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

作者信息

Wahlstrøm Kirsten Lykke, Novovic Srdan, Ersbøll Annette Kjær, Hasbak Philip, Jørgensen Lars Nannestad, Berner Hansen Mark

机构信息

a Digestive Disease Center K , Bispebjerg Hospital , University of Copenhagen, Bispebjerg Hospital , Copenhagen , Denmark.

b Department of Gastroenterology and Gastrointestinal Surgery , University of Copenhagen, Hvidovre Hospital , Copenhagen , Denmark.

出版信息

Scand J Gastroenterol. 2017 Oct;52(10):1140-1147. doi: 10.1080/00365521.2017.1346703. Epub 2017 Jul 5.

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.

摘要

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