Microscopically, lipid containing histiocytes infiltrating into outer muscle layer of gall bladder wall may be seen to from xanthogranulomatous foci and fibrosis owing to extravasation of bile into gallbladder wall through Rokitansky-Aschoff sinuses
or a small ulceration in the mucosa.3 Macroscopically, XGC lesion vary from yellowbrown nodules in the gallbladder wall to diffuse involvement of the entire gallbladder with extension to the surrounding structures.4 The importance of XCG is that it mimics gallbladder carcinoma (GBC) preoperatively on imaging and intra-operatively.
Gallbladder adenomyomatosis (GA) is a disease characterized by epithelial proliferation and hypertrophy of the muscles of the gallbladder wall (1) with an outpouching of the mucosa into or through the thickened muscular layer, i.e., the Rokitansky-Aschoff sinuses
A benign condition such as diffuse adenomyomatosis with numerous Rokitansky-Aschoff sinuses
could be considered, but this case had no cystic changes and the trilaminar appearance of the gallbladder would be an unusual imaging finding.
 The pathogenesis of XGC is the rupture of Rokitansky-Aschoff sinuses
and extravasation of bile into the muscular layer.
The pathogenesis is thought to be related to extravasation of bile into the gallbladder wall from rupture of Rokitansky-Aschoff sinuses
or by mucosal ulceration. This event incites an inflammatory reaction in the interstitial tissue, whereby fibroblasts and macrophages phagocyte the biliary lipids in bile such as cholesterol and phospholipids leading to the formation of xanthoma cells.
At this time, a repeat abdominal sonogram revealed a 4mm echogenic focus adherent to the anterior gallbladder wall with a comet tail sign, suggestive of cholesterol crystals lodged within Rokitansky-Aschoff sinuses
of the gallbladder wall.
Extravasation of bile into the gallbladder wall with involvement of Rokitansky-Aschoff sinuses
is a potential precipitating factor for XGC [6-12].
Adenomyomatosis represents the presence of intramural diverticula of the gallbladder mucosa, the Rokitansky-Aschoff sinuses
, within a thickened, hypertrophied mucosa and muscularis propria of the gallbladder wall.
This is followed by a downward progression of the lesion, possibly reaching the Rokitansky-Aschoff sinuses
. When fully developed, the intestinal metaplasia consists of variable amounts of goblet or columnar cells with a brush border.
A review of 40 cases of xanthogranulomatous cholecystitis suggests that the process in the gallbladder stems from an obstruction of the Rokitansky-Aschoff sinuses
by inspissated bile followed by subsequent rupture and a xanthogranulomatous reaction.
 It is mostly always linked with gallstones with pathogenesis being a mystery, trigger being gallstones, obstruction to bile flow and cholestasis and infection associated with ruptured Rokitansky-Aschoff sinuses
(outpouchings of mucosal epithelium through gall bladder wall).
The gallbladder epithelium, which lines Rokitansky-Aschoff sinuses
, enhances on the arterial phase, which results in cystic intramural collections with a thin rim of enhancement.