Faculty of Medicine, Bakirkoy Dr. Sadi Konuk Training and Research Hospital, Department of Surgery, University of Health Sciences, Istanbul, Turkey.
Faculty of Medicine, Bakirkoy Dr. Sadi Konuk Training and Research Hospital, Department of Radiology, University of Health Sciences, Istanbul, Turkey.
J Invest Surg. 2022 Jan;35(1):119-125. doi: 10.1080/08941939.2020.1833263. Epub 2020 Nov 2.
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.
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).
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 ( = 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 ( = 0.0038 and < 0.0001, respectively). C-Reactive Protein (CRP) and ferritin were significantly higher in those who had pancreatitis ( < 0.0001). D-Dimer and procalcitonin levels had only a small difference ( = 0.1127 and = 0.3403, respectively).
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.
由 SARS-CoV-2 引起的 COVID-19 大流行于 2019 年在中国武汉爆发，随后迅速蔓延至全球。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（GI）系统，尤其是肺部的影响和临床发现已被广泛讨论。然而，对胰腺的影响尚未研究，胰腺也是另一种表达 ACE II 的器官。
本工作前瞻性评估了 316 例确诊为 COVID-19 肺炎患者的数据。根据肺炎严重程度（轻症、重症、危重症）将患者分为三组。分析每组患者的人口统计学数据、胰腺炎发生率、生化参数和影像学图像。将患者分为两组并比较结果：伴有急性胰腺炎的 COVID-19 患者（组 P）和无急性胰腺炎的 COVID-19 患者（组 C）。
中位年龄为 54 岁（18-87 岁），伴有急性胰腺炎患者的中位年龄为 55 岁（26-84 岁）。正如预期的那样，我们发现年龄与死亡率呈正相关（ = 0.0003）。12.6%的患者发生急性胰腺炎。轻症患者中未发现胰腺炎，但危重症患者的胰腺炎发生率为 32.5%。伴有急性胰腺炎的 COVID-19 患者的住院率和死亡率更高（ = 0.0038 和 < 0.0001）。C 反应蛋白（CRP）和铁蛋白明显升高（ < 0.0001）。D-二聚体和降钙素原水平差异较小（ = 0.1127 和 = 0.3403）。
单纯性急性胰腺炎是一种可导致死亡的临床情况，可能是 COVID-19 进展中引发过度免疫反应的原因之一。我们的结果表明，由 SARS-CoV-2 引起的胰腺损伤可能会使患者的临床状况恶化，这些患者的死亡率可能会增加。
