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      Prior cholecystectomy predisposes to acute pancreatitis in codeine-prescribed patients

      case-report

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          Abstract

          In this paper, we report a case of drug-induced pancreatitis just after taking a pain pill including a low-dose combination of acetaminophen and codeine. Codeine-induced pancreatitis has been rarely reported, however, well-established. The proposed mechanism for codeine-induced pancreatitis is by increasing Oddi sphincter pressure. However, the clinically important point is that the codeine-induced pancreatitis is seen almost only in the cholecystectomized patients due to lacking of its reservoir capacity. Codeine is commonly used alone or in combination in pain medicine. Therefore, it is fairly important to question whether a patient underwent cholecystectomy when a physician decides to prescribe codeine-included preparations.

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          Effects of morphine on the human sphincter of Oddi.

          W Hogan, J. Toouli, Alister W Dodds … (1988)
          The effects of morphine on intraluminal pressures recorded from the sphincter of Oddi (SO) at endoscopic retrograde cholangiopancreatography in 19 patients who were without evidence of biliary or pancreatic disease were studied. Morphine was given in four successive doses of 2.5, 2.5, 5, and 10 micrograms/kg iv at five minute intervals. Morphine in subanalgesic doses increased the frequency of SO phasic pressure waves to a maximum of 10-12/min, caused the phasic waves to occur simultaneously along the sphincter segment, increased phasic wave amplitude from 72 (26) (SE) to 136 (31) mmHg, and increased SO basal pressure from 10 (1) to 29 (9) mmHg (p less than 0.05). The effects of morphine on the SO are mediated by more than one opioid receptor type, as naloxone competitively antagonised the increase in phasic wave frequency induced by morphine, but did not affect the increase in SO basal pressure elicited by morphine. When given after naloxone, morphine decreased phasic wave amplitude, an inhibitory effect that is normally masked by morphine's dominant naloxone sensitive excitatory effect. Mu receptors do not appear to be involved in control of spontaneous SO motor function, as naloxone alone did not affect SO motor activity. The excitatory effects of morphine on the SO are not mediated by cholinergic nerves, as they were not blocked by atropine. Cholinergic nerves, however, may have a role in regulating spontaneous SO motor function because atropine alone depressed phasic wave activity and basal pressure. Although morphine does cause 'spasm' of the human SO, its effects are more complex than is commonly believed.
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            A new source of drug-induced acute pancreatitis: codeine.

            P Hastier, N Demuth, F Caroli … (2000)
            A variety of drugs have been reported to cause acute pancreatitis during the past 40 years. We report the first series of four cases of acute pancreatitis related to codeine ingestion. Four patients (three female, mean age 50.2 yr) presented with clinical, biochemical, and radiological evidence of acute pancreatitis. All four had ingested a therapeutic dose of codeine 1-3 h before the onset of abdominal symptoms. Unintentional rechallenge occurred in three cases and was followed by recurrence of acute pancreatitis in all three. All patients made a full recovery. All four patients had had a previous cholecystectomy. The likely underlying pathophysiological mechanism is codeine-induced spasm of the sphincter of Oddi combined with sphincter of Oddi dysfunction related to a previous cholecystectomy. Codeine ingestion leads to acute pancreatitis in some individuals. Previous cholecystectomy seems to predispose to codeine-induced pancreatitis.
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              Influence of cholecystectomy on sphincter of Oddi motility.

              W Luman, R Heading, S. Williams … (1997)
              Gall bladder and sphincter of Oddi (SO) function are coordinated by hormonal and neuronal mechanisms. Nerve fibres pass between the gall bladder and the SO via the cystic duct. It is therefore possible that cholecystectomy may alter SO motility. To investigate the effect of cholecystectomy on SO function. SO manometry was performed in five women (median age 52 years), a few days before and six months after laparoscopic cholecystectomy which was undertaken for uncomplicated cholelithiasis. Basal and post-cholecystokinin (CCK) SO motility were measured. All patients were symptom free after laparoscopic cholecystectomy. Prior to surgery common bile duct pressure, and tonic and phasic SO motility were normal and phasic contractions were inhibited by intravenous CCK (1 Ivy Dog Unit/kg). Six months later, common bile duct pressure and baseline tonic and phasic activity were unchanged but CCK failed to suppress phasic activity. Cholecystectomy, at least in the short term, suppresses the normal inhibitory effect of pharmacological doses of CCK on the SO. The mechanism of this effect is unknown but it could be due to SO denervation.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Crit Illn Inj Sci
                Journal ID (iso-abbrev): Int J Crit Illn Inj Sci
                Journal ID (publisher-id): IJCIIS
                Title: International Journal of Critical Illness and Injury Science
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 2229-5151
                ISSN (Electronic): 2231-5004
                Publication date (Print): Apr-Jun 2015
                Volume: 5
                Issue: 2
                Pages: 114-115
                Affiliations
                [1]Department of Cardiology, Sanko University School of Medicine, Gaziantep, Turkey
                [1 ]Department of Internal Medicine, Gaziantep University School of Medicine, Gaziantep, Turkey
                [2 ]Department of Internal Medicine, Necip Fazil Metropolitan Hospital, Kahramanmaras, Turkey
                [3 ]Department of Internal Medicine, Harran University School of Medicine, Sanliurfa, Turkey
                Author notes
                Address for correspondence: Dr. Hakan Buyukhatipoglu, Gaziantep University, School of Medicine Department of Internal Medicine, Division of Medical Oncology, Kilis Yolu Uzeri - 27310, Gaziantep, Turkey. E-mail: buyukhatipoglu@ 123456gmail.com
                Article
                Publisher ID: IJCIIS-5-114
                DOI: 10.4103/2229-5151.158416
                PMC ID: 4477388
                SO-VID: f38f4921-8ded-4023-b9da-5f5252dc0f05
                Copyright © Copyright: © International Journal of Critical Illness and Injury Science
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Categories
                Subject: Case Report

                ScienceOpen disciplines: Emergency medicine & Trauma
                Keywords: cholecystectomy,codeine,pancreatitis
                Data availability:
                ScienceOpen disciplines: Emergency medicine & Trauma
                Keywords: cholecystectomy, codeine, pancreatitis

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