RESUMO
Hashimoto's thyroiditis and Graves' disease represent two spectrums of the same autoimmune thyroiditis. Evolution from Graves' disease to Hashimoto's thyroiditis is a common scenario but conversion is a rare occurrence that we observed in the presented case of a 56-year-old Hispanic female with a history of Hashimoto's thyroiditis with positive anti-thyroperoxidase (TPO) antibodies who was euthyroid on levothbefore75 µg for six years prior to her presentation to the emergency department (ED) with complaints of palpitations, exertional dyspnea, and unintentional weight loss of 20 lbs for four months. The patient denied any recent change in levothyroxine dosage. The patient was noted to have tachycardia at rest, hyperdynamic circulation, and fine tremors on outstretched hands-on examination but no exophthalmos, thyromegaly, or pedal swellings. Her initial laboratory workup revealed thyroid-stimulating hormone of <0.01 mIU/L, with elevated free T3 and free T4 levels. Levothyroxine was held and beta-blockade therapy was started for symptom control. Further workup showed elevated thyroid-stimulating immunoglobulin and thyroid receptor antibody levels and normalization of anti-TPO antibody levels. The radioactive iodine uptake scan was initially delayed because the patient underwent a pulmonary angiogram in the ED. A later scan showed thyromegaly with heterogeneous uptake of 82% in both lobes. Hence, the patient was diagnosed with Graves' disease and managed with radioactive iodine ablation therapy. On follow-up, the patient developed post-ablation hypothyroidism; she was started back on levothyroxine therapy and became euthyroid. This case highlights that patients can develop Graves' disease in the background of a hypothyroid state, and this conversion might be postulated secondary to a combination of atypical destructive thyroiditis and a switch of autoantibodies from blocking to stimulating ones. Clinicians should suspect the possibility of changing antibodies when there is a change in the patient's euthyroid state.
RESUMO
BACKGROUND Adrenocortical carcinoma (ACC) is a very rare disease, with an incidence of 1.02 per million population per year. The most commonly secreted hormone in ACC is cortisol, often presenting as a rapidly progressive Cushing syndrome (CS). We describe a case of ACC with an unusual presentation, mainly with psychiatric manifestations, including panic attacks and hallucinations. CASE REPORT A 52-year-old woman presented with episodes of acute anxiety, hallucinations, palpitations, hot flashes, gastrointestinal upset associated with paroxysmal hypertension, tachycardia, and flushing for 1 week. The initial workup was aimed at ruling out causes of acute psychosis and/or anxiety such as substance use, and organic diseases such as pheochromocytoma (PCC). Our initial suspicion of PCC was ruled out based on the negative serum and urinary metanephrines (MN) and normetanephrines (NMN). Recurrent metabolic alkalosis and hypokalemia despite fluid and potassium supplementation prompted us to work up for hyperaldosteronism. Her renin level was elevated and the aldosterone level was appropriately suppressed. Elevated cortisol, positive dexamethasone (DXM) suppression test, low adrenocorticotropic hormone (ACTH), imaging revealing an adrenal mass, and postoperative histology confirmed the diagnosis of cortisol-producing ACC. CONCLUSIONS It is essential to recognize psychiatric presentations of CS to achieve early diagnosis and prevent mortality and morbidity. Panic attacks, a common presentation of CS, can present with features mimicking pheochromocytoma (PCC), including palpitations, sweating, tachycardia, and paroxysmal hypertension. A comprehensive workup is warranted to reach a diagnosis, with a combination of hormonal levels, imaging, and histology.
