Endoscopy versus radiology in post-procedural monitoring after peroral endoscopic myotomy (POEM).

BACKGROUND: The newly developed technique of peroral endoscopic myotomy (POEM) has been shown to be effective in several short- and mid-term studies. Limited information is available about the adequacy of immediate post-POEM monitoring tests. METHODS: POEM was performed under general anesthesia in 228 patients (59.6% male, mean age 45.6 ± 15.5 years). Post-procedural checks comprised clinical and laboratory examination, and, during post-procedure days 1-5, endoscopy and-in the first 114 cases-radiologic examination using water-soluble contrast (1st group); the remaining patients underwent post-procedure controls without radiology (2nd group). Main outcome was value of endoscopic compared to radiologic control for recognition of early adverse events. RESULTS: In the first group, routine fluoroscopic contrast swallow suggested minor leakages at the mucosal entry site in two cases which was confirmed endoscopically in only one. Endoscopy revealed two minor entry site leakages and, in six additional cases, dislocated clips without leakage (overall 5.3%). All eight patients underwent reclipping and healed without clinical sequelae. In the 2nd group, endoscopy showed 5 clip dislocations (all reclipped) and one ischemic cardiac perforation in a patient with clinical deterioration on post-POEM day 1 who had to undergo surgery after confirmation of leakage by CT. CONCLUSIONS: Radiologic monitoring (contrast swallow) after POEM is not useful and can be omitted. Even routine endoscopic monitoring for detection and closure of minor defects of the mucosal entry site yields limited information with regards to final outcome; major complications are very rare and probably associated with clinical deterioration. Clinical Trials Gov Registration number of the main study: NCT01405417.

CCK1 and CCK2 receptors are expressed on pancreatic stellate cells and induce collagen production.

The gastrointestinal hormone cholecystokinin (CCK) can induce acute pancreatitis in rodents through its action on acinar cells. Treatment with CCK, in combination with other agents, represents the most commonly used model to induce experimental chronic pancreatitis. Pancreatic stellate cells (PSC) are responsible for pancreatic fibrosis and therefore play a predominant role in the genesis of chronic pancreatitis. However, it is not known whether PSC express CCK receptors. Using real time PCR techniques, we demonstrate that CCK1 and CCK2 receptors are expressed on rat PSC. Interestingly both CCK and gastrin significantly induced type I collagen synthesis. Moreover, both inhibit proliferation. These effects are comparable with TGF-ß-stimulated PSC. Furthermore, the natural agonists CCK and gastrin induce activation of pro-fibrogenic pathways Akt, ERK, and Src. Using specific CCK1 and CCK2 receptor (CCK2R) inhibitors, we found that Akt activation is mainly mediated by CCK2R. Akt activation by CCK and gastrin could be inhibited by the PI3K inhibitor wortmannin. Activation of ERK and the downstream target Elk-1 could be inhibited by the MEK inhibitor U0126. These data suggest that CCK and gastrin have direct activating effects on PSC, are able to induce collagen synthesis in these cells, and therefore appear to be important regulators of pancreatic fibrogenesis. Furthermore, similar to TGF-ß, both CCK and gastrin inhibit proliferation in PSC.