Effect of somatostatin on immune inflammatory response in patients with severe acute pancreatitis

Somatostatin regulates immune inflammatory response via apoptosis and adhesion of leukocytes in many diseases. This article reported a study that aimed to observe the mechanism and effect of somatostatin on the immune inflammatory response through apoptosis and adhesion of leukocytes in severe acute pancreatitis.

Thirty-eight patients with severe acute pancreatitis, that fulfilled the guidelines for the treatment of severe acute pancreatitis of China and Balthazar computed tomography severity index (>or=5) were enrolled consecutively. Nineteen of these patients received our routine treatment and 19 received additional somatostatin. In all patients the expressions of CD4, CD8, CD95/CD95 ligand and CD18/CD62 ligand on leukocytes were determined by flow cytometry, both upon admission and on the fourth day. Thirty healthy volunteers constituted the normal healthy group.

In the treatment group, CD4, CD4:CD8 ratio and CD62 ligand on leukocytes increased from 11.4+/-8.2, 0.47+/-0.10 and 25.5+/-9.2 to 22.1+/-9.7, 0.68+/-0.11 and 36.2+/-11.7 (P<0.05) respectively, while CD95 ligand on both lymphocyte and polymorphonuclear cells increased from 0.65+/-0.21 and 0.76+/-0.29 to 1.18+/-0.32 and 1.58+/-0.43 after treatment with somatostatin (P<0.05). Furthermore, lactate dehydrogenase, aspartate aminotransferase, amylase, C reactive protein and acute physiology and chronic healthy evaluation (APACHE II) score in the treatment group reduced faster than those in the control group (P<0.05), though there was no difference in mortality (15.7% vs 5.3%) between the two patient groups (P>0.05).

Somatostatin can modulate the immune inflammatory response and the severity of severe acute pancreatitis through apoptosis and adhesion of leukocytes, but this modulatory effect by itself is not strong enough to improve the final.