Anakinra
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Ling injury: case report A 17-year-old boy developed possible lung injury during treatment with anakinra for presumed haemophagocytic lymphohistiocytosis (HLH) and macrophage activation syndrome (MAS). The boy was admitted to the hospital due to intermittent fevers, persistent vomiting, headache and weight loss. His history was significant for nicotine and marijuana vaping, including daily E-cigarette use and marijuana. On admission, he was started on azithromycin for presumed pneumonia. His hypoxaemia and respiratory distress worsened. Therefore, cotrimoxazole [trimethoprim/sulfamethoxazole] and ceftriaxone was added to treat suspected Pneumocystis jiroveci pneumonia. However, his condition continued to worsen. An infectious aetiology was not found. At that time, his differential diagnoses included other systemic illnesses, such as iatrogenic and systemic autoimmune disorders, hematologic process, Pneumocystis jiroveci pneumonia and vaping-related acute lung injury. On admission day 11, he was discharged home to complete a cotrimoxazole course for presumed Pneumocystis jiroveci pneumonia. Nine days later, he presented again due to presyncope and was admitted to the PICU. He received empiric treatment with ceftriaxone, vancomycin and cefepime. Subsequently, on the basis of clinical criteria, a presumptive diagnosis of vaping or electronic cigarette-associated acute lung injury (EVALI), with clinical, laboratory and pathologic evidence of MAS and HLH. He was started on pulse therapy with IV methylprednisolone. His laboratory and inflammatory markers improved with the steroid therapy. Subsequently, he was started on IV anakinra at 1 mg/kg/dose every 6h for presumed MAS and HLH on hospital day 11. A further improvement in his clinical condition was observed, but his respiratory status continued to worsen [duration of treatment to reaction onset not stated]. The boy’s anakinra was stopped on admission day 17 due to concern for the possibility of anakinra-related lung injury and lack of further clinical response. He had persistent hypoxemia despite high-flow nasal cannula (HFNC) respiratory support. He showed striking positional changes in oxygen saturation. On admission day 15, he was intubated and started on mechanical ventilation. His pulmonary tests supported a diagnosis of severe acute respiratory distress syndrome. He remained profoundly hypoxemic. On admission day 16, bronchoscopy showed no significant secretions bleeding, endobronchial lesions or mucous plugs. On admission day 17, he was cannulated to venovenous extracorporeal membrane oxygenation (ECMO) to permit lung rest, maximize chances for lung recovery and minimize barotrauma. While he was on ECMO support, his unspecified sedation was stopped, and he was extubated to HFNC on admission day 18. He became agitated within 3h after extubation and had cardiac arrest requiring cardiopulmonary resuscitation for 2 min. He was intubated again and stated on ECMO. An echocardiogram showed decreased left ventricular systolic function. Therefore, he was started on
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