Keywords
Gallbladder cancer - positron emission tomography/computed tomography scan - xanthogranulomatous
            cholecystitis
Introduction
            Based on imaging, it can be difficult to differentiate between xanthogranulomatous
               cholecystitis (XGC) and gall bladder carcinoma by ultrasonography (USG), computed
               tomography scan, or fluorodeoxyglucose (FDG) positron emission tomography-computed
               tomography (PET-CT) scan. The common feature of mural thickening on conventional imaging
               and nonspecific FDG uptake on PET/CT scan makes it very difficult to differentiate
               between these benign and malignant conditions. Histopathology remains the gold standard
               for these conditions. Our case highlights the common imaging characteristics of mural
               thickening and few distinct criteria developed on CT to differentiate between them
               and pitfall of FDG due to nonspecific uptake in inflammatory cells also apart from
               malignant tissue.
         Case Report
            A 71-year-old female presented with pain abdomen and fever since 3 months. USG was
               suggestive of thickened gallbladder wall. Thus, in view of suspicion of malignancy,
               the patient was referred for PET-CT scan. Whole-body 18F-FDG PET/CT scan was suggestive of cholelithiasis with intensely FDG avid [Figure 1a], [Figure 1b], [Figure 1c], [Figure 1d], [Figure 1e], [Figure 1f], [Figure 1g] circumferential nodular mural thickening in gall bladder, more in the fundus region,
               showing loss of fat planes with the adjacent liver with small hypodense areas within
               (arrows). Thus, in view of suspicion of malignancy, cholecystectomy was planned. The
               histopathology [Figure 2] showed gallbladder mucosa was completely ulcerated with only few foci of flattened
               mucosa. There was very dense chronic and xanthogranulomatous inflammation in wall
               suggestive of acute on chronic cholecystitis with xanthogranulomatous inflammation.
             Figure 1 Maximum intensity projection (a) of whole body fluorodeoxyglucose positron emission
                  tomography/computed tomography scan. Axial and coronal computed tomography and fused
                  positron emission tomography/ computed tomography (b-e) Images showing fluorodeoxyglucose
                  avid nodular mural thickening, more in the neck and fundus of gallbladder abutting
                  the adjacent hepatic parenchyma. Axial computed tomography arterial and portovenous
                  phases (f-g) showing asymmetric thickening of gallbladder wall in fundus region, with
                  hypodense areas within, abutting adjacent liver
                  Figure 1 Maximum intensity projection (a) of whole body fluorodeoxyglucose positron emission
                  tomography/computed tomography scan. Axial and coronal computed tomography and fused
                  positron emission tomography/ computed tomography (b-e) Images showing fluorodeoxyglucose
                  avid nodular mural thickening, more in the neck and fundus of gallbladder abutting
                  the adjacent hepatic parenchyma. Axial computed tomography arterial and portovenous
                  phases (f-g) showing asymmetric thickening of gallbladder wall in fundus region, with
                  hypodense areas within, abutting adjacent liver
            
            
             Figure 2 Gallbladder with ulcerated surface epithelium. Wall shows dense mixed inflammatory
                  infiltrate rich in histiocytes (a, H and E × 101). Gallbladder wall shows dense mixed
                  inflammatory infiltrate rich in histiocytes, diffusely infiltrating into the muscle
                  (b, H and E × 200)
                  Figure 2 Gallbladder with ulcerated surface epithelium. Wall shows dense mixed inflammatory
                  infiltrate rich in histiocytes (a, H and E × 101). Gallbladder wall shows dense mixed
                  inflammatory infiltrate rich in histiocytes, diffusely infiltrating into the muscle
                  (b, H and E × 200)
            
            Discussion
            XGC is a rare chronic gallbladder (GB) disease which is characterized by the proliferation
               of xanthoma within the GB wall.[1] Macroscopically, it appears like yellowish tumor like mass in the wall of the gall
               bladder. It is an infrequent chronic granulomatous inflammation of the gall bladder,
               first described by Christensen and Ishak in 1970 as “Fibroxanthogranulomatous inflammation.”[2] The term XGC was coined by McCoy et al. in 1976.[3] Although it is a benign disease, it is often mistaken as GB carcinoma due to the
               thickened GB wall. Histologically, the rupture of the Rokitansky-Aschoff sinuses,
               causes an inflammatory reaction, which can infiltrate adjacent organs, forming dense
               adhesions. It is a variant of cholecystitis. Extravasation of bile into the GB wall
               is supposedly the initiating event in the pathogenesis of XGC, which later triggers
               an inflammatory process that might be acute or chronic. The imaging characteristics
               reported for XGC are a continuous mucosal line in a thickened GB wall, an intramural
               GB wall nodule, and the presence of gallstones on a background of chronic GB disease.[4] Because of the similarity to gall bladder cancer in clinical manifestations and
               radiological findings, makes it difficult to distinguish between them.
            Few articles have been published describing the similarities and differences between
               XGC from gallbladder cancer[5],[6] and few reports about false-positive results on FDG-PET/CT scan.[7] Several studies have shown the strong association between gallstones and XGC,[8] as seen in our case. Ultrasound and CT scan may show nonspecific GB wall thickening.
               The presence of diffuse GB wall thickening, continuous mucosal line, intramural hypoattenuated
               nodules, absence of macroscopic hepatic invasion, and lack of intrahepatic biliary
               dilation on CT scan could help differentiate XGC from GB cancer with sensitivity and
               specificity of 83% and 100%, respectively, when three of these five findings are observed.[9] FDG-PET/CT scan is helpful in differentiating between benign and malignant lesions
               with sensitivity and specificity ranging from 75% to 78% and 82% to 100%, respectively,
               for the detection of GB cancer.[10] However, numerous cases of false-positive results have been seen because inflammatory
               cells in XGC also have high rates of glucose metabolism similar to malignant cells.[11] Thus, XGC is a rare, benign, chronic inflammation of the GB that has clinical, radiological,
               and intraoperative features similar to that of GB cancer and only histopathology can
               definitively differentiate the two conditions.
            Declaration of patient consent
            
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               In the form, the patient has/have given his/her/their consent for his/her/their images
               and other clinical information to be reported in the journal. The patient understands
               that their names and initials will not be published, and due efforts will be made
               to conceal their identity, but anonymity cannot be guaranteed