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.