Serotonin, calcitonin and calcitonin gene-related peptide in acute pancreatitis

Abstract

Objective: The aim of this study was to investigate plasma levels of serotonin, calcitonin and calcitonin gene-related peptide (CGRP) in the course of acute pancreatitis (AP) taking organ failure, etiology and severity into consideration.

Material and methods: Sixty consecutive patients with alcohol- or gallstone-induced AP were included over a 15-month period. Patients were treated according to a standardized algorithm and monitored for organ specific morbidity and mortality. Organ functions and blood samples were assessed on days 0, 1, 2 and 14 after hospital admission. Twenty healthy volunteers, matched for age and gender, comprised the reference group.

Results: Lower levels of serotonin were observed in patients at admission compared to healthy volunteers (p = .021). Serotonin levels increased from day 2 to 14 (p < .001), but with no relation to severity, etiology or organ failure. No difference in calcitonin levels was found in patients at admission compared to healthy volunteers. However, calcitonin levels decreased over time (p < .001) and higher levels were found in patients with respiratory failure (p = .039). No difference was observed in relation to severity or etiology. CGRP levels in patients at admission did not differ from healthy volunteers, nor did CGRP change over time or show any relationship to severity, etiology or organ failure.

Conclusion: Our data suggest serotonin and calcitonin levels to be associated to time-course of AP, and calcitonin levels to organ dysfunction. We hypothesize that serotonin plays a pathogenic role in the compromised pancreatic microcirculation, and calcitonin a role as a biomarker of severity in AP.

Keywords:

• Acute pancreatitis
• calcitonin
• calcitonin gene-related peptide
• coagulation
• microcirculation
• serotonin
• vasoactive

Acknowledgements

This study was supported by grants from the Snedker Master Sophus Jacobsen and Astrid Jacobsen Foundation, the Augustinus Foundation, the Else and Mogens Wedell-Wedellsborg Foundation, and the Danish National Health Research Council (271-05-0770). The authors are indebted to Anders Møller Andersen and Mads Emil Mouritsen for their contributions in conducting the study and preparing the article, respectively.

Disclosure statement

No potential conflict of interest was reported by the authors. This was an academic study with no association to Zealand Pharma with respect to the affiliation of Mark Berner Hansen.

Additional information

Funding

This study was supported by grants from the Snedker Master Sophus Jacobsen and Astrid Jacobsen Foundation, the Augustinus Foundation, the Else and Mogens Wedell-Wedellsborg Foundation, and the Danish National Health Research Council (271-05-0770).