions (Fig. 2). Thus, the persistent radioiodine uptake in the lungs was confirmed to be a spurious finding due to her underlying pulmonary disease rather than metastatic thyroid cancer.

Fig. 2
figure 2

CT chest in coronal and axial reconstructions demonstrating persistent, chronic bilateral inflammation consistent with ground-glass infiltrates and mild bronchiectasis at the a initial and b 1-year follow-up visits. No suspicious metastatic lesions were seen in the corresponding areas of pulmonary radioactive iodine uptake

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Papillary thyroid cancer is the most common endocrine cancer in the US and accounts for almost 2,000 deaths annually [1, 2]. Radioactive iodine (RAI) is frequently used in the evaluation and treatment of PTC because of its high specificity for follicular thyroid cells. However, RAI uptake may mimic metastatic PTC in areas of inflammation or infection [3, 4]. Inflammation is associated with increased vascular flow, capillary permeability, and stasis of radioiodine [3]. Also, leukocytes can induce iodide organification via myeloperoxidase enzymes, which likely mimic thyroid peroxidation [5]. Moreover, recent studies have shown that iodide may play an important role in the innate immune system of the pulmonary tree by acting as a substrate for an oxidative microbicidal system [6, 7]. Iodine accumulation in bronchopulmonary secretions, while acting to defend against respiratory viruses and bacteria in inflammatory lung states [6–10], may also lead to false-positive post-RAI scans resulting in erroneous diagnoses.

Thus, the chronic bronchitis and bronchiectasis secondary to the IgA deficiency in our patient likely contributed to the spurious 123I scan findings. This case of IgA deficiency-related bronchitis masquerading as metastatic thyroid cancer emphasizes the need for vigilance when interpreting radioiodine scintigraphy in patients with comorbid pulmonary conditions.