Bile duct crystals do not contribute to sphincter of Oddi dysfunction

BACKGROUND: Microlithiasis has been proposed as a cause of both occult gallbladder disease and of idiopathic pancreatitis. Theoretically, microlithiasis could also cause postcholecystectomy pain by causing temporary biliary obstruction and may be more common in patients with sphincter of Oddi dysfunction. The frequency of crystals in bile duct aspirates was assessed from patients with symptoms after cholecystectomy with and without elevated baseline sphincter of Oddi pressures. METHODS: A prospective analysis was performed on all patients with recurrent biliary pain after cholecystectomy who presented for ERCP and manometry between January 1998 and June 2000. All patients had aspirates obtained from the common bile duct for crystal analysis by using the aspirating port of the manometry catheter before the injection of contrast. Four to 20 mL of bile was examined by microscopy for both cholesterol and bilirubinate crystals. RESULTS: Sixty patients (83% women, mean age 44 years) were studied. Thirty-five had normal baseline biliary sphincter pressures and 25 elevated biliary baseline sphincter pressures (>40 mm Hg). Two patients in the normal pressure group and 1 in the elevated pressure group had cholesterol crystals present in their aspirate. No patient had bilirubinate crystals present. A 5% frequency of microlithiasis was identified overall. CONCLUSIONS: Bile duct crystals occur infrequently in patients with symptoms after cholecystectomy and are found in patients with normal and abnormal biliary sphincter manometry. This study suggests that the presence of bile duct crystals, or microlithiasis, does not play a role in sphincter of Oddi dysfunction.     

Frequency of biliary crystals in patients with suspected sphincter of Oddi dysfunction

BACKGROUND: The passage of gallstones (macro- or microlithiasis) is theorized to play a role in inducing sphincter of Oddi dysfunction. This study examined the frequency at which biliary crystals are found in patients with suspected type II and type III sphincter of Oddi dysfunction. METHODS: A total of 85 patients (66 women, 19 men; mean age 38 years) with unexplained abdominal pain of suspected pancreatobiliary origin and no prior episode of pancreatitis underwent ERCP with sphincter of Oddi manometry and bile collection for crystal analysis. Eighty-one patients had a gallbladder in situ. No patient had evidence of stones or sludge on prior abdominal imaging. Sphincter of Oddi manometry was performed in standard retrograde fashion by using an aspirating catheter. Patients were classified by sphincter of Oddi dysfunction type by using a modified Hogan-Geenen classification system. Patients with type I sphincter of Oddi dysfunction were excluded. Bile was collected directly from the gallbladder (n=23) or common bile duct (n=62) after an infusion of 3.5 microg of cholecystokinin and was examined by light and polarizing microscopy for cholesterol crystals or calcium bilirubinate granules. RESULTS: The proportion of patients with crystals was 3.5% (3/85). Thirty-five patients (41%) had elevated biliary and/or pancreatic sphincter pressure (type II, 16; type III, 19), of whom one (3%) had cholesterol crystals. Fifty patients had normal sphincter pressure, of whom two (4%) had cholesterol crystals (p=0.6). All 3 patients with cholesterol crystals had a gallbladder in situ. Calcium bilirubinate granules were not found in any patient. CONCLUSIONS: Microlithiasis appears to be rare in patients suspected to have type II or type III sphincter of Oddi dysfunction. Evaluation of bile for crystals appears unproductive in this group of patients.     

ERCP, biliary crystal analysis, and sphincter of Oddi manometry in idiopathic recurrent pancreatitis

