The interaction between severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and autoimmune thyroid disease is an emerging phenomenon. The present study describes the case of a 28-year-old female who experienced a relapse of Graves' disease following SARS-CoV-2 infection. She was biochemically euthyroid for 2 years prior to COVID-19 infection. However, she began experiencing palpitations, increased sweating and tremors of the hands 9 days after being diagnosed with COVID-19-related pneumonia. In addition to presenting this case, a comparison is made of this case to similar reports and the possible mechanisms underlying the association between SARS-CoV-2 and Graves' disease are discussed. One is a direct result of viral uptake by thyroid cells, while another is a result of the hyperinflammatory ʻcytokine storm' and its effects on the hypothalamic-pituitary-thyroid axis and T-cell immunity.

A 34-year-old woman presented with a 3-day history of dyspnea. She denied any preceding fever, night sweats, cough, pleurisy, or coryzal symptoms. She was maintained on sodium valproate 800 mg b.i.d., phenytoin 100 mg o.d., folate 5 mg o.d., and clonazepam 2 mg nocte for a known seizure disorder. Clinical examination and radiologic imaging revealed a large left-sided pleural effusion with the associated collapse of the left lower lung lobe. A chest tube was inserted for diagnostic and therapeutic purposes and ≈500 mls of serous fluid was drained. The pleural fluid analysis confirmed an exudative pleural effusion. Extensive evaluation excluded known causes of exudative pleural effusion, and a diagnosis of sodium valproate-induced pleural effusion was made. Sodium valproate was tapered off and topiramate was added to the patient’s antiepileptic regimen. We recommend physicians be cognizant of sodium valproate-associated pleural effusion, even in the setting of chronic use.

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Kawasaki disease is an acute multisystemic vasculitis occurring predominantly in children and rarely in adults, with sequelae of potentially life-threatening coronary artery aneurysms. “Incomplete” Kawasaki disease is a novel concept and considered a diagnosis of exclusion as it alludes to patients with fever lasting ⩾5 days and 2 or 3 clinical criteria without another reasonable explanation for the illness. The multidisciplinary team should be vigilant for this oligosymptomatic clinical presentation, specifically within this subgroup despite age and ethnicity, and the syndrome should be considered as a differential diagnosis in challenging cases presenting as infectious or autoimmune disease.