The underestimated role of opiates in patients with suspected sphincter of Oddi dysfunction after cholecystectomy

Druart-Blazy, Anne; Pariente, Alexandre; Berthélemy, Philippe; Arotçarena, Ramuntxo

doi:10.1016/s0399-8320(05)82204-3

Cited by 13 publications

(6 citation statements)

References 9 publications

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“…Thus, morphine increases the amplitude and frequency of the phasic wave ( via mu opioid receptors) as well as basal pressure ( via non-mu opioid receptors) of the SO ( 74 , 75 ). These effects have also been demonstrated with fentanyl ( 76 ) and codeine ( 77 ). Morphine shows limited effect on the SO in patients prior to cholecystectomy, whereas it caused a notable rise in basal sphincter pressure postoperatively ( 59 ).…”

Section: Medications and The Risk Of Sodmentioning

confidence: 79%

Sphincter of Oddi Function and Risk Factors for Dysfunction

Afghani

Covington³

et al. 2017

Front. Nutr.

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The sphincter of Oddi (SO) is a smooth muscle valve regulating the flow of biliary and pancreatic secretions into the duodenum, initially described in 1887 by the Italian anatomist, Ruggero Oddi. SO dysfunction (SOD) is a broad term referring to numerous biliary, pancreatic, and hepatic disorders resulting from spasms, strictures, and relaxation of this valve at inappropriate times. This review brings attention to various factors that may increase the risk of SOD, including but not limited to: cholecystectomy, opiates, and alcohol. Lack of proper recognition and treatment of SOD may be associated with clinical events, including pancreatitis and biliary symptoms with hepatic enzyme elevation. Pharmacologic and non-pharmacologic approaches are discussed to help recognize, prevent, and treat SOD. Future studies are needed to assess the treatment benefit of agents such as calcium-channel blockers, glyceryl trinitrate, or tricyclic antidepressants in patients with SOD.

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Section: Medications and The Risk Of Sodmentioning

confidence: 79%

Sphincter of Oddi Function and Risk Factors for Dysfunction

Afghani

Covington³

et al. 2017

Front. Nutr.

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“…• A recent study demonstrated that opiateintake is a frequent cause of suspicion of sphincter of Oddi dysfunction [6] after cholecystectomy, especially in young patients with a narrow common bile duct [7].…”

Section: Discussionmentioning

confidence: 99%

Loperamide-Induced Pancreatitis: Report of Three Cases

Fantin

Peserico

Barbuscio

2018

IGH

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Background: Only 0.1-2% of acute pancreatitis seems to be drug-induced, being this etiology probably underestimated and often classified as idiopathic. Loperamide is an opiate with peripheral action, used in the treatment of diarrhea. Since 2012 it belongs to the FDA list of drugs potentially able to cause acute pancreatitis, because of its capacity of modulating the secretion from the exocrine pancreas and of causing sphincter of Oddi dysfunction.Case presentation: We report the cases of three women, admitted to our hospital for acute pancreatitis. In their medical history two of them referred remote cholecystectomy. They all reported recent loperamide intake, given to acute diarrhea, denying alcohol consumption, smoking or family history for pancreatic disease. During the hospitalization laboratory tests showed increase of pancreatic enzyme and liver function alteration, with a rapid clinical improvement after loperamide suspension. Pancreatic Magnetic Resonance Imaging (MRI), including MR cholangiopancreatography, was performed in all the cases, showing a well-defined pancreatic gland without any sign of acute inflammation and excluding common bile duct lithiasis. Given the absence of common risk factors and the temporal correlation between drug intake and occurrence of symptoms, we considered loperamide responsible of these three cases of acute pancreatitis.Conclusion: In patients with acute pancreatitis, referring recent loperamide intake, in the absence of any other causes, iatrogenic damage must be considered as a possible etiologic factor.

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“…On the basis of their chemical coding, SO ganglia are largely made up of two popu- lations of neurons, one excitatory and the other inhibitory. The excitatory neurons are cholinergic and co-express tachykinin and opiate peptides and the inhibitory neurons are ChAT-negative and express nitric oxide synthase [24][25][26] . Nagasaki et al [27,28] reported that trimebutine inhibits carbachol-induced Ca 2+ release by acting at some point during the coupling of muscarinic receptors through a G-protein to phospholipase C and thus reducing the accumulation of IP3.…”

Section: Discussionmentioning

confidence: 99%