Skip to main content
Medical Principles and Practice logoLink to Medical Principles and Practice
. 2012 Jul 14;22(1):18–23. doi: 10.1159/000339659

Differential Diagnosis and Treatment Options for Xanthogranulomatous Cholecystitis

Yunfeng Cui 1, Hongtao Zhang 1, Erpeng Zhao 1, Naiqiang Cui 1, Zhonglian Li 1,*
PMCID: PMC5586703  PMID: 22814128

Abstract

Objective

To describe the differential diagnosis and treatment options for xanthogranulomatous cholecystitis (XGC), the presentations and management of 68 patients were described.

Subjects and Methods

Demographical and clinical data from 68 cases of XGC treated between January 2004 and January 2010 were analyzed. Clinical characteristics, radiological and surgical findings, histopathological features and postoperative recoveries were recorded. Clinical features of laparoscopic cholecystectomy versus open surgery and XGC versus gallbladder (GB) cancer were compared.

Results

The CA19-9 levels of XGC and coexisting GB cancer were significantly different (p = 0.0034). In radiological findings, focal thickening of the GB wall was more frequent in coexisting GB cancer, early enhancement of the GB was observed more often in coexisting GB cancer, and lymph node enlargement was seen more often in coexisting GB cancer (p < 0.05). There were also significant differences between laparoscopic and open surgery for CA19-9, intramural hypoattenuated nodule, pericholecystic invasion, lymph node enlargement and maximum thickness, focal thickening, heterogeneous enhancement and early enhancement of the GB wall (p < 0.05). These findings were confirmed by multivariate analysis.

Conclusions

Ultrasound, computed tomography scan and intraoperative frozen section were the helpful modalities for XGC diagnosis. CA19-9 (>37 kU/l), pericholecystic invasion, lymph node enlargement (>10 mm), and focal thickening and early enhancement of the GB wall were the criteria for open surgery. In some selected cases, laparoscopic cholecystectomy was preferable.

Key Words: Xanthogranulomatous cholecystitis, Coexisting gallbladder cancer, Tumor marker, Radiological findings, Open surgery, Laparoscopic cholecystectomy

Introduction

Xanthogranulomatous cholecystitis (XGC) is a rare condition of cholecystitis with intense inflammation [1]. It can cause asymmetrical thickening of the gallbladder (GB) wall and demonstrate a tendency to form nodules. The disease is benign but locally invasive and may involve adjacent organs such as the liver, duodenum, colon, and common bile duct. Involvement by the inflammatory process can macroscopically resemble carcinoma of the GB [2,3,4,5]. It is characterized by distinct pathological findings like fat-laden macrophages and foamy histiocytes and is associated with severe fibrosis. Gallstones, biliary stasis, and chronic infection may be possible etiological factors [6,7,8]. The XGC was first reported and named by McCoy et al. [9]. With a low incidence of 0.7–13.2% of all inflammatory diseases of the GB, it occurs mostly in middle-aged and elderly persons [10,11]. In some cases, XGC may be mistaken for malignancy, and it sometimes has coexistent GB cancer [12]. The frequency of the coexistence of these two lesions is approximately 10% in Japan and the USA [13,14].

To contribute to the available experience, we report data of the diagnosis and treatment of 68 patients with XGC. The study involved the use of diagnostic techniques, their impact on surgical indication and the results of surgical treatment and follow-up.

Subjects and Methods

The clinical records of 29,875 patients who had undergone biliary operations in Tianjin Nankai Hospital between January 2004 and January 2010 were reviewed and 68 patients were identified as having a histopathological diagnosis of XGC. The patient records during this period were searched electronically and, if the diagnosis after surgery was XGC, the detailed medical record was checked manually. Details regarding operative approach and pathology were abstracted from the operative and pathological reports.

All patients underwent ultrasonography and computed tomography (CT) preoperatively. The surgical procedures included open cholecystectomy, biliary tract exploration, partial hepatic wedge resection, regional lymphadenectomy and laparoscopic cholecystectomy.

Demographic details, symptoms and signs, investigations, operative details, complications and follow-ups were evaluated. All patients were seen in the outpatient department within 3 months of initial surgery and every 6 months thereafter. Patients were clinically examined, and liver function tests and ultrasound study were evaluated for each follow-up visit. The study was performed after approval was granted by the Ethics Committee of Tianjin Nankai Hospital.

