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 » Introduction
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  Table of Contents  
Year : 2012  |  Volume : 49  |  Issue : 3  |  Page : 303-308

Biological behavior and disease pattern of carcinoma gallbladder shown on 64-slice CT scanner: A hospital-based retrospective observational study and our experience

1 Department of Radiodiagnosis and Imaging, Institute of Medical Sciences, BHU, Varanasi, India
2 Department of Surgery, Institute of Medical Sciences, BHU, Varanasi, India

Date of Web Publication12-Dec-2012

Correspondence Address:
AND Dwivedi
Department of Radiodiagnosis and Imaging, Institute of Medical Sciences, BHU, Varanasi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0019-509X.104496

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 » Abstract 

Purpose: The aim of this diagnostic observational study was to assess the spread and biological behavior of gallbladder cancer using 64-slice computerized tomography (CT) scanner in this particular geographic belt (eastern Uttar Pradesh, western Bihar, and northern Madhya Pradesh provinces of North India). Indians are ethnically and culturally different from their Western counterparts among whom the incidence of this disease is comparatively low. Subjects and Methods: After systemic examination, all patients (87) were subjected to ultrasonographic examination. All cases were histopathologically proven. Confirmed cases were subjected to volumetric CT examination of abdomen and pelvis, plain, post contrast and delayed phase. Results: Majority of the cases were adenocarcinoma. There was female preponderance with majority belonging to fifth and sixth decades. Commonest presentation was diffuse, irregular, enhancing wall thickening in 49.4%. Majority had invasion of liver parenchyma (74.7%). Cholelithiasis was seen in 48.3% cases. Invasion of biliary radicals was high (13.8-18.4%). Eleven cases had invasion of portal vein and tumor thrombus, with hepatic artery invasion in one case. In two cases, both hepatic artery and portal vein invasion was seen. Portal and peripancreatic nodal metastasis was seen in 58.5%. Distant metastasis was reported. Conclusion: Few studies involving the Indian population have attempted to use multi-row detector CT to define the biological behavior of carcinoma gallbladder. The opinion whether the pathology is operable or non-operable can reasonably be given. This large-scale, single-center study gives insight about the epidemiology and biological behavior of carcinoma gallbladder.

Keywords: Carcinoma gall-bladder; multislice computerised tomography; biological behaviour

How to cite this article:
Dwivedi A, Pandey M, Shukla R C, Shukla V K, Gaharwar S, Maurya B N. Biological behavior and disease pattern of carcinoma gallbladder shown on 64-slice CT scanner: A hospital-based retrospective observational study and our experience. Indian J Cancer 2012;49:303-8

How to cite this URL:
Dwivedi A, Pandey M, Shukla R C, Shukla V K, Gaharwar S, Maurya B N. Biological behavior and disease pattern of carcinoma gallbladder shown on 64-slice CT scanner: A hospital-based retrospective observational study and our experience. Indian J Cancer [serial online] 2012 [cited 2022 Oct 2];49:303-8. Available from:

 » Introduction Top

Carcinoma of the gallbladder (Ca GB) is the most common malignancy of the biliary tract and the third most common gastrointestinal malignancy in and around Varanasi region of India. [1] Within the Indian population, it is much higher in northern [2] cities. The incidence of GB cancer (GBC) varies in different parts of the world. Approximately 6500 new cases of GBC are reported annually in the United States, with a 4:1 female:male ratio and the peak incidence occurring in the sixth and seventh decades of life. This sex predilection is thought to be related to the higher incidence of cholelithiasis in women, since 70-80% of GBCs are associated with gallstones. [3],[4],[5] Clinical and radiologic features of GBC overlap with those seen in cholelithiasis and cholecystitis, which often causes a delay in diagnosis until the disease is in the late stage. Ultrasound (US) is the primary imaging modality of investigation. Three patterns have been described on US. The GB fossa is replaced by a heterogeneous mass with internal areas of necrosis; or there may be diffuse, irregular, and asymmetrical wall thickening; or less commonly, a polypoidal, fungating intraluminal mass is seen. The diagnostic accuracy of USG in Ca GB exceeds 80%, but it has limitations in tumor staging. Correct preoperative diagnosis has improved considerably with the use of newer imaging techniques. [6],[7],[8] Epidemiological studies worldwide have implicated dietary factors in the development of GBC. [9],[10],[11],[12] The ecological evidences indicate considerable geographic variation in the incidence of GBC. Variations in the incidence in various populations might be partly determined by their dietary variations. Another predisposing condition is the porcelain GB. [13] Other less frequent associations include inflammatory bowel disease and familial polyposis coli. [14] Ethnic differentials and cultural variations of this disease suggest major environmental influences, rendering the etiology of GBC obscure and hazy. [15] The clinical presentation of GBC includes right upper quadrant pain, anorexia, weight loss, and jaundice. Often, the patient's condition is clinically indistinguishable from that seen in acute or chronic cholecystitis. In this retrospective observational study, the behavior and spread of GBC is interpreted. The knowledge of the patterns of appearance of the primary tumor and familiarity with its typical modes of spread from a distinct geographic belt will be helpful to shed light on the biological behavior of this entity.

