Early immune response in post endoscopic retrograde cholangiopancreatography pancreatitis as a model for acute pancreatitis

Table 1 Differences in clinical presentation of post-endoscopic pancreatitis vs acute pancreatitis

	Post-endoscopic pancreatitis		Acute pancreatitis	Conclusion
Fung et al[11] endoscopic retrograde cholangiopancreatography -induced acute necrotising pancreatitis vs acute necrotising pancreatitis induced by other causes.	Higher APACHE II scores on admission		Lower APACHE II scores on admission	acute necrotising pancreatitis is more severe when induced by endoscopic retrograde cholangiopancreatography
	More extensive pancreatic necrosis		Less extensive pancreatic necrosis
	Higher rate of infected necrosis		Lower rate of infected necrosis
Testoni et al[3] endoscopic retrograde cholangiopancreatography induced acute pancreatitis vs non endoscopic retrograde cholangiopancreatography induced acute pancreatitis	No statistical difference: (1) the severity of the pancreatitis; (2) the mortality rate (double in severe post-endoscopic pancreatitis); (3) hospitalisation
	In the mild form of acute pancreatitis, serum amylase fell by 50% in 38.9 h. Peak serum amylase halved within 48 h in 92% of patients	In the mild form of acute pancreatitis, serum amylase fell by 50% in 46.4 h. Peak serum amylase halved within 48 h in 73.6% of patients	There was a statistical difference (P < 0.001). Mild form of post-endoscopic pancreatitis, a sort of pancreatic reaction, instead of a true episode of acute pancreatitis
Abid et al[12] mild form: Endoscopic retrograde cholangiopancreatography induced acute pancreatitis vs non endoscopic retrograde cholangiopancreatography induced acute pancreatitis	Shorter duration of pain; Shorter time of intravenous hydration; Shorter time to the resumption of an oral diet; Shorter hospital stay. (P < 0.001).		Endoscopic retrograde cholangiopancreatography-induced acute pancreatitis mild attacks run a significantly shorter and milder course than non- endoscopic retrograde cholangiopancreatography related mild attacks

Table 2 Role of immune components in predicting disease severity

	Acute pancreatitis	Post-endoscopic pancreatitis
Monocytes and macrophages	(1) Expression of HLA-DR on monocytes gives a good insight into monocyte function; (2) Decreased monocyte HLA-DR expression may serve as an indicator of immunosuppression[13]; and (3) Decreased monocyte HLA- DR expression predicts the development of organ dysfunction in severe acute pancreatitis[13].
T cells	(1) CD4+ lymphocytes are reported to have a direct cytotoxic effect on acinar cells[14]; (2) Depletion of CD4+ lymphocytes reduces the severity of acute pancreatitis[15]; and (3) Reduction in the number of cytotoxic T lymphocytes (CD3+CD8+) in severe form of acute pancreatitis[16].
Natural Killer cells	(1) Depletion of the natural killer cell population on the first day of severe acute pancreatitis[16]; and (2) No significant change in natural killer cell number in mild acute pancreatitis[16].
IL-10	Predictive marker of organ failure in severe acute pancreatitis[17].	Conflicting results about reducing the incidence of post endoscopic retrograde cholangiopancreatography acute pancreatitis after IL-10 usage[18,19].
IL- 6	Independent factor for predicting severity in acute non- endoscopic retrograde cholangiopancreatography pancreatitis[7].	(1) Peak value 24-48 h after clinical expression of post endoscopic pancreatitis; and (2) In necrotising post endoscopic pancreatitis, the peak levels of IL-6 occur after 24 h[6].
IL-1β	(1) Required for full pancreatic and distal organ injury and inflammation[20]; and (2) Values peak after 24 h and are larger in patients with severe acute pancreatitis compared to mild acute pancreatitis, although a strong correlation with acute pancreatitis severity in humans wasn’t found[21].