Introduction: Tuberculosis (TB) involving the thyroid gland is rare and typically results in hypothyroidism. Here we report a case of thyroid TB that presented with hyperthyroidism. Clinical Case: A 54-year-old woman with a history of hyperthyroidism due to toxic multinodular goiter presented to the emergency department with fever of unknown origin associated with sore throat, non-productive cough, night sweats, diarrhea, and right anterior neck pain that worsened with coughing. Her fevers were intermittent, ranging from 38 to 39 degrees Celsius, and would subside with acetaminophen. She reported that her symptoms had started after getting a thyroid [Tc-99m] pertechnetate scan and 24 hour [I-131] sodium iodide uptake study a month prior. The scan at the time revealed hyperfunctioning thyroid nodules in the lower lobes bilaterally. The 24-hour uptake was 20.2% which is within the normal range of 7 to 30%. TSH on presentation was 0.01 mIU/L (Normal range 0.3-5.50 mIU/L), free T4 was 2.05 ng/dL (Normal range 0.76 -1.7 ng/dL), and free T3 was 5 pg/mL (Normal range 1.9-3.9 pg/mL). Exam revealed a multinodular goiter, which was firm with mild tenderness, and no cervical lymphadenopathy. Infectious workup was unremarkable other than a positive interferon-gamma release assay. As for TB risk factors, the patient immigrated to the United States from Albania about 13 years prior. The patient denied any known TB exposure, neither had she been treated for TB. Radiograph and computed tomography (CT) of the thorax were unremarkable other than re-demonstration of the multinodular goiter. Fluorodeoxyglucose-18 positron emission tomography (FDG-PET), which was performed to identify any focus of active TB, had revealed intense, infiltrative, heterogeneous FDG uptake of the nodular thyroid gland with reactive level 3 and 4 cervical lymph nodes. Also, the scan revealed hyper-metabolic hilar, pre-tracheal, and sub-carinal lymph nodes which could represent latent TB. Further workup for any other foci of active TB including broncho-alveolar lavage, sputum cultures, lumbar puncture, and bone marrow biopsy were unremarkable. Thyroid ultrasound revealed 2 right sided and 3 left sided thyroid nodules, mostly solid and hypoechoic. Fine needle aspiration of nodules revealed benign follicular nodules bilaterally, however the left aspirate contained loose aggregates of histiocytes consistent with non-necrotizing granulomas. Acid-fast bacilli stain of the aspirate was negative. The patient was started on therapy for active TB with isoniazid, rifampin, pyrazinamide, and ethambutol. Six weeks after treatment her fevers had resolved. Conclusion: Thyroid TB should be considered when the severity of symptoms cannot be explained by the degree of hyperthyroidism alone in patients with increased risk of TB. Additionally, TB in the thyroid can be challenging to identify in a patient with known underlying thyroid disease.

Background Thyroid disorders have been described in patients with Covid-19 infection. Although thyrotoxicosis secondary to thyroiditis is mostly reported in several publications worldwide in patients infected with Covid-19, new-onset Graves’ disease is rarely reported. Clinical Case A 41-year-old female without significant past medical history presented to emergency room with nausea, vomiting, palpitations and syncope. She was diagnosed with COVID-19 infection five days prior to her presentation. On admission, patient was normotensive, tachycardic with heart rate of 135 beats/min, and oxygen saturation >90% on room air. Thyroid exam was unremarkable. Initial labs showed suppressed TSH, elevated free T4 of 2.58 ng/dL (0.76–1.70 ng/dL) and elevated total T3 of 210 ng/dL (80–175 ng/dL). The computed tomography pulmonary angiogram (CTPE) was negative for pulmonary embolism. Transthoracic echocardiogram (TTE) showed moderate cardiac effusion without tamponade. Patient had no prior history of thyroid disease, but her mother had hypothyroidism. With Burch-Wartofsky score of 50, treatment for thyroid storm was initiated: Hydrocortisone, propranolol, and propylthiouracil (PTU), followed by cholestyramine, and super saturated potassium iodide (SSKI). Shortly after, patient developed hypotension requiring norepinephrine infusion and transfer to intensive care unit. Repeat TTE showed ejection fraction of 50%, moderate pericardial effusion without tamponade, and global hypokinesis suggestive of myocarditis. Propranolol was held. Although patient's blood pressure improved overnight, patient developed shock liver with AST elevated at 4,095 IU/L (8-30 IU/L), ALT at 2,837 IU/L (<35 IU/L), and total bilirubin at 1.6 mg/dl (0.2-1.2 mg/dl) compared to normal values on admission. PTU was discontinued after two doses due to elevated liver enzymes. Thyroid scan showed diffuse mildly increased radiotracer uptake suggestive of autoimmune thyroid disease. Thyroid stimulating immunoglobulin (TSI) was elevated at 6.5 IU/L (<0.55IU/L) with thyrotropin receptor antibody (TRAb) of 8.39 IU/L (0. 00 - 1.75 IU/L) suggestive of Graves’ disease. On discharge, patient was asymptomatic. At outpatient follow up, patient had improvement in liver enzymes and mild hyperthyroidism, methimazole was started with the plan for close monitoring of liver enzymes and thyroid function tests. Conclusion New-onset Graves’ disease can occur in the setting of Covid-19 infection. It is crucial to report this type of cases to gain more insights in the exact relationship between thyroid disease and Covid-19 infection. Physicians should be aware of the possibility of Graves’ disease in addition to thyroiditis in the setting of thyrotoxicosis and Covid-19 infection. Making the right diagnosis is essential as treatment and course of disease are very different. Presentation: No date and time listed

No abstract