Statistical Analysis

Data were analyzed by using SPSS 16 (version 20.0.0). The χ2 test, Fisher's exact test and Student's t test were used to compare differences between the data. Multivariable logistic regression analysis by binary logistic regression was used to evaluate factors that favored the diagnosis of XGC with GB cancer and features for open surgery. The validation was performed by the Hosmer-Lemeshow test. A p value <0.05 indicated statistical significance.

Results

The demographics and general clinical features of the patients are shown in table 1. The incidence of XGC was approximately 0.2% of inflammatory biliary diseases of this period. Of the 68 cases, 6 (8.8%) were proven to be GB cancer by histological section after surgery. The CA19-9 levels of XGC and coexistent GB cancer were significantly different (p = 0.0034). There were no significant differences between XGC and GB cancer patients for abdominal pain, fever, jaundice, weight loss, WBC, ALT, total bilirubin and CEA (p > 0.05), as shown in table 2.

Table 1.

Demographics and clinical features of all patients who underwent treatment

Item Patients, n
Demographic characteristics
 Mean age, years 62.6 [20–83]
 Sex, F/M 26/32
Symptoms and signs
 Pain 48 (70.6)
 Fever 19 (27.9)
 Jaundice 13 (19.1)
Associated diseases
 Hyperlipidemia 20 (29.4)
 Hypertension 12 (17.6)
 Diabetes mellitus type 2 5 (7.4)
Tumor markers
 CEA (positive) 12 (5.9)
 CA19-9 (>37 kU/l) 28 (41.2)
Radiologic findings (ultrasound and CT)
 Gallstone 39 (57.4)
 Acute cholecystitis 20 (29.4)
 Chronic cholecystitis 48 (70.6)
 GB carcinoma 8 (11.8)
Surgical procedures
 Open cholecystectomy 26 (38.2)
 Laparoscopic cholecystectomy 22 (32.4)
 Cholecystectomy and biliary tract exploration 9 (13.3)
 Cholecystectomy and partial hepatic wedge resection 6 (8.8)
 Radical correction of GB carcinoma 5 (7.4)
Rate of conversion from laparoscopic to open
 surgery 4.2
Morbidity 3 (4.4)
 Wound infection 2
 Bile leakage 1
Mortality 0
Median follow-up, years 2.8 [1–6]

Values in square brackets indicate ranges and values in parentheses indicate percentages.

Table 2.

Comparison of clinical features between XGC patients with and without GB cancer

Item XGC XGC with GB cancer p value
Patients 62 6
Symptoms and signs
 Abdominal pain 46 (78.0%) 2 (33.3%) 0.1756
 Fever 18 (30.5%) 1 (16.7%) 1.0000
 Jaundice 10 (16.9%) 3 (50%) 0.0789
 Weight loss 15 (25.4%) 2 (33.3%) 0.6352
Laboratory findings
 WBC/mm3 9,326 ± 2,564 8,321 ± 2,896 0.5440
 ALT, U/l 75.2 ± 56.3 64.3 ± 25.9 0.1260
 Total bilirubin, mg/dl 1.9 ± 2.3 2.8 ± 2.6 0.1630
 CA19-9 (>37 kU/l) 22 (35.5%) 6 (100%) 0.0034
 CEA (positive) 10 (16.1%) 2 (33.3%) 0.2846
CT scan findings
 Maximum thickness of GB wall, mm 10.5 ± 4.6 11.2 ± 3.2 0.1530
 Focal thickening of GB wall 17 (27.4%) 5 (83.3%) 0.0117
 Heterogeneous enhancement of the GB wall 39 (62.9%) 3 (50%) 0.6827
 Early enhancement of GB wall 21 (33.9%) 5 (83.3%) 0.0255
 Disrupted mucosal line 26 (41.9%) 4 (66.7%) 0.3937
 Intramural hypoattenuated nodule 32 (51.6%) 3 (50%) 1.0000
 Gallstone 35 (56.4%) 4 (66.7%) 1.0000
 Pericholecystic invasion 30 (48.4%) 5 (83.3%) 0.1978
 Lymph node enlargement (>10 mm) 15 (24.2%) 4 (66.7%) 0.0471
Surgical procedures
 Open cholecystectomy 26 (41.9%) 0 0.0753
 Laparoscopic cholecystectomy 23 (37.1%) 0 0.0892
 Cholecystectomy and biliary tract exploration 9 (14.5%) 0 1.0000
 Cholecystectomy and partial hepatic wedge resection 5 (8.1%) 1 (16.7%) 0.4383
 Radical correction of GB carcinoma 0 5 (83.3%) 0.0001
Morbidity 1 (1.6%) 2 (33.3%) 0.1690
 Wound infection 1 1 NA
 Bile leakage 0 1 NA

NA = Not applicable.

