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Sphincterotomy for patients with SO dyskinesia has been shown not to improve symptoms and cannot be recom­mended, especially in view of the increased risk of pancreati­tis in patients with SO dysfunction. The role of pharmacotherapy is somewhat unclear because there are few well conducted studies using manometric criteria for the di­agnosis of SO dysfunction. The main drawback is that there are no drugs that appear to be specific for the SO, are long acting and free of side effects. Nifedipine has been shown to reduce significantly SO basal pressure when given sublin- gually to patients with SO dyskinesia during SO manometry.       Two studies have evaluated oral nifedipine for up to 12 weeks in patients with manometrically diagnosed ‘SO spasm’  and suspected type 2 SO dyskinesia (ie, no manometry). Both studies found that, compared with placebo, there was a significant decrease in pain episodes and pain scores. The therapy was well tolerated, but concerns still exist re­garding the potential for systemic side effects of hypotension, flushing and headaches.

Glyceryl trinitrate given sublingually during SO manome- try has been shown to decrease SO basal pressure in patients with suspected pancreatobiliary disease. However, no long term study has been undertaken using nitrates in pa­tients with SO dysfunction.

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TREATMENT OF SO STENOSIS

In a prospective study, patients with biliary-like pain were randomly assigned to endoscopic sphincterotomy or sham procedure. Manometry was done but was not used to de­termine therapy. The results of manometry were correlated with the clinical outcome (Table 3). After four years of follow-up, it was found that patients with SO stenosis treated by sphincterotomy were more likely to show improvement in symptoms than patients with sphincter stenosis who had the sham procedure. If the manometric diagnosis was SO dyski- nesia, significant differences were not observed. The results from this study led to the conclusion that patients with sig­nificant SO dysfunction as characterized by an elevated ba­sal pressure (SO stenosis) should be treated by division of the SO. Similar results were reported around that time, and, subsequently, other prospective nonrandomized trials have confirmed the benefit of sphincterotomy for pa­tients with an elevated basal pressure. As dis­cussed above, sphincterotomy for type 3 patients with an elevated basal pressure may not be associated with longlast- ing benefit.

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The development of techniques to measure pressure across the SO has enhanced our understanding of the normal physiology of the human SO and has also defined, with accu­racy and reproducibility, the presence of manometric disor­ders of the sphincter. The miniaturized manometry catheters that are used for pressure measurement have three lumens and are made of either polyethylene or teflon. They have an outer diameter of 1.7 mm. Three side holes are made at the recording tip of the catheter at 2 mm intervals, start­ing at 10 mm from its distal tip. Thus, the three lumens rec­ord across a length of 5 mm from within the SO. The catheter is connected to a pneumohydraulic capillary perfu- sion system with pressure force transducers in series. The catheter is perfused with deionized, bubble-free water at a flow rate of 0.13 mL/min to 0.25 mL/min, and the whole sys­tem is capable of accurately recording pressure changes of up to 300 mmHg/s. Mild sedation is usually achieved with intra­venous benzodiazepine (diazepam or midazolam) or propofol. These medications have been shown not to be associated with alterations in SO manometirc recordings. Be­fore and during the manometric recording, drugs that alter sphincter motility, such as atropine and opiate analgesics, are avoided.

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Blood screens during an acute attack of pain reveal a normal white cell count. About 10% to 20% of patients, however, show increases in serum concentrations of liver transaminases, particularly in blood specimens that are taken 3 to 4 h after the onset of pain. This is occasionally accompanied by increases in serum bilirubin and AP. In a subgroup of patients, serum amylase may be ele­vated either alone or in conjunction with changes in liver en­zymes, and these patients are then considered to have the pancreatic form of the disorder.

Typical pain episodes of SO dysfunction are quite charac­teristic, but often other functional bowel disturbances can coexist, making diagnosis on history alone difficult. A trial of therapy for suspected irritable bowel syndrome can be con­sidered where the history is vague, in the hope that this may improve symptoms and exclude SO dysfunction as a diagnos­tic possibility. Common bile duct stones need to be excluded in all patients with suspected SO dysfunction. The role of magnetic resonance cholangiopancreatography (MRCP) in evaluating the biliary tree in patients with a low likelihood of having common bile duct stones is unclear. At present, MRCP has not been shown to be superior than an ultrasound in detecting common bile duct stones. ERCP has the obvious advantage of being able to remove common bile duct stones at the time of the procedure and can also give an indi­cation as to the possibility of SO dysfunction being present by an objective measurement of common bile duct diameter and whether contrast drains adequately. While these factors have not been shown to predict SO dysfunctions reliably, they can help in deciding whether to proceed to other inves­tigations once common bile duct stones have been excluded. Pain on injection of contrast during ERCP has not been found to correlate with SO dysfunction. Biopsies from the papilla in a large series of patients with SO dysfunction found a 4.3% incidence of adenoma. If there is any sus­picion that the papilla appears abnormal, biopsies should be considered.

