Journal of Steroids & Hormonal Science

Acute Pancreatitis Caused by Drugs in Hospitalized COVID-19 Patients

Seongcheol Kim^{* *}Correspondence: Seongcheol Kim, Department of Medicine, Harvard University, Massachusetts, United States, Email:

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Introduction

Acute severe respiratory syndrome. The Coronavirus disease-19 (COVID-19) pandemic is caused by Coronavirus 2 (SARS-CoV-2). Asymptomatic instances to life-threatening respiratory infections are among the clinical symptoms of COVID-19. The most frequent and potentially fatal complication is Acute Respiratory Distress Syndrome (ARDS), while others include renal and pancreatic damage, thrombosis of smaller pulmonary capillaries, arterial and venous lung vasculopathy, and cardiac issues. SARS-CoV-2 and certain medications given to COVID-19 patients in hospitals were linked to the emergence of illnesses, most specifically severe pancreatitis. In 80% of patients, AP pancreatic inflammatory disease does not result in life threatening consequences. In a small percentage of instances (20%), it might gradually result in the irreparable loss of the pancreatic parenchyma and be fatal. The main clinical sign of AP is belt like abdominal pain that is felt in the upper abdomen and spreads to the back. Vomiting, nausea, and fever with grade variations (from low to moderate) are other symptoms that frequently coexist. There are numerous reasons why AP can develop. Alcohol consumption (35%) and stone blockage of the common bile duct (40%) are the most common. Medication has been identified as a second, albeit less frequent, cause of AP (2%). According to the Revised Atlanta Classification (RAC), two of the following three criteria must be met in order to diagnose AP:

• Abdominal pain consistent with AP.
• Elevated pancreatic serum enzymes, with amylase or lipase three times above the normal rate.
• Typical AP findings on imaging tests such as abdominal ultrasonography, Magnetic Resonance Imaging (MRI), or Computed Tomography (CT).

Additionally, SARS-CoV-2 is an RNA virus that infects cells by syncing with the ACE2 receptor and spiking spike protein.

Description

These proteins are mostly expressed in pancreatic, gastric luminal, and lung parenchyma cells islet, ductal, and acinar cells. Trans Membrane Serine Protease 2 (TMPRSS2), another enzyme that aids viral entry in addition to ACE2, is expressed in ductal cells. Although the precise mechanism by which SARS-CoV-2 infection affects pancreatic cells is not yet established, it is possible that the infection of those cells is one of the causes of AP. Some reports claim that the uncontrolled cytokine storm that results from SARS-CoV-2 infection may increase the AP's severity. Another theory is that various degrees of AP may be brought on by pancreatic ischemia. Additionally, an unbalanced hemostasis and enhanced coagulation could result from the inflammatory process that initiates the coagulation cascade. It is important to highlight that infection related hyperglycemia strongly promotes inflammation and, as a result, increases the levels of inflammatory mediators. To varying degrees, each of the aforementioned techniques helps to materialise AP. Additionally, it was discovered that COVID-19 patients with pancreatic injury also had higher serum lipase or amylase levels. It's interesting to note that patients with COVID-19 may have developed AP because of the medications they took while they were in the hospital, in addition to the direct viral damage to pancreatic cells and COVID-19's thrombogenic status. The World Health Organization (WHO) has identified over 525 distinct medicines as potentially causative agents, despite the fact that Drug Induced Acute Pancreatitis (DIAP) accounts for fewer than 5% of all instances of AP. Many of these medications have been given to COVID-19 patients and have resulted in direct or indirect pancreatic injury, primarily through the development of Hypertriglyceridemia (HGT). Direct toxic effects, accumulation of toxic metabolites or intermediates, immunological response, and hypersensitive reaction are a few of the mechanisms involved in the pathogenesis of DIAP. Due to the rarity of DIAP, there are few scientific investigations and precise information, particularly for more recent medicines that have been linked to AP.

Conclusion

As a result, data have been gathered through case reports written after medications have been used or by regional drug safety committees. The purpose of this review is to enumerate and evaluate the medications that have been used to treat COVID-19 infections and are linked to DIAP in COVID-19 patients who are hospitalised.