BACKGROUND: This study investigated the role of ERCP, analysis of bile for microcrystals, and sphincter of Oddi manometry in idiopathic recurrent pancreatitis. METHODS: One hundred twenty-six patients met criteria for idiopathic recurrent pancreatitis. Patients with a normal ERCP underwent sphincter of Oddi manometry and analysis of bile. Bile was also collected in patients with papillary stenosis (defined as ductal dilation with delayed drainage of contrast, sphincter basal pressures greater than 40 mm Hg, and positive analysis for cholesterol and/or calcium bilirubinate crystals). RESULTS: ERCP alone identified a cause of idiopathic recurrent pancreatitis in 47 (37%) patients: papillary stenosis in 26 (21%), pancreas divisum in 9 (7%), and choledocholithiasis in 6 (5%). Among patients with a gallbladder, microcrystals were found in 27 (50%) and sphincter dysfunction in 17 (31%). Among patients who have undergone cholecystectomy, sphincter dysfunction was identified in 24 (47%). Minor papilla sphincterotomy was performed in 8 patients (89%) with pancreas divisum. Biliary sphincterotomy was performed in 85 patients and included all patients with choledocholithiasis, choledochocele, microcrystals, papillary stenosis, and sphincter dysfunction except 2 patients with microcrystals who underwent cholecystectomy. Additionally, pancreatic sphincterotomy was performed in 32 (78%) patients with pancreatic sphincter hypertension and in 6 (23%) of 26 patients with papillary stenosis with dilated pancreatic ducts. Thus, among the 126 patients, 93 of the 100 patients with a detected abnormality underwent endoscopic sphincterotomy. Response rates varied from 67% to 100% during follow-up (mean 29.6 months, range 18 to 33 months). CONCLUSION: ERCP techniques including minor papilla cannulation, analysis of bile for microcrystals, and sphincter of Oddi manometry identified a cause of idiopathic recurrent pancreatitis in 79% (endoscopically treatable in 75%) of patients, with or without prior cholecystectomy.     

Idiopathic recurrent pancreatitis: long-term results after ERCP, endoscopic sphincterotomy, or ursodeoxycholic acid treatment

OBJECTIVE: In about 30% of cases, the etiology of acute recurrent pancreatitis remains unexplained, and the term "idiopathic" is currently used to define such disease. We aimed to evaluate the long-term outcome of patients with idiopathic recurrent pancreatitis who underwent endoscopic cholangiopancreatography (ERCP) followed by either endoscopic biliary (and seldom pancreatic) sphincterotomy or ursodeoxycholic acid (UDCA) treatment, in a prospective follow-up study. METHODS: A total of 40 consecutive patients with intact gallbladder entered the study protocol after a 24-month observation period during which at least two episodes of pancreatitis occurred. All patients underwent diagnostic ERCP, followed by biliary or minor papilla sphincterotomy in cases of documented or suspected bile duct microlithiasis and sludge, type 2 sphincter of Oddi dysfunction, or pancreas divisum with dilated dorsal duct. Patients with no definite anatomical or functional abnormalities received long-term treatment with UDCA. After biliary sphincterotomy, patients with further episodes of pancreatitis underwent main pancreatic duct stenting followed by pancreatic sphincterotomy if the stent had proved to be effective. RESULTS: ERCP found an underlying cause of pancreatitis in 70% of cases. Patients were followed-up for a period ranging from 27 to 73 months. Effective therapeutic ERCP or UDCA oral treatment proved that occult bile stone disease and type 2 or 3 sphincter of Oddi dysfunction (biliary or pancreatic segment) had been etiological factors in 35 of the 40 cases (87.5%) After therapeutic ERCP or UDCA, only three patients still continued to have episodes of pancreatitis. CONCLUSIONS: Diagnostic and therapeutic ERCP and UDCA were effective in 92.5% of our cases, over a long follow-up, indicating that the term "idiopathic" was justified only in a few patients with acute recurrent pancreatitis.     

Sphincter of Oddi dysfunction and bile duct microlithiasis in acute idiopathic pancreatitis

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.     

Biliary microcrystals in idiopathic acute pancreatitis: clue for occult underlying biliary etiology