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Mechanism of SO dysfunction

The cause of SO dysfunc­tion and the pain mechanism involved are uncertain. One potential mechanism is a neural defect leading to disturbed SO motility that may be due to a defect of the neural connec­tions that coordinate the interaction between the duode­num, biliary tract and SO. In animals and humans, the response to CCK is altered following cholecystectomy, suggesting that the surgery may in some way affect these neu­ral connections. The neural pathways from the gallbladder and common bile duct to the SO are thought to have an in­hibitory effect on the SO. Interruption of these inhibi­tory neural pathways may lead to an increased tonicity of the SO with resistance to outflow in a biliary system that has lost its pressure reservoir, the gallbladder. In a small human study of patients with abdominal pain suspected to be SO dysfunc­tion that was performed during endoscopic SO manometry, some patients after cholecystectomy did not show SO relaxa­tion in response to artificial elevations of the common bile duct pressure by infusing saline. Normally, the SO should relax in response to elevations in the common bile duct pressure. It has also been shown that in the absence of the gallbladder, bile duct pressure is increased and the bile duct pressure increases in response to SO spasm induced by morphine, which was not seen with an intact gallbladder. There are reports of SO dysfunction following liver transplantation. After liver transplantation, the SO is essentially denervated. However, surgical interruption of neural pathways cannot be the only mechanism for SO dys­function because patients with intact gallbladders have been shown to have manometrically proven SO dysfunction.

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Two classification sys­tems for SO dysfunction have been developed for patients with biliary type pain. One system involves a ‘clinical’ classi­fication based on endoscopic retrograde pancreato- cholangiography (ERCP) and liver function test abnormali­ties and the other, SO manometry.

The clinical classification system stratifies patients into three groups (types 1, 2 and 3), depending on the likelihood that SO dysfunction is present. Type 1 patients have all three abnormalities: a dilated common bile duct (12 mm) on ERCP; delayed drainage of contrast for the common bile duct (45 mins); and, on two occasions in association with pain epi­sodes, abnormal alkaline phosphatase (AP) or abnormal ratio of alanine aminotransferase to aspartate aminotransferase (twice the upper limit of normal) on liver function testing. Type 2 patients have one or two abnormalities, and type 3 patients experience pain with none of the above abnormali­ties. It is thought that SO dysfunction is present in all type 1 patients, approximately 50% to 60% of type 2 patients and fewer than 10% of type 3 patients. Type 3 patients are be­lieved to be the patients most likely to have irritable bowel syndrome.

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SO dysfunction has been known by many names in the past, including biliary dyskinesia, biliary spasm, biliary dyssynergia, papillary stenosis, papillitis, odditis and postcholecystectomy syndrome. There are two main clinical conditions that relate to what portion of the sphincter mal­functions. The more common problem is biliary SO dysfunc­tion. Patients with dysfunction of the pancreatic portion of the sphincter usually include patients with idiopathic recur­rent pancreatitis. Pancreatic pain without pancreatitis has also been suggested, but the definition of discrete pancreatic pain without clear pancreatitis is unclear.

Patients with biliary SO dysfunction are typically females (females to males seven to one) in their mid-40s and usually present five to seven years after having undergone cholecys- tectomy for cholelithiasis. Acute attacks can be associ­ated with severe pain, as in patients with true biliary colic. However, apart from localized tenderness, signs of periton- ism or fever are not present. The pain is situated in the epi­gastrium or right upper quadrant, often radiates into the back, and may be associated with nausea and vomiting. The pain generally occurs in episodes lasting up to several hours or until relieved by analgesics. Initial treatment of patients presenting with the above clinical symptoms is directed at relieving the pain, usually achieved by the administration of a systemic analgesic or buscopan. Pethidine (meperidine) is thought to be the most appropriate analgesic in patients with suspected SO dysfunction. These pain episodes may occur at intervals of weeks or months. Some patients also describe discomfort in the upper abdomen that is more frequent and may occur every day. The attacks of pain can occur after fatty meals and are often nocturnal. Patients may complain of sen­sitivity to codeine and other opiates, but this is nonspecific. Indeed, the first episode of pain may have been experienced following opiate medication, usually for an unrelated proce­dure. SO dysfunction is commonly associated with work ab­senteeism and health care use. One study found that patients over-report nongastroenterological somatic complaints (ie, somatization disorder) and childhood sexual abuse, suggesting a role for broad psychiatric assessment and treatment of some patients with SO dysfunction.

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