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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been more than 100 years since Rugero Oddi described the sphincter that bears his name. In that time, investigators have determined its precise anatomy and they have demonstrated its independence from the duodenal muscle wall. Modern manometric techniques have defined the motor activity of the sphincter and motility abnormalities in patients presenting with either recurrent biliary-type pain or idiopathic recurrent pancreatitis. The term Sphincter of Oddi dysfunction is used to describe motility disorders of the sphincter. Clinical studies have shown that in patients with manometrically determined stenosis, division of the sphincter is associated with cure of the symptoms in more than 70%. For patients with biliary-type pain, division of the bile duct sphincter is all that is required, whereas in patients with idiopathic recurrent pancreatitis, division of the septum between the bile duct and the pancreatic duct is mandatory.
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PMID:Sphincter of Oddi. 868 45

Sphincter of Oddi dysfunction has been reported as a cause of acute idiopathic recurrent pancreatitis (IRP). Octreotide, a long-acting somatostatin analogue, is an antisecretory drug used in the treatment and prevention of acute pancreatitis. Its action on sphincter of Oddi motility is controversial and no data are available for IRP patients. The aim of this study was to assess sphincter of Oddi motor response to acute administration of octreotide in patients with past attacks of acute pancreatitis without identification of any evident aetiological factor. Six patients (four male, two female; mean age +/-SD, 38.8+/-9 years) suffering from acute pancreatitis for at least 3 months before the examination were submitted to sphincter of Oddi manometry. After a basal recording lasting at least 2 min, octreotide, 0.05 mg i.v., was administered and the recording repeated. Intraduodenal pressure was taken as the zero reference and the basal sphincter of Oddi pressure and amplitude and frequency of phasic contractions were calculated before and after octreotide administration. No significant pre- vs post-octreotide differences were observed in basal pressure (41.9+/-24 vs 47.5+/-33 mm Hg, respectively) or in amplitude of phasic contractions (164.6+/-33 vs 170.8+/-18 mm Hg). With a latency of about 1 min, octreotide administration caused a high-frequency phasic activity in all cases (mean frequency, 5.5+/-2.2 contractions/min before and 9.8+/-2 after octreotide; P < 0.04). After the procedure acute pancreatitis (prolonged abdominal pain and serum amylase levels more than three-fold the normal values) developed in five patients. In conclusion, our data suggest that acute administration of octreotide may induce tachyoddia and thus a rise in sphincter of Oddi pressure, with possible impairment of biliary-pancreatic outflow.
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PMID:Effect of octreotide on sphincter of Oddi motility in patients with acute recurrent pancreatitis: a manometric study. 901 48

Disordered motility of the biliary tract may be associated with the aetiology of common biliary tract conditions, such as gallstones. In this instance, treatment of the gallstone disease alleviates symptoms in the majority of patients. However, in up to 10% of patients, biliary motility disorders may present in the absence of gallstones or in patients after cholecystectomy. Gallbladder dyskinesia results in biliary-type pain. This abnormality may be objectively identified using the radionuclide gallbladder ejection fraction. The majority of patients with an abnormal test are improved or cured following cholecystectomy. Sphincter of Oddi dysfunction presents with either recurrent biliary-type pain or recurrent pancreatitis. Manometry of the sphincter of Oddi objectively identifies patients with manometric stenosis. The majority of these patients are improved or cured following division of the sphincter of Oddi.
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PMID:Biliary motility disorders. 951 7

