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Acute Pancreatitis in a Teenager With SARS-CoV-2 Infection

Paz, Liborio MD*; Eslava, Edgar MD*; Ribes, María MD*; Mayer, Erick F. MD, MSc*,†

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The Pediatric Infectious Disease Journal: April 2021 - Volume 40 - Issue 4 - p e161-e162
doi: 10.1097/INF.0000000000003046
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A 14-year-old child presented after 5 hours of severe abdominal pain of acute onset. The pain was located in the epigastrium and radiated toward the left hypochondrium and back. He had no history of fever, diarrhea, vomiting, or flu-like symptoms. His personal and family histories were unremarkable. Family members were all healthy and had been compliant with lockdown measurements during the SARS-CoV-2 pandemic. Upon arrival to the Emergency Department, his temperature was 36.3°C, heart rate 52 bpm, respiratory rate 20 bpm, and blood pressure 104/61 mm Hg. He was stable but in significant pain. Abdomen was soft with normal bowel sounds, although it was tender to palpation on epigastric area. The rest of physical examination was unremarkable.

Table 1 summarizes the initial workup, which was significant for moderately elevated lipase (247 U/L, normal range (NR) 0–50 U/L), amylase (196 U/L, NR 8–53 U/L), creatine kinase (3204 U/L, NR 24–195 U/L), and lactic dehydrogenase levels (913 U/L, NR 230–460 U/L). The SARS-CoV-2 polymerase chain reaction was positive, and the PCR for influenza A and B were negative. He had a normal chest radiogram. Electrocardiogram showed sinus bradycardia. Initial abdominal ultrasound showed biliary sludge, and a distended gallbladder with diffuse wall thickening and a scant amount of surrounding free fluid. Choledochal channel and intrahepatic biliary ducts had a normal caliber. The pancreas was not visualized because of air-filled bowel loops.

TABLE 1. - Laboratory Results on Admission
Laboratory Test Results
White-blood cell count 7310 cells/mm3
 Neutrophil count 4760 cells/mm3
 Lymphocyte count 2060 cells/mm3
 Monocyte count 430 cells/mm3
Hemoglobin 13 g/L
Platelet count 291,000 cells/mm3
Amylase 196 U/L
Lipase 247 U/L
Creatine kinase 3204 U/L
Alanine aminotransferase 161 U/L
Aspartate aminotransferase 87 U/L
Bilirubin, total 0.37 mg/dL
Lactate dehydrogenase 912 U/L
Blood urea nitrogen 78.5 mg/dL
Creatinine 1.17 mg/dL
Trygliceride 55 mg/dL
Cholesterol 155 mg/dL
C-reactive protein <1 mg/L
D-dimer 0.27 µg/mL

He was admitted to the pediatric unit for pain management, administration of intravenous fluids, and further workup. The following day, a magnetic resonance cholangiopancreatography was consistent with acute pancreatitis, showing a normal-size pancreas with edematous changes. The pancreatic boundaries were blurred because of peripancreatic fluid exudation. It also showed a hydropic gallbladder without lithiasis. The rest of the study was within normal limits. Pain responded to bowel rest, IV fluids, and analgesia. Laboratory markers of pancreatitis slowly trended down on following days. Diet was advanced as tolerated, and he was discharged home after 5 days.


We present the case of a 14-year-old boy with acute pancreatitis in the setting of a SARS-CoV-2 infection. The diagnosis of acute pancreatitis requires at least 2 of the 3 following criteria: (1) abdominal pain, (2) amylase or lipase >3 times the upper normal limit, and (3) characteristic findings on diagnostic imaging.1 Our patient fulfilled all 3 criteria. Furthermore, he did not have a history of systemic or metabolic diseases; trauma or drug ingestion; or evidence of other infections known to cause pancreatitis, like mumps, Epstein-Barr, hepatitis A, cytomegalovirus, rubella, enterovirus, measles, influenza, or human immunodeficiency virus infections. The development of acute pancreatitis is usually multifactorial and requires both predisposition and a significant injury.