 » Subjects and Methods Top

All patients underwent detailed systemic examination. Next they were subjected to ultrasonographic examination using color flow (Philips IU 22). Cases suspicious of primary carcinoma of GB were subjected to histopathologic examination. Only proven cases by fine needle aspiration cytology/ biopsy (FNAC/FNAB) were further subjected to volumetric computed tomographic (CT) examination of abdomen and pelvis, plain, post contrast and delayed phase (64-slice VCT scanner GE). All patients were screened to rule out bleeding disorders and coagulopathies. Test dose of non-ionic contrast was given to lower the risk of adverse contrast reactions. Pertinent clinical history regarding the risk factors was taken. Meticulous note was made of the primary pathology and locoregional and distant spread of disease. In cases where warranted additional scans of brain and chest were obtained, the images were independently analyzed by two experienced radiologists of the same department who were blinded of each other's findings. In case of difference in opinion, common consensus was taken.

 » Results Top

Eighty percent of cases were adenocarcinoma and the remaining 20% cases were squamous cell carcinoma. There was female preponderance in our study (4:1). Majority of the patients belonged to fifth and sixth decades. Focal irregular GB wall thickening was seen in 17.2% (n = 15), diffuse irregular enhancing wall thickening in 49.4% (n = 43) [Figure 1], and mass was seen replacing the GB fossa with non-visualization of GB in 33.3% (n = 29). In 43.7% (n = 38), focal mass lesion was seen arising from GB, with intraluminal component of mass in 4 (4.5%) patients. Size of the mass varied widely; taking the longest axis of mass into account, 23 (33.8%) cases had size less than 4 cm, 27 (39.7%) between 4 and 8 cm, 13 (19.1%) were of 8-12 cm, with 5 (7.4%) being more than 12 cm. Intralesional low attenuation non-enhancing areas suggestive of necrosis were seen in 38 (43.7%) cases. Out of 87 patients, 74.7% (n = 65) had invasion of liver parenchyma [Figure 2]. Mass lesion was seen closely abutting adjacent hepatic segments with relatively maintained fat plane in 7 (8%) cases. Associated cholelithiasis was seen in 48.3% (n = 42) cases [Figure 1], [Figure 2]. Extensive pericholecystic fat stranding s/o locoregional spread was seen in 13.8% (n = 12) cases, with mild fat stranding in 72.4% (n = 63) cases. Satellite/metastatic lesions in liver were seen in 34.5% cases. 8% (n = 7) had invasion of lesser sac up to bed of stomach. Extension of the lesion to porta hepatis with maintained fat plane was seen in 34.5% (n = 30) cases. Invasion of the confluence of right and left hepatic ducts was seen in 16.1% (n = 14) with proximal intrahepatic biliary radical dilatation (IHBRD). Infiltration of common hepatic ducts with visualization of confluence was observed in 14.9% (n = 13) cases; however, involvement of both confluence and extension along intrahepatic biliary radicals and common hepatic duct (CHD) up to cystic duct was seen in 13.8% (n = 12) cases [Figure 3]. In 2 (2.3%) cases, fat plane with common ducts appeared lost, however, with no proximal IHBRD. In 18.4% (n = 16) cases, invasion of common bile duct (CBD) was seen with or without CHD involvement. 33.3% (n = 29) showed involvement of hepatic flexure and mesocolon, as demonstrated by eccentric or circumferential wall thickening [Figure 4]; however, in 2 (2.3%) cases, GB mass lesion was seen closely abutting hepatic flexure with no obvious eccentric wall thickening. Eleven (12.6%) cases had invasion of portal vein and tumor thrombus, with hepatic artery invasion in 1 (1.1%) case. In 2 (2.2%) cases, both hepatic artery and portal vein invasion were seen with luminal narrowing and intraluminal enhancing filling defects, suggestive of tumor thrombus. In 41.4% (n = 36) cases, lesion was seen closely abutting lateral wall of second part of duodenum with relatively maintained fat plane. Obvious infiltration as demonstrated by eccentric wall thickening or intraluminal growth causing luminal obstruction was observed in 48.3% (n = 42) cases [Figure 5]. Circumferential involvement was seen in 1 (1.1%) case. Extension of the lesion to involve pyloric antrum of stomach was seen in 9.2% cases. Portal and peripancreatic nodal metastasis was seen in 58.5% (n = 51) cases [Figure 1], with 18 (20.6%) cases showing enlarged, mild enhancing retroperitoneal lymph nodes, a few showing conglomeration and necrosis. Lung metastasis was seen in 3.4% (n = 3) cases, which were later confirmed histopathologically. Bone metastasis was seen in 1.1% (n = 1) case. Ascites was seen in 31% (n = 27) of cases, with 19.5% (n = 17) cases showing discrete, irregular, enhancing soft tissue density lesions in the peritoneal cavity or along the peritoneal lining, with or without omental thickening and stranding s/o deposits [Figure 6]. In 2.3% (n = 2) cases, infiltration of anterior parietal wall in right hypochondrium was seen contiguous with the main mass lesion [Table 1].
Figure 1: Diffuse, irregular GB wall thickening with cholelithiasis. Enlarged portal and peripancreatic nodes with areas of necrosis seen

