曾患急性胰腺炎和未患急性胰腺炎的慢性胰腺炎患者的代谢后遗症和全因死亡率:基于全国人口的队列研究》。

M. E. Cook, Niels Henrik Bruun, Line Davidsen, P. Vestergaard, A. M. Drewes, S. S. Olesen
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引用次数: 0

摘要

目的:在一个基于人群的慢性胰腺炎(CP)患者队列中,调查曾患急性胰腺炎(AP)和未患急性胰腺炎(AP)的患者发生代谢后遗症和全因死亡的风险。方法:我们利用全国范围内的健康登记来识别 2000-2018 年间所有发生 CP 的丹麦居民(年龄大于 18 岁)。有关急性胰腺炎/慢性胰腺炎诊断、代谢后遗症(胰腺炎后糖尿病(PPDM)、胰腺外分泌功能障碍(EPD)和骨质疏松症)以及全因死亡率的信息均来自丹麦国家健康登记处。根据确诊 CP 之前是否患有 AP 对 CP 病例进行了分层。代谢后遗症和全因死亡率的风险用危险比(HRs)表示,95% 置信区间(CIs)采用多变量 Cox 比例危险模型计算。在 CP 患者中,3913 人(40.5%)曾被诊断为 AP。与无 AP 病史的患者相比,有 AP 病史的患者死亡风险降低(HR 0.79 (95% CI, 0.74-0.84)),这主要发生在 CP 诊断后的初期。既往有 AP 的患者发生 PPDM 的风险增加(HR 1.53 (95% CI, 1.38-1.69)),这种风险在 CP 诊断后的十年内持续存在。在 EPD(HR 0.97(95% CI,0.87-1.07))和骨质疏松症(HR 0.87(95% CI,0.74-1.02))方面未观察到总体风险差异。有和没有 AP 的 CP 患者在 PPDM 和全因死亡率方面具有不同的风险特征。
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Metabolic Sequelae and All-Cause Mortality in Chronic Pancreatitis With and Without Prior Acute Pancreatitis: A Nationwide Population-Based Cohort Study.
OBJECTIVES To investigate the risk of metabolic sequelae and all-cause mortality in a population-based cohort of chronic pancreatitis (CP) patients with and without prior acute pancreatitis (AP). METHODS We used nationwide health registries to identify all Danish residents (>18 years) with incident CP from 2000-2018. Information on AP/CP diagnoses, metabolic sequelae (post-pancreatitis diabetes mellitus (PPDM), exocrine pancreatic dysfunction (EPD), and osteoporosis), and all-cause mortality were obtained from Danish national health registries. CP cases were stratified based on the presence of AP prior to CP diagnosis. The risk of metabolic sequelae and all-cause mortality was expressed as hazard ratios (HRs) with 95% confidence intervals (CIs), calculated using multivariate Cox proportional hazards models. RESULTS A total of 9655 CP patients were included. Among CP patients, 3913 (40.5%) had a prior AP diagnosis. Compared to patients without a history of AP, patients with prior AP had a decreased risk of death (HR 0.79 (95% CI, 0.74-0.84)), which was largely confined to the initial period after CP diagnosis. Patients with prior AP had an increased risk of PPDM (HR 1.53 (95% CI, 1.38-1.69)), which persisted for up to a decade after CP diagnosis. No overall differences in risk were observed for EPD (HR 0.97 (95% CI, 0.87-1.07)) and osteoporosis (HR 0.87 (95% CI, 0.74-1.02)). CONCLUSIONS This nationwide study revealed that the majority of CP patients have no prior episode(s) of AP, indicating that an attack of AP sensitizing the pancreas is not essential for CP development. CP patients with and without prior AP have different risk profiles of PPDM and all-cause mortality.
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