International journal of rheumatic diseases · 2025
Seropositive Rheumatoid Arthritis and Polyhexamethylene Guanidine/Oligo(2-(2-Ethoxy)ethoxyethyl)guanidinium Chloride Exposure Are Associated With a Synergistic Effect on the Risk of Developing Interstitial Lung Disease: Registry Based Cohort-Study.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
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.
Choi Hyowon, Ryu Seungjun, Ahn Yeon-Soon
Аннотация
BACKGROUND: Humidifier disinfectants (HDs) containing polyhexamethylene guanidine/oligo(2-(2-ethoxy)ethoxyethyl)guanidinium chloride (PHMG/PGH) have a strong association with interstitial lung disease (ILD). Whether PHMG/PGH increases seropositive rheumatoid arthritis (RA) or interacts with RA to raise ILD risk is unknown.
METHODS: We constructed a registry-linked retrospective cohort by linking HD-claimant from the Korean Environmental Industry & Technology Institute (KEITI) to the National Health Insurance Service. Individuals who were aged ≥ 20 years as of January 1, 2003, were followed until death or December 31, 2021. PHMG/PGH exposure was modeled time-varyingly (pre vs. post). Seropositive RA (ICD-10 M05) was identified through claims screening with medical record review; ILD was defined by J84 claims. RA incidence was estimated using Poisson regression. For ILD, we applied time-dependent Cox models for PHMG/PGH exposure and post-RA status, adjusting for demographics, smoking, residence, and other HD components. Additive interaction was quantified by the relative excess risk due to interaction (RERI), attributable proportion (AP), and synergy index (S).
RESULTS: Total 3452 adults (mean follow-up 15.9 ± 5.6 person-years) were analyzed; 1.7% developed seropositive RA and 21.6% ILD. RA incidence was 0.830 before exposure and 1.105 after (per 1000 person-years; p = 0.61). ILD hazards were elevated for PHMG/PGH exposure (HR 3.62, 95% CI 3.11-4.20) and for seropositive RA (HR 3.80, 2.70-5.34). Co-occurrence was observed more-than-additive risk: RERI 1.467 (95% CI 0.814-2.120), AP 0.143 (0.079-0.206), S 1.188 (1.049-1.326).
CONCLUSIONS: PHMG/PGH exposure was not associated with increased incidence of seropositive RA. PHMG/PGH and seropositive RA each independently raised ILD risk, with more-than-additive association when combined. Given the retrospective, internally compared design, mechanistic work is warranted.
METHODS: We constructed a registry-linked retrospective cohort by linking HD-claimant from the Korean Environmental Industry & Technology Institute (KEITI) to the National Health Insurance Service. Individuals who were aged ≥ 20 years as of January 1, 2003, were followed until death or December 31, 2021. PHMG/PGH exposure was modeled time-varyingly (pre vs. post). Seropositive RA (ICD-10 M05) was identified through claims screening with medical record review; ILD was defined by J84 claims. RA incidence was estimated using Poisson regression. For ILD, we applied time-dependent Cox models for PHMG/PGH exposure and post-RA status, adjusting for demographics, smoking, residence, and other HD components. Additive interaction was quantified by the relative excess risk due to interaction (RERI), attributable proportion (AP), and synergy index (S).
RESULTS: Total 3452 adults (mean follow-up 15.9 ± 5.6 person-years) were analyzed; 1.7% developed seropositive RA and 21.6% ILD. RA incidence was 0.830 before exposure and 1.105 after (per 1000 person-years; p = 0.61). ILD hazards were elevated for PHMG/PGH exposure (HR 3.62, 95% CI 3.11-4.20) and for seropositive RA (HR 3.80, 2.70-5.34). Co-occurrence was observed more-than-additive risk: RERI 1.467 (95% CI 0.814-2.120), AP 0.143 (0.079-0.206), S 1.188 (1.049-1.326).
CONCLUSIONS: PHMG/PGH exposure was not associated with increased incidence of seropositive RA. PHMG/PGH and seropositive RA each independently raised ILD risk, with more-than-additive association when combined. Given the retrospective, internally compared design, mechanistic work is warranted.