Biliary pain is commonly reported in household surveys with the presumed cause being gallstones. When gallstones are absent or other abnormalities as a potential cause of similar pain do not exist, a different approach is necessary. Although trans-abdominal ultrasound can detect stones down to 3-5 mm, the advent of endoscopic ultrasound provides an even better definition for microlithiasis of < 3 mm. Duodenal aspiration of bile can further detect cholesterol microlithiasis or bilirubin granules, another potential source of biliary-type pain and perhaps even pancreatitis. Only in this way can acalculous gallbladder disease be clearly defined. The percentage of cholecystokinin-stimulated gallbladder emptying has been reputed to be the most sensitive diagnostic test for 'biliary dyskinesia', but abnormality of gallbladder emptying can be due to a smooth muscle defect of the gallbladder itself or heightened tone in the sphincter of Oddi. The value of surgical intervention has not been clearly established. The advent of laparoscopic cholecystectomy, however, has increased the number of patients with acalculous biliary disease who undergo surgery. Surgery is best done using impaired gallbladder emptying as the criterion for operation with improved outcome. Often, following cholecystectomy, biliary pain does not resolve the so-called 'post cholecystectomy syndrome'. Absence of the gallbladder as a pressure reservoir leaves the sphincter of Oddi as the prime determinant of bile duct pressure. Sphincter of Oddi dysfunction also exists in patients with an intact biliary tract and may become evident following cholecystectomy. Biliary manometry has clarified who might benefit from sphincterotomy. Choledochoscintigraphy is a non-invasive preliminary test. Advent of visceral hypersensitivity and better definition of this entity has shown, that in some of these patients with type III sphincter of Oddi, dysfunction appears to reside in duodenal hyperalgesia. It is clear that improved criteria are required to perform gallbladder emptying and better techniques to detect visceral hypersensitivity. Nonetheless, functional biliary pain in the absence of gallstone disease is a definite entity and a challenge for clinicians.
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PMID:Acalculous biliary pain: new concepts for an old entity. 1297 5

Sphincter of Oddi dysfunction (SOD) is a benign noncalculous obstruction of bile or pancreatic drainage at the level of the sphincter of Oddi. The disorder is clinically associated with either biliary pain or idiopathic pancreatitis, depending on the portion of the sphincter affected. Patients with suspected SOD are subdivided into three categories: these are type I, II, and III, depending on associated clinical evidence for the diagnosis. Multiple noninvasive tests have been utilized to aid in the diagnosis but have been complicated by poor sensitivity and specificity. Sphincter of Oddi manometry is the gold standard for confirming the diagnosis, although questions remain about its sensitivity and specificity. Sphincterotomy of the affected portion of the sphincter is the treatment of choice and has been shown effective for palliation of symptoms in two sham-controlled studies of patients with suspected type II biliary SOD.
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PMID:Sphincter of Oddi Dysfunction. 1576 32

Sphincter of Oddi dysfunction (SOD) is a clinical entity caused by a primary motility alteration of either the biliary or the pancreatic sphincter. SOD is a rare condition that has been scarcely reported in children. Most of the reported literature has been in children with idiopathic recurrent pancreatitis. These children are treated endoscopically by dual sphincterotomy of the pancreatic and common duct sphincters. However, the safety and efficacy of sphincter of Oddi manometry and sphincterotomy in the pediatric population await further study.
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PMID:Sphincter of Oddi dysfunction in children. 1653 81

Sphincter of Oddi dysfunction (SOD) is a syndrome of chronic biliary pain or recurrent pancreatitis due to functional obstruction of pancreaticobiliary flow at the level of the sphincter of Oddi. The Milwaukee classification stratifies patients according to their clinical picture based on elevated liver enzymes, dilated common bile duct and presence of abdominal pain. Type I patients have pain as well as abnormal liver enzymes and a dilated common bile duct. Type II SOD consists of pain and only one objective finding, and Type III consists of biliary pain only. This classification is useful to guide diagnosis and management of sphincter of Oddi dysfunction. The current gold standard for diagnosis is manometry to detect elevated sphincter pressure, which correlates with outcome to sphincterotomy. However, manometry is not widely available and is an invasive procedure with a risk of pancreatitis. Non-invasive testing methods, including fatty meal ultrasonography and scintigraphy, have shown limited correlation with manometric findings but may be useful in predicting outcome to sphincterotomy. Endoscopic injection of botulinum toxin appears to predict subsequent outcome to sphincterotomy, and could be useful in selection of patients for therapy, especially in the setting where manometry is unavailable.
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PMID:Sphincter of Oddi dysfunction: managing the patient with chronic biliary pain. 1680 61

