We thank the European Society of Endocrinology (ESE) for providing the global endocrinology community with the statement on coronavirus disease (COVID-19) and endocrine disorders [1]. Regarding Addison’s disease, the ESE statement affirms that there is no evidence that patients with adrenal insufficiency are at increased risk of contracting COVID-19, and there are no reported data on the outcomes of COVID-19 infection in adrenal-insufficient individuals. Herein, we present the case of a 32-year-old woman with autoimmune polyglandular syndrome type 1 who developed COVID-19 caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); she lived closed to the first Lombardy cluster spreading from Codogno, Italy. Her clinical, immunological, and genetic patterns have been previously described (as patient no. 4) in a case series of autoimmune polyendocrinopathy–candidiasis–ectodermal dystrophy (APECED), also known as autoimmune polyendocrine syndrome type 1 (APS-1)[2]. In summary, she carries a homozygous R203X mutation in exon five of the autoimmune regulator (AIRE) gene, resulting in primary adrenal insufficiency (PAI), hypoparathyroidism, hypogonadism, ectodermal dystrophy, candidiasis, pernicious anemia, and gastrointestinal dysfunction.

Because her chronic hypoparathyroidism was inadequately controlled by standard treatment alone, the patient had been on hormonal replacement therapy with recombinant human parathyroid hormone (rhPTH)(1–84) since January 2018. After starting rhPTH (1–84) 50 µg once daily as a subcutaneous injection, she stopped calcitriol and calcium supplementation, having achieved optimal and stable serum calcium levels. Her treatment was specifically approved by the Italian Medicines Agency (AIFA) before the marketing authorization in Italy, and the patient underwent regular follow-up at the University of Turin (Piedmont, Italy). On February 19, the patient presented to the emergency department of the Cremona Hospital (Lombardy, Italy) with fever, cough, and dyspnea. High-resolution computed tomography showed multiple and bilateral ground-glass opacities of the lungs. Bronchoalveolar lavage fluid was positive for SARS-CoV-2. After an unsuccessful trial of non-invasive ventilation, her progressive respiratory failure required endotracheal intubation and mechanical ventilation. Therefore, she was transferred to the Intensive Care Unit (ICU) of San Matteo Hospital in Pavia (Lombardy, Italy) on February 22. Pharmacological treatment included empirical antiviral regimens with lopinavir/ritonavir and ribavirin, and prophylaxis with hydroxychloroquine, azithromycin, piperacillin/tazobactam, and trimethoprim-sulfamethoxazole. Hemodynamic support required norepinephrine and dobutamine infusion; intravenous hydrocortisone was subsequently introduced at a dose of 300 mg divided in bolus injections over 24 h. After 6 days, the patient was extubated and started helmet continuous positive airway pressure. During hospitalization, the intravenous glucocorticoid dose was gradually tapered and eventually switched back to the pre-admission oral regimen. Unfortunately, the patient’s rhPTH treatment was interrupted after admission. Although the summary of product