Letter to the EditorTo the Editor, Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation (ROHHAD) is an extremely rare disease having a high risk of mortality. Death usually occurs around the age of 10, but very few patients can survive beyond this age. [1,2] During the novel coronavirus (COVID-19) outbreak, the specific risks for patients with genetic disorders were not fully disclosed; however, available data indicated that they have a more severe course of infection compared to the general population requiring intensive care support. [3] We described the critical care management of a 20-year-old patient with ROHHAD syndrome presenting with COVID-19 and discussed the clinical challenges. The patient was admitted to the emergency department with complaints of shortness of breath and fever. His previous history revealed ROHHAD syndrome associated with intellectual delay, severe obstructive sleep apnea requiring continuous positive airway pressure, autonomic nervous system, and endocrine abnormalities. His computed tomography of the thorax demonstrated bilateral ground-glass infiltrates and pulmonary congestion. Laboratory investigations showed leucopenia (1.5x10 3 /uL), hypernatremia (169 mmol/L), impairment of renal and hepatic function (creatinine: 1.85 mg/dl, blood urea: 84mg/dl, alanine aminotransferase: 65 U/L, aspartate aminotransferase: 110 U/L, international normalized ratio: 1.82 and prothrombin time: 23.7 sec), elevated level of D-dimer (2690 µgr/L), ferritin (63.2 µg/L), C reactive protein (CRP) (27.4 mg/L) and interleukin-6 (IL-6): 84.39 pg/ml). His nasopharyngeal swab for real-time polymerase chain reaction resulted positive. The patient was initially admitted to the pandemic clinic and the COVID-19 treatment protocol was commenced. However, he developed severe hypoxia that required emergency intubation and was transferred to the intensive care unit three days after hospitalization. He received mechanical ventilation, which required intravenous sedatives with a high fraction of inspired oxygen, high positive end-expiratory pressure, low tidal volume strategy, and concomitant rescue therapies (infusion of neuromuscular blocking agents, prone positioning, and inhaled vasodilators). Nevertheless, he had persistent hypoxemia and respiratory acidosis. Blood glucose levels were consistently high despite the adjusting insulin infusion. Serum sodium level measurements demonstrated fluctuations and required frequent blood sampling and correction of the imbalance. During his course in intensive care unit, his condition gradually deteriorated with hemodynamic alterations refractory to supportive treatment, spiked inflammatory markers (D-dimer: 13.500 µgr/L, CRP: 263.6 mg/L, ferritin: 281.8 µg/L and IL-6: 427.2 pg/ml), impaired liver and renal function tests. He was not suitable for extracorporeal therapies due to hemodynamic instability and died ten days later in the intensive care unit. Udrea et al. [4] described the first case of COVID-19 infection in a pediatric pati...