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Is the role of secretin in causing a choleresis clinically significant enough to be a “stress test” for biliary SOD?
Every specialty in Medicine has its orphan diagnosis; in ophthalmology it’s “dry eyes”, in gynaecology “dyspareunia”, in rheumatology “fibromyalgia” and the list goes on. In gastroenterology, the vast diagnostic and therapeutic wasteland is irritable bowel syndrome (IBS). However, deep within IBS (or more correctly, chronic functional abdominal pain syndrome) there is an almost impenetrable jungle, called sphincter of Oddi Dysfunction (SOD). It is not a place for the faint-hearted. SOD as a fashionable diagnosis first appeared on the radar screen in a 1989 N Engl J Med paper: a group of US investigators published their experience of endoscopic (biliary) sphincterotomy (EBS) in patients with postcholecystectomy pain.1 The authors divided SOD into three categories depending on the presence or absence of transiently abnormal liver serologies and/or common bile duct (CBD) dilatation. “Typical” biliary-type pain was needed to make the SOD diagnosis. Type I patients had “typical” biliary pain, transient serum transaminase elevations to at least 1.5 times the upper limit of normal with normalisation between attacks on ⩾2 occasions, and a CBD ⩾12 mm in diameter. Type II patients had pain and enzyme elevations or a dilated CBD, but not both. Type III patients had a pain syndrome alone. (The original classification included delayed drainage of contrast from the bile duct after ERCP as an addition criterion. Most investigators have dropped this from the classification, as it has been shown to be unreliable). The so-called Milwaukee Classification of SOD has survived unchanged for 17 years, despite growing evidence that it is flawed and in need of revision.2 This is not intended as a criticism of the original investigators, who tried their best to make sense of a difficult pain …
Competing interests: None.
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