The spectrum of COVID-19, the disease caused by the novel SARS-CoV-2, ranges from an asymptomatic carrier state to a severe and frequently fatal disease. SARS-CoV-2 infections usually affect the lower respiratory tract, where the virus binds to the angiotensin-converting enzyme-2 (ACE2) receptor, but there is evidence that this virus can infect other tissues. The SARS-CoV-2 virus has been detected in fecal samples in patients with COVID-19, even if they had negative nasopharyngeal PCRs.2,3 Clinically, this correlates with symptoms like nausea, vomiting, and diarrhea, that have been reported as part of the clinical manifestations of COVID-19.4

The ACE2 receptor, the transmembrane protein required for viral entry into the cell, is expressed in multiple systems.2,3,5,6 In a study done in survivors of SARS-CoV infection, closely related to SARS-CoV-2, the organ involvement correlated with the expression of ACE2 demonstrated by significantly higher immunostaining in the lung, kidney, heart, and pancreas, including the exocrine and endocrine pancreatic tissue.6 Furthermore, ACE2 expression measured by mRNA levels is higher in the pancreas than in the lungs.5 While less than 20% of patients with COVID-19 can have a mild elevation of amylase and lipase,5 pancreatitis is not a common finding and seems to occur more often in the context of COVID-19 and multiorgan failure.3 In these cases, patients presented with respiratory insufficiency that later deteriorated into multiorgan dysfunction that included pancreatitis. Nevertheless, there are few reports of adult patients with COVID-19 presenting with pancreatitis. A 36-year-old obese woman presented with abdominal pain consistent with pancreatitis after experiencing cough, fever, and progressive dyspnea for over a week, later confirmed to have COVID-19.7 Another paper reported a 24-year-old man with acute pancreatitis and SARS-CoV-2 infection. The later diagnosis had been done the day prior when the patient presented to the Emergency Department because of mild upper respiratory tract symptoms.8

To our knowledge, this is the first case of a pediatric patient infected with SARS-CoV-2 that presents with acute pancreatitis as the sole clinical manifestation. This case report cannot prove that the SARS-CoV-2 caused the pancreatitis, and it is also not possible for us to determine if the SARS-CoV-2 infection was acute or occurred days before the onset of abdominal pain. Nevertheless, the review of the literature summarized above suggests that this is biologically plausible. Although this is an unusual presentation, we think that SARS-CoV-2 infection should be included in the differential diagnosis of patients with acute pancreatitis or elevation of lipase and amylase in the absence of other causes. Further reports will be necessary to confirm this possible association and to better characterize and define the characteristics and impact of this novel infection.


1. Banks PA, Bollen TL, Dervenis C, et al.; Acute Pancreatitis Classification Working Group. Classification of acute pancreatitis–2012: revision of the Atlanta classification and definitions by international consensus. Gut. 2013; 62:102–111
2. Xiao F, Tang M, Zheng X, et al. Evidence for gastrointestinal infection of SARS-CoV-2. Gastroenterology. 2020; 158:1831–1833.e3
3. Hadi A, Werge M, Kristiansen KT, et al. Coronavirus disease-19 (COVID-19) associated with severe acute pancreatitis: case report on three family members. Pancreatology. 2020; 20:665–667
4. Centers for Disease Control and Prevention. Coronavirus disease 2019 (COVID-19)—Symptoms. Centers for Disease Control and Prevention. Available at: Accessed July 10, 2020.
5. Liu F, Long X, Zhang B, et al. ACE2 expression in pancreas may cause pancreatic damage after SARS-CoV-2 infection. Clin Gastroenterol Hepatol. 2020; 18:2128–2130.e2
6. Yang JK, Lin SS, Ji XJ, et al. Binding of SARS Coronavirus to its receptor damages islets and causes acute diabetes. Acta Diabetol. 2010; 47:193–199
7. Aloysius MM, Thatti A, Gupta A, et al. COVID-19 presenting as acute pancreatitis. Pancreatology. 2020; 20:1026–1027
8. Mazrouei SSA, Saeed GA, Al Helali AA. COVID-19-associated acute pancreatitis: a rare cause of acute abdomen. Radiol Case Rep. 2020; 15:1601–1603

SARS-CoV-2 infection; COVID-19; acute pancreatitis

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