The main causes of pancreatic inflammation worldwide are biliary lithiasis and alcoholism. However, 10 to 30% of patients have been considered to have "idiopathic" acute pancreatitis. Recently, some studies showed that a significant rate of the so called idiopathic pancreatitis are caused by microlithiasis and/or biliary sludge, identified by the presence of cholesterol monohidrate and/or calcium bilirubinate microcrystals in the biliary sediment. In the present study, the analysis of microcrystals from bile obtained during endoscopic retrograde cholangiopancreatography was done in patients with pancreatitis (idiopathic, biliary or alcoholic--20 in each group). Patients with idiopathic pancreatitis and microcrystals in the bile underwent cholecystectomy whenever possible. Those who refused or were inapt to surgery underwent endoscopic sphincterotomy or received continuous therapy with ursodeoxycholic acid. Patients with idiopathic pancreatitis without biliary crystals did not receive any specific treatment. The prevalence of biliary microcrystals in patients with idiopathic pancreatitis (75%) and biliary pancreatitis (90%) was significantly higher than in those with alcoholic pancreatitis (15%). In the identification of the etiology of biliary pancreatitis, the presence of microcrystals had a sensitivity of 90%, specificity of 85%, positive predictive value of 85.7%, negative predictive value of 89.4% and accuracy of 87.5%. In the patients with recurrent idiopathic pancreatitis, with biliary crystals, there was an statistically significant reduction in the number of pancreatitis episodes after specific treatment. In the follow-up of this group during 23.3 +/- 4.8 months, recurrence of pancreatitis occurred only in patients with "persistent biliary factor" (choledocholithiasis and/or persistence of cholesterol monohidrate). All patients with idiopathic pancreatitis who underwent cholecystectomy had chronic cholecystitis. Moreover, cholelithiasis was present in one case. In the ultrassonographic follow-up of the patients with idiopathic acute pancreatitis with microcrystals in the bile, cholelithiasis was detected in one case. In the subgroup of five patients with idiopathic pancreatitis without biliary microcrystals recurrence occurred in one case. Ultrassonographic study during follow-up did not reveal biliary stones in any of these patients. We concluded that the detection of biliary microcrystals in "idiopathic" pancreatitis suggested an underlying biliary etiology, even if occult. What's more, early specific therapeutic procedure (cholecystectomy, endoscopic sphincterotomy or ursodeoxycholic acid) in patients with recurrent idiopathic pancreatitis with microcrystals in the bile reduced significantly the recurrence during the follow-up. Finally, acute pancreatitis (specially recurrent) should not be called idiopathic before the microscopic analysis of the bile, aiming to detect or exclude the presence of microcrystals.     

The relationship of bile duct crystals to sphincter of Oddi Dysfunction

Bile duct crystals collected either from the duodenum after gallbladder contraction or directly from bile duct aspiration are surrogates for gallbladder stones and microlithiasis. Whether bile crystals also serve as surrogates for bile duct stones or microlithiasis that forms in the bile duct after cholecystectomy is not known based on current data. Sphincter of Oddi dysfunction (SOD), due either to muscular spasm or sphincter fibrosis, is a cause of bile duct obstruction. Almost all of the literature on SOD involves patients who have had a prior cholecystectomy. Intuitively, obstruction at the SO following cholecystectomy would seem to lead to biliary stasis and predispose patients to bile duct microlithiasis. However, a recent study did not find bile duct crystals in patients with manometrically diagnosed SOD. The reason for this is unknown, although we hypothesize that cholesterol and bilirubinate crystals are not surrogates for brown pigment stones commonly found in patients following cholecystectomy.     

Biliary microlithiasis in patients with idiopathic acute pancreatitis and unexplained biliary pain: response to therapy

BACKGROUND AND AIMS: Microlithiasis has been suspected to cause acute pancreatitis and biliary pain. We studied the frequency of microlithiasis and response to treatment in recurrent idiopathic acute pancreatitis (RIAP) and unexplained biliary pain. METHODS: Gallbladder bile was examined microscopically for cholesterol monohydrate crystals (CMC) and calcium bilirubinate granules (CBG) in patients with RAIP (n = 24; mean age 36 years, range 18-56 years; 14 men), unexplained biliary pain (n = 12; mean age 32 years, range 22-55 years; six men), gallstones (n = 22; mean age 40 years, range 30-58 years; 12 men) and patients without clinical or imaging evidence of gallstone disease (n = 12; mean age 32 years, range 14-54 years; six men). The presence of a single CMC or >25 CBG/slide was considered abnormal. RESULTS: Bile microscopy was abnormal in 75% patients with RAIP (18/24; CMC in 10, CBG in six, CMC and CBG in two), 83.3% patients with unexplained biliary pain (10/12; CMC in seven, CBG in one, CMC and CBG in two) and 95.4% patients with gallstones (21/22; CMC in 12, CBG in one, CMC and CBG in eight). None of the controls without gallstone disease had CMC while three patients had low counts of CBG. Twenty-eight patients with RAIP and biliary pain having microlithiasis agreed to be treated with cholecystectomy (n = 2), endoscopic sphincterotomy (n = 21) or ursodeoxycholic acid (UDCA; n = 5). The 23 patients treated with cholecystectomy or sphincterotomy remained asymptomatic during follow up (mean 23 months, range 6-48 months). Four of five patients treated with UDCA remained asymptomatic for a follow-up period of 9, 10, 11 and 18 months, respectively. One patient who had refused cholecystectomy or sphincterotomy continued to experience pain at the same frequency as before during a follow-up period of 12 months. One patient, who was asymptomatic on UDCA for 9 months, agreed to undergo sphincterotomy and remained asymptomatic over a follow-up period of 14 months. CONCLUSIONS: Microlithiasis is a common cause for idiopathic acute pancreatitis and unexplained biliary pain. Lasting relief is obtained in most patients after treatment with UDCA, cholecystectomy or sphincterotomy.     

