The journal of medical investigation : JMI · 2026
Successful treatment for collagen vascular disease-related respiratory failure with inhaled nitric oxide as a bridging therapy:A case report.
СтатьяКлинический случайНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Sato Hiroki, Saijo Saki, Miyoshi Kota, Terazawa Masaki, Otani Shotaro, Moriwaki Konomi, Momota Kazuki, Takashima Takuya, Nunomura Toshiyuki, Ishihara Manabu, Itagaki Taiga, Oto Jun
Аннотация
BACKGROUND: Inhaled nitric oxide (iNO) is approved in Japan for perioperative pulmonary hypertension and persistent pulmonary hypertension in newborns;however, its role in non-cardiac respiratory failure is unclear.
CASE PRESENTATION: A 47-year-old woman with Sjögren's syndrome developed severe acute type I respiratory failure due to collagen vascular disease. Despite high-FIO2 ventilation, her PaO2/FIO2 ratio remained <80, and extracorporeal membrane oxygenation (ECMO) was considered. Administration of iNO at 10 ppm improved oxygenation, with a rapid increase in PaO2/FIO2 ratio. This response allowed time for steroid pulse therapy, rituximab, plasma exchange, and pleural drainage, which stabilized the patient's condition without ECMO. Notably, the temporal association between iNO initiation and rapid oxygenation improvement suggests that pulmonary vascular dysfunction was a major contributor to hypoxemia. Subsequent stabilization with immunosuppressive therapy highlights the role of iNO as a bridging therapy rather than a definitive treatment.
CONCLUSION: In this case, iNO may have served as a bridging therapy, improving oxygenation until immunosuppressive treatment was effective. iNO may serve as a useful interim measure for avoiding ECMO in collagen vascular disease-associated respiratory failure, particularly when pulmonary hypertension is suspected. J. Med. Invest. 73 : 270-273, February, 2026.
CASE PRESENTATION: A 47-year-old woman with Sjögren's syndrome developed severe acute type I respiratory failure due to collagen vascular disease. Despite high-FIO2 ventilation, her PaO2/FIO2 ratio remained <80, and extracorporeal membrane oxygenation (ECMO) was considered. Administration of iNO at 10 ppm improved oxygenation, with a rapid increase in PaO2/FIO2 ratio. This response allowed time for steroid pulse therapy, rituximab, plasma exchange, and pleural drainage, which stabilized the patient's condition without ECMO. Notably, the temporal association between iNO initiation and rapid oxygenation improvement suggests that pulmonary vascular dysfunction was a major contributor to hypoxemia. Subsequent stabilization with immunosuppressive therapy highlights the role of iNO as a bridging therapy rather than a definitive treatment.
CONCLUSION: In this case, iNO may have served as a bridging therapy, improving oxygenation until immunosuppressive treatment was effective. iNO may serve as a useful interim measure for avoiding ECMO in collagen vascular disease-associated respiratory failure, particularly when pulmonary hypertension is suspected. J. Med. Invest. 73 : 270-273, February, 2026.