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Acute transient thyroid swelling after fine‐needle aspiration biopsy: rare complication of unknown origin

Our patient’s plasma normetanephrine and noradrenaline levels did not suppress sufficiently during the test, which was consistent with the presence of phaeochromocytoma. During this test and the initial workup, the patient was not consuming any drugs or medication. Follow-up imaging studies were carried out over the next 12 months and were still negative (Table 1). Genetic testing for phaeochromocytoma was also performed including examination for mutations in ret proto-oncogene (RET), succinate dehydrogenase complex, subunits B,C,D (SDHB/SDHC/SDHD) and von Hippel-Lindau tumour suppressor gene (VHL), which were also negative. In parallel to the medical workup, he was followed by medical psychiatry for his depression, anxiety and physical complaints. Two months after his initial presentation, the antidepressant citalopram was prescribed, but the patient was poorly adherent and did not take the medication. Treatment with fluoxetine was initiated 7 months post-presentation, with better adherence, and titrated up to 30 mg daily. He also underwent occupational and physical therapy. This led to some improvement in his mood, anxiety, somatic complaints and functioning, and a concomitant, progressive drop in his catecholamine levels, which on last measurement had normalized (Table 1). Phaeochromocytoma is a challenging but important diagnosis, with plasma metanephrines being the gold standard for diagnosis. In cases where this is insufficient, a clonidine suppression test is considered the most sensitive and specific additional diagnostic test. This test was introduced to address the problem of how to distinguish patients with phaeochromocytoma from those with false-positive biochemical results. By activating a2-adrenoceptors in the brain and on sympathetic nerve endings, clonidine suppresses noradrenaline release by sympathetic nerves. Therefore, decreases in elevated plasma noradrenaline concentrations after clonidine suggest sympathetic activation, whereas a lack of decrease suggests phaeochromocytoma. This patient had a convincing biochemical profile of phaeochromocytoma which led to an extensive diagnostic imaging workup, which was all negative. During his entire workup, he was followed by medical psychiatry and demonstrated anxiety and depression, which were felt to be secondary to an organic medical condition. However, treating his psychiatric condition with supportive therapy and treatment with a selective serotonin reuptake inhibitor (SSRI) led to marked improvement in his catecholamine production. Unlike tricyclic antidepressants, which are reported to cause a false-positive elevation of catecholamines, the SSRIs are not reported to influence the measurement of catecholamines. Previous reports in adults have shown that an elevation of noradrenaline and dopamine, as in our case, rather than adrenaline, can occur in the setting of anxiety, depression or a bipolar disorder. To our knowledge, no similar data have been reported in children. The patient presented had multiple constitutional complaints and, 2 years after his initial presentation, is still being investigated and treated by a multidisciplinary team and receiving psychiatric treatment. Although all the medical and psychiatric issues have not been fully resolved, it is now clear that catecholamine elevations were false-positives and the ongoing concern of phaeochromocytoma was unwarranted. The elevations resolved with improvement in his psychiatric condition. In conclusion, although depression can be primary or secondary to organic causes, if depression is suspected in the presence of abnormal catecholamine levels, a false-positive result should be considered.