Biliary Sphincter of Oddi Dysfunction Type I Versus Occult Biliary Microlithiasis in Post-cholecystectomy Patients: Are They Both Part of the Same Clinical Entity?

We speculate that biliary sphincter of Oddi dysfunction type I and symptomatic migrating biliary microlithiasis may be part of the same disease process. A retrospective analysis of prospectively collected data was carried out using procedure and diagnosis codes during the period of 1997–2006. Seventeen patients (age 51 ± 17; 94% women) with prior cholecystectomy, right upper quadrant/epigastric abdominal pain, elevated liver enzymes, dilated biliary ducts seen on ultrasound/CT scan were identified. The patients underwent ERCP with biliary endoscopic sphincterotomy. Nine (53%) had biliary microlithiasis and eight (47%) had biliary sphincter of Oddi dysfunction type I. They were followed for 2–108 weeks (median 9 weeks). 6/8 (75%) in biliary sphincter of Oddi dysfunction type I and 6/9 (67%) in biliary microlithiasis group had resolution of abdominal pain (P = 1.00). We conclude that the clinical improvement with biliary sphincterotomy for biliary sphincter of Oddi dysfunction type I versus occult biliary microlithiasis was not significantly different.     

Role of endoscopic evaluation in idiopathic pancreatitis: a systematic review

In approximately 20% of patients with acute pancreatitis, a cause is not established by history, physical examination, routine laboratory testing, and abdominal imaging. For those with a single unexplained attack, the role of invasive evaluation with endoscopic retrograde cholangiopancreatography is unsettled but has been generally limited to those patients with suspected bile duct stones or malignancy. Recent studies suggest that microlithiasis is causative in up to 75% of patients with an unexplained attack and gallbladder in situ, whereas sphincter of Oddi dysfunction is most prevalent in those with recurrent attacks who have previously undergone cholecystectomy. EUS has been shown to be highly accurate for the identification of gallbladder sludge, common bile duct stones, and pancreatic diseases. Given this apparent diagnostic utility, an EUS-based strategy may be a reasonable approach to evaluate patients with a single idiopathic attack. ERCP and sphincter of Oddi manometry should generally be reserved for patients with multiple unexplained attacks and negative EUS results, especially for those patients who have previously undergone cholecystectomy.     

Sphincter of Oddi Dysfunction After Successful Gallstone Lithotripsy (Postlithotripsy Syndrome) Manometric Data and Results of Endoscopic Sphincterotomy

After successful gallstone lithotripsy, biliarypain recurs in about one third of patients. However,gallstone recurrence can be shown in only 40-60% ofthese patients. Therefore, other causes, such as sphincter of Oddi dysfunction (SOD), may besuspected. Twenty-two consecutive patients withrecurrent biliary pain after successful gallstonelithotripsy without evidence of gallstone recurrence atultrasonography were enrolled. Liver tests were elevated in 13patients and ERC showed a dilated bile duct in nine. All22 patients underwent sphincter of Oddi (SO) manometry,bile sample analysis for microlithiasis, endoscopic sphincterotomy (ES), and bile duct explorationwith a Dormia basket. Thereafter, the patients wereclinically followed at bimonthly intervals. SO manometryrevealed SOD in 15/22 patients. This was more often the case in patients with initiallylarger (>2 cm) or multiple stones than afterlithotripsy for solitary small stones (P < 0.01).Microlithiasis was detected in one patient, anotherpatient had small biliary calculi at bile ductexploration (both without SOD). After ES, 14/15 patientswith biliary SOD but none of the five without SODimproved (median follow-up: two years; P < 0.01). The one patient with CBD stones became symptom-freeafter ES, while the patient with microlithiasis improvedafter additional cholecystectomy only. Overall, ESproved to be the adequate therapy in 15/22 patients (68%, median follow-up: 22 months). Aftergallstone lithotripsy, SOD is found in about two thirdsof patients with recurrent symptoms but withoutgallstone recurrence. In this group CBD stones ormicrolithiasis are rare. Therefore, SOD has to be suspected inthis situation and ES gives favorable results, even whenperformed on a clinical basis only (without SOmanometry).     

Acute recurrent pancreatitis.

