Speed your diagnosis of this gallbladder disorder

CASE Dionne J, a 38-year-old woman with a BMI of 32, presents with a 2-month history of right upper abdominal pain. The pain is intermittent and often begins after eating, she reports, particularly when a meal includes fatty foods. She has no nausea, vomiting, diarrhea, constipation, or fever, and the pain is not getting progressively worse.

When the pain comes on, Ms. J says, it lasts about an hour, sometimes less. It is colicky in nature, and not relieved with bowel movements or position change. The patient tried ranitidine 150 mg twice a day for 2 weeks, with no relief. You suspect functional gallbladder disorder. But is Ms. J a candidate for a cholecystectomy? What would you do next?

Over the past 2 decades, the incidence of cholecystectomies due to functional gallbladder disorder (FGBD) has multiplied, going from about 5% to 20% to 25%.¹ But definitive information about the etiology of FGBD has not kept pace.

Although the Rome III diagnostic guidelines for FGBD, published in 2006,² remain the standard of care, a number of more recent studies have added to our understanding of this disorder. This review of the diagnosis and treatment of FGBD incorporates both the Rome III guidelines and the latest findings. The text and tables that follow can help you recognize this clinical entity earlier, minimize the number of tests needed to arrive at a definitive diagnosis, and establish a plan of care that is consistent with both the guidelines and the evidence.

As obesity rates rise, so does gallbladder dysfunction

Obesity has been shown to produce a chronic proinflammatory state throughout the body,^3-6 which has been linked to fatty infiltration of the gallbladder (among other organs) and impaired contractility.^3,6-9

A study by Al-Azzawi et al highlighted the importance of increased fat in the gallbladder wall as a key cause of dysmotility.¹⁰ The researchers compared wall thickness, inflammation, and the amount of fat in the walls of gallbladders that had been removed for both acalculous and calculous disease with the characteristics of gallbladders removed for reasons unrelated to organ dysfunction (the controls). Those with dysmotility, they found, had more fat in the wall but the same wall thickness as the controls. The amount of fat in the walls was similar for the acalculous and the calculous groups, but the gallbladders in which stones were found had more inflammation and increased wall thickness.¹⁰

Several other studies have found evidence of both inflammation and fatty deposits in the walls of gallbladders removed for acalculous disease.^2,4,11-13

In one study, researchers found chronic inflammation in 99% of gallbladders removed from patients who had classic biliary symptoms but no gallstones.¹¹

FGBD appears to be initiated by fatty infiltration of the gallbladder wall, causing increasing levels of inflammation and steatocholecystitis that lead to poor motility.^3,4,6-10 This in turn alters bile composition, which can lead to sludge and stone formation.^2,6,10 The finding by Al-Azzawi et al of greater thickness and inflammation in the walls of gallbladders with calculi suggests that gallstones result from progressively worsening inflammation and dysmotility.¹⁰

Steps to take for a definitive diagnosis

A diagnosis of FGBD requires a history of classic gallbladder symptoms, many but not all of which are specified in the Rome III diagnostic criteria (TABLE). Classic symptoms include nausea, vomiting, right upper quadrant pain, pain after eating, and reproduction of pain with cholecystokinin (CCK) injection. Cramping, bloating, reflux, diarrhea, fullness, and epigastric pain are atypical symptoms.^2,11

TABLE
Rome III diagnostic criteria for functional gallbladder disorder