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Figure 2: Irregular GB mass lesion seen arising from fundus and body with invasion of seg IVb and V of liver. Laminated hyperdense focus s/o calculus seen in GB lumen

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Figure 3: GB mass lesion seen invading CHD and CBD with proximal IHBRD

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Figure 4: Invasion of hepatic flexure and mesocolon

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Figure 5: GB mass lesion extending and circumferentially invading second part of duodenum and closely abutting head of pancreas with relatively maintained fat plane

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Figure 6: Omental deposits in left paracolic gutter

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Table 1: loco-regional and distant invasive spread of carcinoma gall bladder

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 » Discussion Top

Ca GB has been notorious to have poor prognosis with overall 5-year survival rate reported to be 4%. [16] It is relatively rare in the West; a high incidence has been noted in various ethnic groups and populations. [17] It is a common occurrence in this geographic belt (eastern Uttar Pradesh, western Bihar, and northern Madhya Pradesh provinces of North India), constituting 4.4% of all malignancies. [1] Etiology of GBC remains obscure although cholelithiasis, [3],[4],[5] cholecystitis, [18] racial and ethnic factors, blood groups, carcinogens, lipid peroxidation products, benign tumors, and secondary bile acids have been implicated as possible causes. [19],[20],[21],[22] We noted 48.3% of cases to have associated cholelithiasis. Other studies have reported similar association with gall stones. [3],[4],[5] Majority of patients belong to fifth and sixth decades, with a male to female ratio of 1:4. Various workers have reported the age of peak incidence to be in the seventh decade of life. [23],[24] The most common CT finding in GBC reported in various studies is a mass that fills most of an enlarged and deformed GB. [16] These masses are typically low in attenuation with variable enhancement. Polypoid masses are the second most common presentation; differentiation from benign polyps is based on size, with the polypoid masses typically larger than 1 cm. Ancillary findings on CT include gall stones, wall calcification, dilated biliary radicals, hepatic metastasis, lymphadenopathy, ascites, and peritoneal deposits, and extension into stomach, duodenum, colon, or pancreas. The lymph nodes may show necrotic center.

