Естественный эксперимент по заболеваемости нейро-воспалительными заболеваниями и инфекциям связывает до и после COVID-19.
Обработка статьи · этапы, ошибки и управление
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Akada Masahiro, Hata Masayuki, Miyake Masahiro, Ishihara Kenji, Muraoka Yuki, Morooka Satoshi, Tamura Hiroshi, Tsujikawa Akitaka
Аннотация
Оригинал публикации
Natural experiment on neuroinflammatory disease incidence and infection links pre- and post-COVID-19.
Infections are recognized triggers for several neuroinflammatory disorders. The coronavirus disease 2019 (COVID-19) pandemic's non-pharmaceutical interventions sharply curtailed pathogen exposure, creating a natural experiment to test infection-disease links. Using Japan's National Claims Database, we first validated the nationwide decline with two strictly infection-dependent conditions-epidemic keratoconjunctivitis and influenza-associated encephalopathy-whose monthly incidences fell by >60% after April 2020. Next, we applied an interrupted time series design, a causal-inference method for longitudinal data, to nine immune-mediated inflammatory diseases. Unsupervised clustering of model-derived level and slope changes identified three data-driven clusters. The first cluster, comprising Guillain-Barré syndrome and acute disseminated encephalomyelitis, showed large, statistically significant level reductions (P < 0.001), particularly in women, consistent with infection-susceptible pathophysiology. The second cluster, including myasthenia gravis and optic neuritis, exhibited transient declines followed by significant positive post-intervention slopes (P < 0.001), suggesting deferred diagnosis, treatment interruption or immune rebound. The third cluster, consisting of sarcoidosis, neuromyelitis optica, multiple sclerosis, Vogt-Koyanagi-Harada disease and Behçet's disease, remained stable, suggesting limited or complex infectious links. These data-driven trajectories mirror clinical pathophysiology and demonstrate that reduced pathogen exposure affects neuroinflammatory disease onset to varying degrees. This framework supports infection-related risk stratification, preventive strategies and continuity planning in neuroimmunology practice.