Syed Jaan Naqvi, MD1, Saad Karamat, MD2, Demetrios Tzimas, MD3, Stephanie Dibble, PA-C1, Seth Clohosey, MD1; 1St. Mary's Hospital, Waterbury, CT; 2Desert Regional Medical Center, Santa Clarita, CA; 3Saint Mary's Hospital, Waterbury, CT
Introduction: Over seven million cases of Coronavirus Disease 2019 (COVID-19) have been confirmed thus far with over four hundred thousand deaths (1). Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes COVID-19 with a spectrum of disease severity with pneumonia being the most common manifestation. Studies have shown SARS-CoV-2 inducing damage to heart, kidney and pulmonary tissue through possible binding of the ACE2 receptor (10). As the incidence of COVID-19 cases increase, there is increased reporting of gastrointestinal manifestations. In view of this, we report a case of COVID-19 induced pancreatitis.
Methods: 69-year-old lady initially admitted for respiratory failure in the setting of SARS-CoV-2 pneumonia presents 3 days after discharge with epigastric pain. Her medical history significant for a prior cholecystectomy. Patient never smoked, drank alcohol, or used illicit drugs. Labs and imaging significant for leukocytosis, mildly elevated lipase, and CT abdomen suggestive of acute pancreatitis. Given her findings, she was diagnosed with mild acute pancreatitis. She was volume resuscitated, pain managed with hydromorphone, and started on early parenteral nutrition. She tolerated a diet by hospital day 5 and discharged home. Discussion: Diagnosis of acute pancreatitis is met when patients fulfill two of the following criteria: typical symptoms, lipase/amylase three times the upper limit of normal, or imaging findings consistent with acute pancreatitis. In our case presentation, our patient met the criteria confirming the diagnosis. In regards to the etiology, a comprehensive evaluation found no particular etiology for our patient’s pancreatitis. However, viruses can be a potential cause of acute pancreatitis. Previous theories suggest direct destruction of pancreatic acinar cells via inflammation and edema particularly in HBV induced pancreatitis. We suggest there may be a similar state of inflammation occurring from coronavirus infection. It is speculated SARS-CoV-2 may use its spike (S) protein to bind angiotensin-converting enzyme 2 (ACE2) on the host cell membrane to gain entry into the cell (14). Liu et. al showed expression of ACE2 in both exocrine gland and islets of the pancreas. At this time, pathogenesis remains unclear, but one can extrapolate SARS-CoV-2 may induce pancreatitis due to direct cytopathic effects of viral entry and replication. As COVID-19 pandemic continues, it would be worthwhile to suspect SARS-CoV-2 as an etiology of acute pancreatitis.
Disclosures: Syed Jaan Naqvi indicated no relevant financial relationships. Saad Karamat indicated no relevant financial relationships. Demetrios Tzimas indicated no relevant financial relationships. Stephanie Dibble indicated no relevant financial relationships. Seth Clohosey indicated no relevant financial relationships.