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a Chair, Committee on
Functional Biliary and Pancreatic Disorders, Multinational Working
Teams to Develop Diagnostic Criteria for Functional Gastrointestinal
Disorders (Rome II), Cattedra di
Gastroenterologia I, Clinica Medica II,
Università "La Sapienza," Rome,
Italy, b Co-Chair, Committee
on Functional Biliary and Pancreatic Disorders, Multinational Working
Teams to Develop Diagnostic Criteria for Functional Gastrointestinal
Disorders (Rome II), Department of Medicine,
University of Calgary,
Calgary, Alberta, Canada, c Division of Gastroenterology and Hepatology,
Milwaukee, WI, USA, d Division of Gastroenterology and Hepatology,
Indiana University School of Medicine,
Indianapolis, IN, USA, e Gastrointestinal Surgical Unit,
Flinders Medical Centre,
SA, Australia
Correspondence to: Eldon Shaffer, MD, Professor and Head, Department of Medicine, Foothills Medical Centre, 1403 29th Street NW, Calgary, Alberta T2N 2T9, Canada. Email: eldon.shaffer{at}crha-health.ab.ca
The term "dysfunction" defines the motor disorders of
the gall bladder and the sphincter of Oddi (SO) without note of the potential etiologic factors for the difficulty to differentiate purely
functional alterations from subtle structural changes. Dysfunction of
the gall bladder and/or SO produces similar patterns of biliopancreatic
pain and SO dysfunction may occur in the presence of the gall bladder.
The symptom-based diagnostic criteria of gall bladder and SO
dysfunction are episodes of severe steady pain located in the
epigastrium and right upper abdominal quadrant which last at least 30 minutes. Gall bladder and SO dysfunctions can cause significant
clinical symptoms but do not explain many instances of biliopancreatic
type of pain. The syndrome of functional abdominal pain should be
differentiated from gall bladder and SO dysfunction. In the diagnostic
workup, invasive investigations should be performed only in the
presence of compelling clinical evidence and after non-invasive testing
has yielded negative findings. Gall bladder dysfunction is suspected
when laboratory, ultrasonographic, and microscopic bile examination
have excluded the presence of gallstones and other structural
abnormalities. The finding of decreased gall bladder emptying at
cholecystokinin-cholescintigraphy is the only objective characteristic
of gall bladder dysfunction. Symptomatic manifestation of SO
dysfunction may be accompanied by features of biliary obstruction
(biliary-type SO dysfunction) or significant elevation of pancreatic
enzymes and pancreatitis (pancreatic-type SO dysfunction). Biliary-type
SO dysfunction occurs more frequently in postcholecystectomy
patients who are categorized into three types. Types I and II, but not
type III, have biochemical and cholangiographic features of biliary
obstruction. Pancreatic-type SO dysfunction is less well classified
into types. When non-invasive investigations and endoscopic retrograde
cholangiopanreatography show no structural abnormality, manometry of
both biliary and pancreatic sphincter may be considered.
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