The radiological findings of the XGC and the coexisting GB cancer group showed focal thickening of the GB wall was more frequent in XGC patients with GB cancer than those without (p = 0.0117). For the CT enhancement time, early enhancement of the GB was observed more often in patients with GB cancer than those without (p = 0.0255). Lymph node enlargement (minimum diameter >1 cm) was seen more often in patients with GB cancer than those without (p = 0.0471). There were no significant differences between XGC and GB cancer for maximum thickness of the GB wall, heterogeneous GB enhancement, disrupted mucosal line, intramural hypoattenuated nodule, or accompanied gallstone and pericholecystic invasion, as shown in table 2. Multivariable logistic analysis for GB cancer revealed that CA19-9 (>37 kU/l), focal thickening of the GB wall, early enhancement of the GB wall and lymph node enlargement (>10 mm) were the independent variables for making the diagnosis of XGC with GB cancer (table 3).

Table 3.

Multivariate logistic regression analysis for clinical features in XGC patients with GB cancer

Item Odds ratio 95% CI
CA19-9 (>37 kU/l) 10.256 1.665–21.369
Focal thickening of GB wall 6.354 0.986–10.554
Early enhancement of GB wall 9.446 1.336–20.559
Lymph node enlargement (>10 mm) 15.677 3.999–36.222
Radical correction of GB carcinoma 16.846 5.221–25.336

The surgical procedures for the 68 patients are shown in table 1. Two patients with Mirizzi syndrome that had internal fistula with common bile duct and duodenum were repaired intraoperatively. Of the 8 patients with suspected carcinoma of the GB preoperatively, 2 were definitively diagnosed with XGC from excised tissue during surgery by frozen section histopathologically. Specimens from all 68 patients were examined pathologically, which indicated that 6 patients had coexisting GB cancer. Complications were observed in 3 patients, including 2 with infection of the incision and 1 patient with bile leakage who recovered 4 weeks after the operation. Follow-up lasted 1–6 years. One patient died of a cardiovascular accident, 1 died of primary kidney carcinoma 1 year after the operation, and 6 patients died of GB cancer. The rest of the patients survived.

The clinical data of laparoscopic cholecystectomy and open surgery are listed in table 4. There were significant differences between laparoscopic cholecystectomy and laparatomy for CA19-9 (p = 0.003), maximum thickness of the GB wall (p = 0.03), focal thickening of the GB wall (p = 0.005), heterogeneous enhancement of the GB wall (p = 0.03), early enhancement of the GB wall (p = 0.0001), intramural hypoattenuated nodule (p = 0.0001), pericholecystic invasion (p = 0.0001) and lymph node enlargement (p = 0.0001). The operation time and postoperative hospital stay of the laparoscopic cholecystectomy group were shorter than those of the laparotomy group (p < 0.01), as shown in table 4. Multivariable logistic analysis for open surgery revealed that CA19-9 (>37 kU/l), focal thickening of the GB wall, early enhancement of the GB wall, pericholecystic invasion and lymph node enlargement (>10 mm) were the independent variables for making the choice of open surgery (table 5).

Table 4.

Comparison of patients’ clinical data between laparoscopic cholecystectomy and open operation groups

Item Laparoscopic cholecystectomy group Open operation group p value Total number
Patients 22 46 NA 68
Tumor markers
 CEA (positive) 0 4 (8.7%) 0.300 4
 CA19-9 (>37 kU/l) 22 (9.1%) 28 (60.9%) 0.0001 30
CT scan findings
 Maximum thickness of GB wall, mm 7.3 ± 5.4 11.2 ± 4.3 0.031 NA
 Focal thickening of GB wall 2 (9.1%) 20 (43.5%) 0.005 22
 Heterogeneous enhancement of the GB wall 18 (81.8%) 24 (52.2%) 0.032 42
 Early enhancement of GB wall 1 (4.5%) 25 (54.3%) 0.0001 26
 Disrupted mucosal line 6 (27.3%) 14 (30.4%) 1.0000 20
 Intramural hypoattenuated nodule 19 (86.4%) 16 (34.8%) 0.0001 35
 Gallstone 16 (72.7%) 23 (50%) 0.12 39
 Pericholecystic invasion 2 (9.1%) 32 (69.6%) 0.0001 34
 Lymph node enlargement (>10 mm) 0 19 (41.3%) 0.0001 19
Mean duration of surgery, min 89 135 0.001 NA
Mean postoperative hospital stay, days 7.6 17.5 0.001 NA
Morbidity 0 3 0.54 3