Sphincter of Oddi dysfunction and pancreas divisum are very distinct anatomic abnormalities, yet are diagnosed in similar clinical situations. While both entities are uncommon, they are most often discovered during the evaluation of postcholecystectomy syndrome, recurrent idiopathic pancreatitis, and biliary or pancreatic pain when first line studies are normal. Treatment consists of surgical sphincteroplasty or endoscopic sphincterotomy for both diagnoses, which result in reliable relief of symptoms for most sphincter of Oddi dysfunction patients but less predictable response in pancreas divisum.
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PMID:Diagnosis and management of sphincter of Oddi dysfunction and pancreas divisum. 1805 39

Sphincter of Oddi dysfunction (SOD) is a term used to describe a group of heterogenous pain syndromes caused by abnormalities in sphincter contractility. Biliary and pancreatic SOD are each sub-classified as type I, II or III, according to the Milwaukee classification. SOD appears to carry an increased risk of acute pancreatitis as well as rates of post ERCP pancreatitis of over 30%. Various mechanisms have been postulated but the exact role of SOD in the pathophysiology of acute pancreatitis is unknown. There is also an association between SOD and chronic pancreatitis but it is still unclear if this is a cause or effect relationship. Management of SOD is aimed at sphincter ablation, usually by endoscopic sphincterotomy (ES). Patients with type I SOD will benefit from ES in 55%-95% of cases. Sphincter of Oddi manometry is not necessary before ES in type I SOD. For patients with types II and III the benefit of ES is lower. These patients should be more thoroughly evaluated before performing ES. Some researchers have found that manometry and ablation of both the biliary and pancreatic sphincters is required to adequately assess and treat SOD. In pancreatic SOD up to 88% of patients will benefit from sphincterotomy. Therefore, there have been calls from some quarters for the current classification system to be scrapped in favour of an overall system encompassing both biliary and pancreatic types. Future work should be aimed at understanding the mechanisms underlying the relationship between SOD and pancreatitis and identifying patient factors that will help predict benefit from endoscopic therapy.
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PMID:Sphincter of Oddi dysfunction and pancreatitis. 1808 Dec 21

Although there are numerous causes of acute panc-reatitis, an etiology cannot always be found. Two potential etiologies, microlithiasis and sphincter of Oddi dysfunction, are discussed in this review. Gallbladder microlithiasis, missed on transcutaneous ultrasound, is reported as the cause of idiopathic acute pancreatitis in a wide frequency range of 6%-80%. The best diagnostic technique for gallbladder microlithiasis is endoscopic ultrasound although biliary crystal analysis and empiric cholecystectomy remain as reasonable options. In contrast, in patients who are post-cholecystectomy, bile duct microlithiasis does not appear to have a role in the pathogenesis of acute pancreatitis. Sphincter of Oddi dysfunction is present in 30%-65% of patients with idiopathic acute recurrent pancreatitis in whom other diagnoses have been excluded. It is unclear if this sphincter dysfunction was the original etiology of the first episode of pancreatitis although it appears to have a causative role in recurring episodes since sphincter ablation decreases the frequency of recurrent attacks. Unfortunately, this conclusion is primarily based on small retrospective case series; larger prospective studies of the outcome of pancreatic sphincterotomy for SOD-associated acute pancreatitis are sorely needed. Another problem with this diagnosis and its treatment is the concern over potential procedure related complications from endoscopic retrograde cholangiopancreatography (ERCP), manometry and pancreatic sphincterotomy. For these reasons, patients should have recurrent acute pancreatitis, not a single episode, and have a careful informed consent before assessment of the sphincter of Oddi is undertaken.
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PMID:Sphincter of Oddi dysfunction and bile duct microlithiasis in acute idiopathic pancreatitis. 1828 82


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