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Mizoribine treatment in an elderly diabetic patient with antisynthetase-associated interstitial lung disease

Objective: Immunosuppressive therapy for interstitial lung disease (ILD) is often necessary, but the standard regimen for antisynthetase-associated ILD has not been established. Patient: An 80-year-old man was hospitalized for severely progressive dyspnea. Bilateral interstitial shadows occurred 1 m...

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Detalles Bibliográficos
Autores principales: Nagai, Kei, Niisaka, Masahiro, Nakajima, Masayuki, Sakata, Yoshinori, Nakamura, Yoshiharu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Japanese Association of Rural Medicine 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7530592/
https://www.ncbi.nlm.nih.gov/pubmed/33033547
http://dx.doi.org/10.2185/jrm.2020-018
Descripción
Sumario:Objective: Immunosuppressive therapy for interstitial lung disease (ILD) is often necessary, but the standard regimen for antisynthetase-associated ILD has not been established. Patient: An 80-year-old man was hospitalized for severely progressive dyspnea. Bilateral interstitial shadows occurred 1 month before the event. Serological findings showed that he had antisynthetase-associated ILD, as identified by strong positivity for anti-aminoacyl-transfer RNA synthetase (ARS) antibody, despite no evidence of myositis. He was treated transiently with noninvasive positive pressure ventilation and steroid-pulse therapy followed by 60 mg/day of oral prednisolone. However, his diabetes mellitus was aggravated by corticosteroid therapy; thus, a combination of low-dose steroid and mizoribine (MZB), which has a low risk of aggravating glucose intolerance, was used. Results: The patient’s clinical symptoms and daily life activities have been well persevered as an outpatient and well maintained with 200 mg of MZB and 10 mg of prednisolone for several months without obvious clinical recurrence and without any remarkable steroid- and MZB-related side effects. Conclusion: The use of MZB appeared to suppress the pathophysiology of anti-ARS antibody-associated ILD.