NA = Not applicable.

Table 5.

Multivariate logistic regression analysis of clinical features for open surgery

Item Odds ratio 95% CI
CA19-9 (>37 kU/l) 13.264 3.332–27.889
Maximum thickness of GB wall (>10 mm) 4.776 1.227–9.354
Focal thickening of GB wall 8.897 2.332–15.012
Early enhancement of GB wall 18.553 9.633–30.959
Pericholecystic invasion 8.766 3.334–33.863
Lymph node enlargement (>10 mm) 19.654 6.122–32.778

Adjusted for age and sex by binary logistic regression.

Discussion

In our data, 8.8% of cases were proven to coexist with GB cancer, 57.4% coexisted with stones in the GB and 26.5% had stones stuck in the cyst neck and led to the enlargement of the GB. These findings indicate that XGC formation may be associated with gallstones, which is consistent with the report of Kwon et al. [15]. Most of the patients in this study presented with chronic symptoms and signs, as previously reported [16]. Chronic inflammation in XGC always causes persistent thickening of the GB wall and adhesions to adjacent tissues and organs, and in some cases Mirizzi syndrome is found [17], similar to our findings. Another important finding in our study was that elevated CA19-9 correlated with an increased risk of coexistent GB cancer in XGC patients, so CA19-9 may be considered as a marker for coexisting GB cancer.

Some features highly suggestive of XGC on ultrasound and CT have been reported, including thickening of the GB wall, GB stone shadow, and adhesion to neighboring tissues and organs [18,19]. Owing to the sensitivity of stones and the thickness of the GB wall, ultrasonographic examination shows some clinical values in diagnosing XGC. These reports are consistent with our findings. Where the lesion was concomitant with a stuck stone, enlargement of the GB and fistula formation, XGC was highly suspected. However, other diseases such as GB cancer or adenomyomatosis also present with wall thickening. Radiological findings of ultrasound and CT were used to differentiate XGC from XGC patients with GB cancer. Focal thickening of the GB wall, early enhancement of the GB wall and lymph node enlargement (>10 mm) were the independent factors for making a diagnosis of GB cancer. These characteristics could be helpful in making a correct preoperative diagnosis for XGC.

Frozen sections are necessary in patients in whom the differentiation of XGC from malignant lesions is difficult during surgery [20]. From our experience, when lesions had such features as GB wall focal thickening, suspicious invasion and lymph node enlargement, frozen section was preferred. Microscopically, typical granuloma (consisting of flaky foam cells, rhagiocrine cells, fibroblasts, and inflammatory cells) is the gold standard for the pathological diagnosis of XGC [21,22]. The appropriate selection of surgery strategy should be based on intraoperative frozen section investigation, which may prevent an unnecessary enlargement of the operation.

Owing to the invasiveness and destruction of XGC, surgery should be performed as soon as the diagnosis of XGC is made to prevent the occurrence of complications such as fistula [23], which is consistent with our findings. It is also reported that if there is no suspicion of cancer, percutaneous GB drainage may be an efficient method for the initial treatment of severe cases, which gives the opportunity for an elective cholecystectomy with an excellent outcome [24]; there was no such case, however, in our series. In this study, open surgery was still the main surgical procedure for the treatment of XGC. Fistula repairs were performed on 2 patients with Mirizzi syndrome. Special attention should be paid to the dissection of fistula in these cases. In this study, there were 6 patients who had coexisting adenocarcinoma. Of these, 5 underwent radical corrections of GB carcinoma and 1 patient had cholecystectomy and partial hepatic wedge resection because of its early staging, hence the principle for coexisting cancer was still radical surgery.

