Rheumatology (Oxford, England) · 2026
High levels of vascular cell adhesion molecule-1 associate with a 'vasculopathic' phenotype in systemic sclerosis with higher mortality.
СтатьяПоддержка исследования: вне правительства СШАНазвание 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.
Parker Matthew J S, Nikpour Mandana, Hansen Dylan, Hanson Aimee L, Sahhar Joanne, Brown Matthew A, Corte Tamera J, Proudman Susanna, Kenna Tony J, Australian Scleroderma Interest Group
Аннотация
OBJECTIVES: To determine disease-specific associations of serum vascular cell adhesion molecule-1 (VCAM-1) and associated mortality in SSc.
METHODS: Participants were identified from the Australian Scleroderma Cohort Study. Data were linked with the National Death Index for cause-specific mortality. VCAM-1 was measured using a magnetic Luminex assay. Participant characteristics and information on organ specific manifestations were extracted until February 2024. Participants were stratified into VCAM-1 quartiles.
RESULTS: Of 388 participants, 87.1% were female and 76.8% had limited cutaneous disease. Median age at diagnosis was 45.7 years (interquartile range 36.4-56.7). Participants with upper quartile VCAM-1 (quartile 4; Q4) had increased mortality compared with others [hazard ratio (HR) 2.17, 95% CI 1.54-3.04; P < 0.001]. Despite the significant increased mortality in Q4, there were no statistically significant differences in sex, age, disease duration, disease subtype, autoantibody profile or forced vital capacity across the VCAM-1 quartiles. Q4 were more likely to have pulmonary arterial hypertension (PAH; P = 0.028), SSc-attributable myocardial disease (P = 0.009) and digital ulcers (P = 0.003). In cause-specific mortality analysis, Q4 were more likely to have PAH (HR 3.08, 95% CI 1.68-5.65; P < 0.001), SSc-attributable myocardial disease (HR 2.85, 95% CI 1.51-5.38; P = 0.001) and all-cause cardiovascular disease (HR 2.50, 95% CI 1.60-3.89; P < 0.001) listed as a cause or contributor to death. Q4 VCAM-1 level was not associated with interstitial lung disease presence, severity or cause-specific mortality.
CONCLUSION: The increased mortality in participants with SSc and Q4 VCAM-1 levels is attributable to increased frequency of vascular disease manifestations. Q4 participants do not have a disproportionate frequency of other established risk factors for increased mortality, suggesting an independent role for VCAM-1 in disease pathophysiology.
METHODS: Participants were identified from the Australian Scleroderma Cohort Study. Data were linked with the National Death Index for cause-specific mortality. VCAM-1 was measured using a magnetic Luminex assay. Participant characteristics and information on organ specific manifestations were extracted until February 2024. Participants were stratified into VCAM-1 quartiles.
RESULTS: Of 388 participants, 87.1% were female and 76.8% had limited cutaneous disease. Median age at diagnosis was 45.7 years (interquartile range 36.4-56.7). Participants with upper quartile VCAM-1 (quartile 4; Q4) had increased mortality compared with others [hazard ratio (HR) 2.17, 95% CI 1.54-3.04; P < 0.001]. Despite the significant increased mortality in Q4, there were no statistically significant differences in sex, age, disease duration, disease subtype, autoantibody profile or forced vital capacity across the VCAM-1 quartiles. Q4 were more likely to have pulmonary arterial hypertension (PAH; P = 0.028), SSc-attributable myocardial disease (P = 0.009) and digital ulcers (P = 0.003). In cause-specific mortality analysis, Q4 were more likely to have PAH (HR 3.08, 95% CI 1.68-5.65; P < 0.001), SSc-attributable myocardial disease (HR 2.85, 95% CI 1.51-5.38; P = 0.001) and all-cause cardiovascular disease (HR 2.50, 95% CI 1.60-3.89; P < 0.001) listed as a cause or contributor to death. Q4 VCAM-1 level was not associated with interstitial lung disease presence, severity or cause-specific mortality.
CONCLUSION: The increased mortality in participants with SSc and Q4 VCAM-1 levels is attributable to increased frequency of vascular disease manifestations. Q4 participants do not have a disproportionate frequency of other established risk factors for increased mortality, suggesting an independent role for VCAM-1 in disease pathophysiology.