Discussion
The first report of pancreatic involvement in CoViD-19 infection described 9 patients in which receptor of angiotensin-converting enzyme 2 (ACE 2) was found to be expressed in both exocrine pancreas and islet3,4. The proposed mechanism of pancreatic injury in CoViD-19 infection include a direct cytopathic effect mediated by local viral replication or a damage due to immune response with locoregional vasculitis and thrombotic microangiopathy, as occurs in other organs4.
In the lung the virus attaches to ACE 2 receptors and the spike protein (SP) attaches to alveolar cells, with a cytokine storm resulting in alveolar flooding and denudation of the lining epithelium, hampering oxygen exchange, and manifesting clinically as acute respiratory distress syndrome 5. A similar mechanism may occur in the pancreas, where ACE 2 receptor expression and messenger RNA levels of ACE 2 are higher than in the lung 3. Binding of the virus to ACE 2 receptor mediates pancreatic injury. To entry the pancreatic cells, SP needs ACE 2 as key receptor, and the priming of transmembrane protease serine 2 (TMPRSS2) 6. Pancreatic injury is higher in severe CoViD-19 infection compared to milder disease, probably as consequence of the cytokine burst and immune dysregulated response 7.
However, the causal role of CoViD-19 in pancreatitis development has been questioned 8,9.
We described two cases of mild CoViD-19 infection with development of AP with PP treated with endoscopic ultrasound-guided trans-gastric drainage by a lumen apposing stent. In both patients, other causes of AP, such as alcohol, drugs, trauma, ischemia, hypotension, previous thrombotic event, metabolic disorders, autoimmune diseases, toxins, iatrogenic events, or other viral infections, were excluded by an accurate anamnesis and evaluation of the personal health record. Furthermore, no therapies for CoViD-19, potentially responsible for AP, were performed. The detection of CoV-19 in the pseudocyst fluid, lead us to indicate the possible causal relationship between the viral infection and the development of AP. Moreover, the timing of the AP presentation, following the onset of CoViD-19, seems to be another important element.
In conclusion, the association between CoViD-19 infection and AP has been reported in several papers. However, it is crucial to differentiate between a simple coexistence and a causal relationship between these two pathologies. An unequivocal demonstration of this relationship should require a clear exclusion of any other known etiology, including drugs used in CoViD-19 treatment. Considering literature data and direct experience, we believe that a direct coronavirus damage to pancreatic tissue is possible, as demonstrated mainly by the finding of viral RNA in pancreatic pseudocyst fluid and, also, by the temporal association between the two pathologies, in case of lack of other etiologies. Anyway, our knowledge about this topic is still limited and available data are difficult to interpret. Further experiences on wider series and multicenter cohort studies are needed to confirm our findings.
Conflicts of Interest : The Authors have no potential conflicts of interest or financial ties to disclose about this article.
Funding: No grants or other external sources of founding have supported this work.