A comparison between the clinical data of laparoscopic cholecystectomy and open surgery revealed that elevated CA19-9, focal thickening of the GB wall, early enhancement of the GB wall, pericholecystic invasion, lymph node enlargement and fistula formation were characteristic features of open surgery. These features might be helpful for the surgeon in making a correct decision between laparoscopic and open cholecystectomy surgery, as shown in table5. However, laparoscopic cholecystectomy has a shorter operating time and postoperative hospital stay than open surgery, thereby indicating that in some strictly selected cases, laparoscopic surgery has its advantage over open surgery in treating XGC.

Although XGC is a benign disease with a low mortality rate, patients usually have more postoperative complications including leakage of bile, bile peritonitis, bleeding, hepatic abscess, and infection of incision as was observed in only 3 patients in this study. The factors essential for lowering the complication rate may include adequate preoperative evaluation, accurate intraoperative diagnosis, correct choice of surgery and careful surgical manipulation.

Conclusions

Ultrasound and CT scan were the helpful modalities for preoperative diagnosis. If the malignant situation could not be eliminated, intraoperative frozen section was carried out to differentiate XGC from GB cancer. CA19-9, focal thickening of the GB wall, early enhancement of the GB wall, pericholecystic invasion and lymph node enlargement (>10 mm) were indications for making a decision for open surgery. Open surgery was the main surgical procedure for the treatment of XGC, but for some selected cases laparoscopic cholecystectomy was preferable to open surgery.