History, physical examination, simple laboratory and radiological tests, and endoscopic retrograde cholangiopancreatography (ERCP) are able to establish the cause of recurrent acute pancreatitis in 70% to 90% of patients. Dysfunction of the biliary and/or pancreatic sphincter, as identified by sphincter of Oddi manometry, accounts for the majority of the remaining cases. The diagnosis may be missed if the pancreatic sphincter is not evaluated. Pancreas divisum is a prevalent congenital abnormality that is usually innocuous but can lead to recurrent attacks of acute pancreatitis or abdominal pain. In select cases, endoscopic sphincterotomy of the minor papilla can provide relief of symptoms and prevent further attacks. A small proportion of patients with idiopathic pancreatitis have tiny stones in the common bile duct (microlithiasis). Crystals can be visualized during microscopic analysis of bile that is aspirated at the time of ERCP. Neoplasia is a rare cause of pancreatitis, and the diagnosis can usually be established by computerized tomography or ERCP. A wide variety of medications can also cause recurrent pancreatitis. ERCP, sphincter of Oddi manometry, and microscopy of aspirated bile should be undertaken in patients with recurrent pancreatitis in whom the diagnosis is not obvious.     

Evidence-based approach to idiopathic pancreatitis

The causes of recurrent acute pancreatitis, including the newly recognized genetic causes, are reviewed. The pitfalls of overcalling the diagnosis of pancreatitis in patients with abdominal pain or other symptoms and the role of a careful history are emphasized. The presence of undetectable microlithiasis in patients with unexplained pancreatitis is discussed. The popular notion of pancreas divisum and sphincter of Oddi dysfunction as causes of pancreatitis is challenged, as is the role of endotherapy in these conditions.     

Sphincter of Oddi: Function, dysfunction, and its management

The most common functional disorder of the biliary tract and pancreas relates to the activity of the Sphincter of Oddi. The Sphincter of Oddi is a small smooth muscle sphincter strategically placed at the junction of the bile duct, pancreatic duct, and duodenum. The sphincter controls flow of bile and pancreatic juices into the duodenum and prevents reflux of duodenal content into the ducts. Disorder in its motility is called Sphincter of Oddi dysfunction. Clinically this presents either with recurrent abdominal biliary type pain or episodes of recurrent pancreatitis. Manometry may identify the motility abnormalities, the most clinically significant being an abnormally elevated basal pressure. The most effective treatment once an abnormal basal pressure is identified is division of the sphincter. This is associated with good long-term results.     

Sphincter of oddi dysfunction

Opinion statement 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.     

Frequency of abnormal pancreatic and biliary sphincter manometry compared with clinical suspicion of sphincter of Oddi dysfunction.

BACKGROUND: Sphincter of Oddi manometry as performed at ERCP is the most accepted method to evaluate for sphincter of Oddi dysfunction. To fully assess for sphincter of Oddi dysfunction, both the pancreatic and the bile ducts must be evaluated. We assessed the frequency of pancreatic and biliary sphincter abnormalities in a large series of patients. METHODS: A total of 593 patients underwent manometry of the biliary and pancreatic ducts at one endoscopic retrograde cholangiopancreatography session. Basal sphincter pressure greater than or equal to 40 mm Hg was considered abnormal. Phasic waves were not evaluated. Manometric abnormalities were correlated with the clinical presentation as categorized using a modified Geenen/Hogan classification. RESULTS: Of 360 patients with intact sphincters, 18.9% had abnormal pancreatic sphincter basal pressure alone, 11.4% had abnormal biliary basal sphincter pressure alone, and in 31.4% the basal pressure was abnormal for both sphincters; thus, 60.1% of the patients had sphincter dysfunction. The frequency of sphincter of Oddi dysfunction did not differ whether typed by biliary or pancreatic criteria: approximately 65% type II and 59% type III. Of patients without pancreatitis, 55.9% had an abnormal basal sphincter pressure, whereas sphincter dysfunction was present in 72.3% of those with idiopathic pancreatitis and 53.9% of patients with chronic pancreatitis. Of patients with an ablated biliary sphincter, 45.9% had abnormal basal pancreatic sphincter pressure and only 0.6% had an abnormal biliary sphincter pressure alone. Abnormal pressure in both sphincters was found in 9.3%. CONCLUSION: If both portions of the sphincter of Oddi are studied simultaneously, abnormalities are found very commonly (55% to 72%). Assessment of both sides of the sphincter is necessary. Classifying patients according to both pancreatic and biliary sphincter segments is cumbersome, and may be replaced by an overall type. Using this modified classification, the frequency of sphincter of Oddi dysfunction is similar in both type II and type III patients (59% to 67%).     

