Finnberg-Kim Amanda, Pihlsgård Mats, Önnerhag Kristina, Melander Olle, Enhörning Sofia
Department of Clinical Sciences in Malmö, Lund University, Malmö, Sweden.
Department of Gastroenterology and Hepatology, Skåne University Hospital, Malmö, Sweden.
Liver Int. 2025 Jun;45(6):e70132. doi: 10.1111/liv.70132.
Previous studies have shown that procalcitonin (PCT) concentration is elevated in patients with liver disease without evidence of bacterial infection. We aimed to investigate the association between elevated PCT and the future risk of liver disease.
PCT was measured in 3897 individuals without known liver disease in the Malmö Diet and Cancer Cardiovascular Cohort (MDC-CC) and in 3854 individuals in the Malmö Preventive Project cohort (MPP). Cox proportional hazards regression models were used to analyse the risk of register-verified incident liver disease by PCT levels. We performed our analyses in a pooled sample of both the MPP and MDC-CC cohorts, as well as separate analyses for each cohort.
70 subjects in MDC-CC and 49 subjects in MPP were diagnosed with non-viral liver disease during a median follow-up of 27.1 and 14.8 years, respectively. In multivariate adjusted models in the pooled sample, individuals with high PCT (> 0.05 ng/mL) had a significantly increased risk of developing liver disease compared to subjects with PCT concentrations below the cutoff (hazard ratio (HR) 3.4, 95% confidence interval (CI) 2.07-5.63, p < 0.001). The HR per standard deviation increase of log-transformed PCT was 1.56 (95% CI 1.32-1.85, p < 0.001) in multivariate adjusted models. Separate cohort-specific sensitivity analyses, including additional adjustment for C-reactive protein, showed similar effect estimates as the pooled analyses.
Elevated concentration of PCT independently predicts non-viral liver disease. These findings could have implications for risk assessment but also highlight the possibility of PCT as a direct cause of hepatocyte damage.
既往研究表明,在无细菌感染证据的肝病患者中,降钙素原(PCT)浓度会升高。我们旨在研究PCT升高与未来肝病风险之间的关联。
在马尔默饮食与癌症心血管队列(MDC - CC)中,对3897名无已知肝病的个体以及马尔默预防项目队列(MPP)中的3854名个体进行了PCT检测。采用Cox比例风险回归模型,根据PCT水平分析登记确认的新发肝病风险。我们在MPP和MDC - CC队列的合并样本中进行了分析,同时也对每个队列进行了单独分析。
在MDC - CC队列中,70名受试者,在MPP队列中,49名受试者在分别为期27.1年和14.8年的中位随访期内被诊断为非病毒性肝病。在合并样本的多变量调整模型中,与PCT浓度低于临界值的受试者相比,PCT高(>0.05 ng/mL)的个体患肝病的风险显著增加(风险比(HR)3.4,95%置信区间(CI)2.07 - 5.63,p < 0.001)。在多变量调整模型中,对数转换后的PCT每增加一个标准差,HR为1.56(95% CI 1.32 - 1.85,p < 0.001)。包括对C反应蛋白进行额外调整的单独队列特异性敏感性分析显示,效应估计值与合并分析相似。
PCT浓度升高可独立预测非病毒性肝病。这些发现可能对风险评估有影响,但也凸显了PCT作为肝细胞损伤直接原因的可能性。