References

  • 1.Guzman-Valdivia G. Xanthogranulomatous cholecystitis: 15 years experience. World J Surg. 2004;28:254–257. doi: 10.1007/s00268-003-7161-y. [DOI] [PubMed] [Google Scholar]
  • 2.Solanki RL, Arora HL, Gaur SK, Anand VK, Gupta R. Xanthogranulomatous cholecystitis (XGC): a clinicopathological study of 21 cases. Indian J Pathol Microbiol. 1989;32:256–260. [PubMed] [Google Scholar]
  • 3.Tyagi SP, Maheshwari V, Sahoo P, Tyagi N, Ashraf SM. Chronic granulomatous cholecystitis: a clinicopathological study of 17 cases. J Indian Med Assoc. 1991;89:284–287. [PubMed] [Google Scholar]
  • 4.Houston JP, Collins MC, Cameron I, Reed MW, Parsons MA, Roberts KM. Xanthogranulomatous cholecystitis. Br J Surg. 1994;81:1030–1032. doi: 10.1002/bjs.1800810735. [DOI] [PubMed] [Google Scholar]
  • 5.Eriguchi N, Aoyagi S, Tamae T, Kanazawa N, Nagashima J, Nishimura K, Hamada S, Kawabata M, Kodama T. Xanthogranulomatous cholecystitis. Kurume Med J. 2001;48:219–221. doi: 10.2739/kurumemedj.48.219. [DOI] [PubMed] [Google Scholar]
  • 6.Dixit VK, Prakash A, Gupta A, Pandey M, Gautam A, Kumar M, Shukla VK. Xanthogranulomatous cholecystitis. Dig Dis Sci. 1998;43:940–942. doi: 10.1023/a:1018802028193. [DOI] [PubMed] [Google Scholar]
  • 7.Kumar A, Krishnani N, Saxena R, Kapoor VK, Kaushik SP. Xanthogranulomatous cholecystitis. Ind J Gastroenterol. 1996;15:122–125. [PubMed] [Google Scholar]
  • 8.Rao RV, Kumar A, Sikora SS, Saxena R, Kapoor VK. Xanthogranulomatous cholecystitis: differentiation from associated gall bladder carcinoma. Trop Gastroenterol. 2005;26:31–33. [PubMed] [Google Scholar]
  • 9.McCoy JJ, Jr, Vila R, Petrossian G, McCall RA, Reddy KS. Xanthogranulomatous cholecystitis. Report of two cases. J S C Med Assoc. 1976;72:78–79. [PubMed] [Google Scholar]
  • 10.Guzman-Valdivia G. Xanthogranulomatous cholecystitis in laparoscopic surgery. J Gastrointest Surg. 2005;9:494–497. doi: 10.1016/j.gassur.2004.09.036. [DOI] [PubMed] [Google Scholar]
  • 11.Cárdenas-Lailson LE, Torres-Gómez B, Medina-Sánchez S, Mijares-García JM, Hernández-Calleros J. Epidemiology of xanthogranulomatous cholecystitis (in Spanish) Cir Cir. 2005;73:19–23. [PubMed] [Google Scholar]
  • 12.Afifi El-Sayed M, Juma TH. Primary cystic duct carcinoma. Med Princ Pract. 1998;7:147–149. [Google Scholar]
  • 13.Kitagawa S, Nakagawa M, Yamada T, Mori Y, Simizu H, Rin S, Kurumaya H. Clinico-pathological study of xanthogranulomatous cholecystitis (in Japanese) Nihon Geka Gakkai Zasshi. 1990;91:1001–1010. [PubMed] [Google Scholar]
  • 14.Roberts KM, Parsons MA. Xanthogranulomatous cholecystitis: clinicopathological study of 13 cases. J Clin Pathol. 1987;40:412–417. doi: 10.1136/jcp.40.4.412. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 15.Kwon AH, Matsui Y, Uemura Y. Surgical procedures and histopathologic findings for patients with xanthogranulomatous cholecystitis. J Am Coll Surg. 2004;199:204–210. doi: 10.1016/j.jamcollsurg.2004.03.018. [DOI] [PubMed] [Google Scholar]
  • 16.Reaño G, Sanchez J, Ruiz E, Celis J, Payet E, Berrospi F, Chavez I, Young F, Doimi F. Xanthogranulomatous cholecystitis: retrospective analysis of 6 cases (in Spanish) Rev Gastroenterol Peru. 2005;25:93–100. [PubMed] [Google Scholar]
  • 17.Lee KC, Yamazaki O, Horii K, Hamba H, Higaki I, Hirata S, Inoue T. Mirizzi syndrome caused by xanthogranulomatous cholecystitis: report of a case. Surg Today. 1997;27:757–761. doi: 10.1007/BF02384992. [DOI] [PubMed] [Google Scholar]
  • 18.Kim PN, Ha HK, Kim YH, Lee MG, Kim MH, Auh YH. US findings of xanthogranulomatous cholecystitis. Clin Radiol. 1998;53:290–292. doi: 10.1016/s0009-9260(98)80129-3. [DOI] [PubMed] [Google Scholar]
  • 19.Chun KA, Ha HK, Yu ES, Shinn KS, Kim KW, Lee DH, Kang SW, Auh YH. Xanthogranulomatous cholecystitis: CT features with emphasis on differentiation from gallbladder carcinoma. Radiology. 1997;203:93–97. doi: 10.1148/radiology.203.1.9122422. [DOI] [PubMed] [Google Scholar]
  • 20.Pinocy J, Lange A, König C, Kaiserling E, Becker HD, Kröber SM. Xanthogranulomatous cholecystitis resembling carcinoma with extensive tumorous infiltration of the liver and colon. Langenbecks Arch Surg. 2003;388:48–51. doi: 10.1007/s00423-003-0362-x. [DOI] [PubMed] [Google Scholar]
  • 21.Hsu C, Hurwitz JL, Schuss A, Katz DS. Radiology-Pathology Conference: xanthogranulomatous cholecystitis. Clin Imaging. 2003;27:421–425. doi: 10.1016/s0899-7071(02)00589-2. [DOI] [PubMed] [Google Scholar]
  • 22.Krishnani N, Dhingra S, Kapoor S, Pandey R. Cytopathologic diagnosis of xanthogranulomatous cholecystitis and coexistent lesions. A prospective study of 31 cases. Acta Cytol. 2007;51:37–41. doi: 10.1159/000325680. [DOI] [PubMed] [Google Scholar]
  • 23.Srinivas GN, Sinha S, Ryley N, Houghton PW. Perfidious gallbladders – a diagnostic dilemma with xanthogranulomatous cholecystitis. Ann R Coll Surg Engl. 2007;89:168–172. doi: 10.1308/003588407X155833. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 24.Psarras K, Baltatzis ME, Symeonidis N, Pavlidis ET, Miha A, Pavlidis TE, Sakantamis AK. A severe case of xanthogranulomatous cholecystitis along with a review of CT indications for nonoperative management including percutaneous drainage. Surg Laparosc Endosc Percutan Tech. 2012;22:e42–e44. doi: 10.1097/SLE.0b013e318241bf29. [DOI] [PubMed] [Google Scholar]

Articles from Medical Principles and Practice are provided here courtesy of Karger Publishers

RESOURCES