Which Mechanism is Effective on the Hyperamylasaemia After Coronary Artery Bypass Surgery?

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dc.contributor.authorAlgin, Halil Ibrahim
dc.contributor.authorParlar, Ali Ihsan
dc.contributor.authorYildiz, Ismail
dc.contributor.authorAltun, Zekiye Sultan
dc.contributor.authorIslekel, Gul Huray
dc.contributor.authorUyar, Ibrahim
dc.contributor.authorTulukoglu, Engin
dc.date.accessioned2024-04-24T16:14:51Z
dc.date.available2024-04-24T16:14:51Z
dc.date.issued2017
dc.departmentDicle Üniversitesien_US
dc.description.abstractBackground and Aim Acute pancreatitis is one of the less frequently diagnosed lethal abdominal complications of cardiac surgery. The incidence of early postoperative period hyperamylasaemia was reported to be 30-70% of patients who underwent coronary artery bypass grafting (CABG) with cardiopulmonary bypass (CPB). The mechanism of pancreatic enzyme elevation after cardiac surgery is not clear. Our aim was to determine the relationship between ischaemia associated temporary renal dysfunction and elevation of pancreatic enzymes after CABG. Methods Forty-one consecutive patients undergoing CABG under CPB were prospectively studied to determine serum total amylase, phospholipase A2, macroamylase, Cystatin C and urine NAG levels. Results Hyperamylasaemia was observed in 88% of the cases, with a distribution of 6% at the beginning of cardioplegic arrest, 5% at the 20th minute after cardioplegic arrest, 7% at the 40th minute after cardioplegic arrest, 14% when the heart was re-started, 26% at the 6th hour of intensive care and 30% at the 24th hour of intensive care. All of these patients had asymptomatic isolated hyperamylasaemia, and none of them presented with clinical pancreatitis. As indicators of renal damage; Cystatin C and NAG levels were higher compared to baseline values. Conclusion Amylase began to rise during initial extracorporeal circulation and reached a maximum level postoperatively at 6 and 24 hours. Decreased amylase excretion is the main reason for post CABG hyperamylasaemia.en_US
dc.identifier.doi10.1016/j.hlc.2016.09.006
dc.identifier.endpage508en_US
dc.identifier.issn1443-9506
dc.identifier.issn1444-2892
dc.identifier.issue5en_US
dc.identifier.pmid27939744
dc.identifier.scopus2-s2.0-85008230365
dc.identifier.scopusqualityQ2
dc.identifier.startpage504en_US
dc.identifier.urihttps://doi.org/10.1016/j.hlc.2016.09.006
dc.identifier.urihttps://hdl.handle.net/11468/15449
dc.identifier.volume26en_US
dc.identifier.wosWOS:000402465300011
dc.identifier.wosqualityQ3
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherElsevier Science Incen_US
dc.relation.ispartofHeart Lung and Circulation
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAmylaseen_US
dc.subjectCoronary Artery Bypass Graftingen_US
dc.subjectCystatin Cen_US
dc.subjectHyperamylasaemiaen_US
dc.subjectLipaseen_US
dc.subjectRenal Dysfunctionen_US
dc.titleWhich Mechanism is Effective on the Hyperamylasaemia After Coronary Artery Bypass Surgery?en_US
dc.titleWhich Mechanism is Effective on the Hyperamylasaemia After Coronary Artery Bypass Surgery?
dc.typeArticleen_US

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