Effects of colectomy on bile composition, cholesterol saturation and cholesterol crystal formation in humans

Total or subtotal colectomy is the surgical treatment of choice for patients with ulcerative colitis. Recently it has been reported that colectomy may lead to increased lithogenicity of bile, short nucleation time, cholesterol crystal formation, and gallstone disease. We examined whether colectomy in patients with ulcerative colitis leads to changes in bile composition that predisposes to cholesterol crystal formation and cholesterol gallstone disease. Ten consecutive patients who had previously undergone ileostomy and colectomy because of ulcerative colitis were admitted for ileal pouch surgery. At operation bile was obtained by puncture of the gallbladder. Controls were 35 patients undergoing cholecystectomy (23 for cholesterol gallstone disease and 12 for reasons other than gallstone disease). The gallbladder bile was analyzed for cholesterol crystals, bile acid, and biliary lipid composition, cholesterol saturation, and nucleation time. The colectomized patients had normal biliary lipid composition, normal cholesterol saturation, and normal nucleation time, in contrast to gallstone patients who displayed highly supersaturated bile with a short nucleation time. Thus patients with ileostomy after colectomy because of ulcerative colitis have normal cholesterol saturation and nucleation time of bile.     

Sphincter of Oddi dysfunction: an evidence-based review

Sphincter of Oddi dysfunction is a painful syndrome that presents as recurrent episodes of right upper quadrant biliary pain, or recurrent idiopathic pancreatitis. It is a disease process that has been a subject of controversy, in part because its natural history, disease course and treatment outcomes have not been clearly defined in large controlled studies with long-term follow-up. This review is aimed at clarifying the state-of-the-art with an evidence-based summary of the current diagnostic and therapeutic approaches and modalities for sphincter of Oddi dysfunction.     

Idiopathic acute recurrent pancreatitis

Acute recurrent pancreatitis (ARP) results most commonly from alcohol abuse or gallstone disease. Initial evaluation fails to detect the cause of ARP in 10-30% of patients, and as a result the diagnosis of "idiopathic" ARP is given. In these patients, a more extensive evaluation including specialized labs, ERCP, endoscopic ultrasound, or magnetic resonance cholangiopancreatography typically leads to a diagnosis of microlithiasis, sphincter of Oddi dysfunction, or pancreas divisum. Less commonly, hereditary pancreatitis, cystic fibrosis, a choledochocele, annular pancreas, an anomalous pancreatobiliary junction, pancreatobiliary tumors, or chronic pancreatitis are diagnosed. Determining the etiology is important, as it helps to direct therapy, limits further unnecessary evaluation, and may improve a patient's long term prognosis.     

Biliary tract motor dysfunction

Gallbladder and sphincter of Oddi motility regulates the flow of bile from the liver to the duodenum. During the interdigestive period most secreted bile is diverted into the gallbladder where it is concentrated, but a significant minority of the biliary secretion passes directly into the duodenum. Regulation of this flow is mainly via the phasic contractions of the sphincter of Oddi and the sphincter basal tone. The phasic contractions expel small volumes of fluid into the duodenum, but most of the flow occurs between the contractions and is therefore not dependent on peristaltic pumping, but rather on a small pressure gradient. During fasting, just prior to duodenal phase III activity, the gallbladder expels up to 40% of its volume and the sphincter phasic contractions increase. Following a meal, the gallbladder empties its contents, and the sphincter of Oddi resistance is reduced via a fall in basal pressure and inhibition of the amplitude of phasic contractions. Control of this activity is via an interplay of both neuronal and hormonal factors which together have an effect on both gallbladder and sphincter of Oddi motility. Abnormalities in motility are recognized for both the gallbladder and the sphincter of Oddi. Gallbladder dyskinesia is objectively diagnosed using the radionuclide GBEF. In patients with a GBEF less than 40% cholecystectomy results in relief of symptoms. In postcholecystectomy patients sphincter of Oddi dysfunction presents as either biliary-like pain or idiopathic recurrent pancreatitis. Endoscopic sphincter of Oddi manometry provides the most objective diagnostic information. In patients with a sphincter of Oddi stenosis, characterized manometrically as an elevated basal pressure, division of the sphincter results in relief of symptoms. For patients with biliary-like pain, division is performed as an endoscopic sphincterotomy, whereas for patients with idiopathic recurrent pancreatitis, a sphincteroplasty and pancreatic duct septectomy are required.