Association between Acute Pancreatitis and COVID-19: Could Pancreatitis Be the Missing Piece of the Puzzle about Increased Mortality Rates?

Cevher Akarsu, Mehmet Karabulut, Husnu Aydin, Nuri Alper Sahbaz, Ahmet Cem Dural, Duygu Yegul, Kivanc Derya Peker, Sina Ferahman, Sezer Bulut, Turgut Dönmez, Sinan Asar, Kadriye Kart Yasar, Gokhan Tolga Adas
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引用次数: 51

Abstract

Background: The COVID-19 pandemic caused by SARS-CoV-2 commenced in Wuhan China in 2019 and soon spread worldwide. SARS-CoV-2 enters the cell by binding to the ACE II receptor and begins viral replication. The effects and clinical findings of SARS-CoV-2 on the liver, kidney, heart, gastrointestinal (GI) system and especially lungs have been widely discussed. However, the effects on the pancreas-another organ that also expresses ACE II-have not been studied.

Methods: This work prospectively evaluated data from 316 patients who were admitted with a diagnosis of COVID-19 pneumonia. The patients were categorized into three according to the severity of pneumonia (mild, severe, critical). Demographic data, rate of pancreatitis, biochemical parameters, and radiological images from each group were analyzed. The patients were divided into two groups and outcomes were compared: COVID-19 patients with acute pancreatitis (Group P) and without acute pancreatitis (Group C).

Results: The median age was 54 (18-87), and the median age for patients with acute pancreatitis was 55 (26-84). As an expected finding, we found a positive correlation between advanced age and mortality (p = 0.0003). 12.6% of the patients had acute pancreatitis. While pancreatitis was not seen in patients on mild status, the rate of pancreatitis was 32.5% in critical patients. Hospitalization and mortality rates were higher in patients with COVID-19 accompanied by acute pancreatitis (p = 0.0038 and p < 0.0001, respectively). C-Reactive Protein (CRP) and ferritin were significantly higher in those who had pancreatitis (p < 0.0001). D-Dimer and procalcitonin levels had only a small difference (p = 0.1127 and p = 0.3403, respectively).

Conclusion: Acute pancreatitis alone is a clinical condition that can lead to mortality and may be one of the reasons for the exaggerated immune response developing in the progression of COVID-19. Our results point out that the presence of pancreatic damage triggered by SARS-CoV-2 can deteriorate the clinical condition of patients and the mortality rate may increase in these patients.

急性胰腺炎与COVID-19之间的关系:胰腺炎是否可能是死亡率增加之谜的缺失部分?
背景:2019年由SARS-CoV-2引起的COVID-19大流行始于中国武汉,并迅速蔓延至全球。SARS-CoV-2通过与ACE II受体结合进入细胞并开始病毒复制。SARS-CoV-2对肝脏、肾脏、心脏、胃肠道系统特别是肺的影响和临床表现已被广泛讨论。然而,对胰腺(另一个也表达ACE ii的器官)的影响尚未研究。方法:前瞻性评估316例诊断为COVID-19肺炎的住院患者的资料。根据肺炎的严重程度将患者分为轻度、重度、危重三类。分析各组患者的人口学资料、胰腺炎发生率、生化指标及影像学资料。将患者分为合并急性胰腺炎的COVID-19患者(P组)和未合并急性胰腺炎的患者(C组)。结果:患者中位年龄为54岁(18-87岁),合并急性胰腺炎患者中位年龄为55岁(26-84岁)。正如预期的发现,我们发现高龄与死亡率呈正相关(p = 0.0003)。12.6%的患者有急性胰腺炎。轻症患者未见胰腺炎,危重症患者胰腺炎发生率为32.5%。新冠肺炎合并急性胰腺炎患者住院率和死亡率较高(p = 0.0038, p = 0.1127, p = 0.3403)。结论:急性胰腺炎是一种可导致死亡的临床疾病,可能是COVID-19进展中出现夸大免疫反应的原因之一。我们的研究结果指出,SARS-CoV-2引发的胰腺损伤的存在可使患者的临床状况恶化,并可能增加患者的死亡率。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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