We came across polypoidal masses ranging from 4 cm to more than 12 cm. GBC can present as asymmetric GB wall thickening that may be difficult to distinguish from the scarred GB wall seen in chronic cholecystitis. In our study, the commonest presentation was diffuse, irregular, enhancing wall thickening in 49.4% (n = 43), followed by focal mass lesion arising from GB (43.7%), with intraluminal component. Other signs are the result of disease progression, including biliary obstruction and liver involvement, features that are commonly confused with carcinoma of the pancreas or even liver. Ca GB frequently spreads by direct extension to the liver, although lymph node involvement is also common. In our study, 65 patients (74.7%) had obvious hepatic parenchymal invasion. Portal and peripancreatic adenopathy was as high as 58.1% in our study. Vascular metastases are much less frequent, but can occur. We found invasion of portal vein in 11 cases (12.6 %). Biliary obstruction can be due to either lymphadenopathy or direct spread to the biliary radicals. We came across large number of cases with direct invasion of biliary radicals (13.8-18.4%). Advanced stage disease spreads to the gastrointestinal tract, omentum, and pancreas. We found a high percentage of patients with invasion of duodenum (41.4-48.3%). Invasion of hepatic flexure was reported in 33.3% patients. Peritoneal deposits were found in 19.5% and ascites in 31% of patients. Distant metastasis to lung was seen in three cases, whereas bone metastasis was present in one case. In a study [25] on 69 patients of GBC who underwent exploratory laparotomy, 76.8% had liver involvement, 71% had lymph node involvement, and 24.6% had peritoneal deposits. Preoperative staging using multislice CT has had an overall accuracy ranging from 83 to 86%, [26],[27] although the ability to identify early-stage disease on CT remains disappointing. Our study stresses the fact that by the time majority of cases are diagnosed, they are no longer resectable. [28],[29],[30] Endoscopic USG can depict the depth of tumor invasion and can characterize polypoidal lesions. Dynamic contrast-enhanced CT or magnetic resonance imaging (MRI) with Magnetic resonance cholangiopancreatography (MRCP) is useful in staging. MRCP depicts biliary involvement better than USG or CT and can differentiate adenomyomatosis or chronic cholecystitis from Ca GB. Radiologically, direct invasion of the liver parenchyma, invasion of the duodenum, stomach, colon, and pancreas, hematogenous metastases to the liver, peritoneal dissemination, biliary obstruction at the time of presentation typically due to direct tumor invasion of the hepatoduodenal ligament, often at the porta hepatis, metastatic spread to the lymph nodes, and vascular invasion are the findings which make curative surgery difficult and augur poor prognosis. (Unresectable in our study does not include wedge extended cholecystectomy and radical surgery which is limited to Ib or low stage II.)

Most of the time, the disease is diagnosed in advanced stage, making the prognosis poor. In a study, the stage distribution according to the TNM system revealed 6, 10, 12, and 53 patients at stages I-IV, respectively. The curative resection rate was 22.2%. Stage-dependent surgical procedures resulted in cumulative survival rates of 33.3%for stages I and II, 8.3% for stage III, and 1.9% for stage IV. The overall prognosis was significantly determined by metastatic spread to the lymph nodes. [28]

Incidence of Ca GB is higher in this geographic belt. Diagnostic efforts should focus on detecting the low stages I and II of GBC. Studies from India suggest that cases from this geographic belt are more aggressive. [31]

 » Conclusions Top

This retrospective diagnostic observational study of 87 patients from a single hospital gives valuable information about the spread and biological behavior of Ca GB, its epidemiology, and role of multi-scanner CT in defining this disease. Indians are ethnically and culturally different from their Western counterparts among whom the incidence of this disease is comparatively low.

 » References Top

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3.Kapoor VK, Mc Michael AJ. Gall Bladder Cancer: An 'Indian" disease. Natl Med J India 2003;16:209-13.  Back to cited text no. 3
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10.Strom BL, Soloway RD, Rioz-Palenz JL, Rodriguez-Martinez HA, West SL, Kinman JL, et al. Risk factors for gallbladder cancer. Cancer 1995;76:1747-56.  Back to cited text no. 10
11.Zatonski WA, Lowenfels AB, Boyle P, Maisonneuve P, Bruno De Mesquita HB, Ghadirian P, et al. Epidemiologic aspects of gall bladder cancer. A case control study of the search programme of the International agency for Research on Cancer. J Natl Cancer Inst 1997;89:1132-8.  Back to cited text no. 11
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13.Waterhouse J, Muir C, Correa P, Powell J, editors. Cancer incidence in five continents, Vol 3, IARC Publication No. 15. Lyon: IARC; 1976.  Back to cited text no. 13
14.Zeman RK, Burrell Ml, editors. Gallbladder and Bile Duct Imaging: A clinical radiologic approach. New York: Churchill Livingstone; 1987. p. 292-307.  Back to cited text no. 14
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16.Furlan A, Ferris JV, Hosseinzadeh K, Borhani AA. Gallbladder carcinoma update: Multimodality imaging evaluation, staging and treatment options. AJR Am J Roentgenol 2008;191:1440-7.  Back to cited text no. 16
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18.Piehler JM, crichlow RW. Primary carcinoma of gall bladder. A collective review. Surg Gynecol Obstet 1978;147:929-42.  Back to cited text no. 18
19.Pandey M, Gautam A, Shukla VK. ABO and Rh blood groups in patients with cholelithiasis and carcinoma of the gall bladder. Br Med J 1995;310:1639.  Back to cited text no. 19
20.Shukla VK, Shukla PK, Pandey M, Rao BR, Roy SK. Lipid peroxidation products in bile from patients with carcinoma of the gall bladder. A preliminary study. J Surg Oncol 1994;54:258-62.  Back to cited text no. 20
21.Pandey M, Shukla PK, Gautam A, Rao BR, Roy SK, Shukla VK. Increased peroxidation of polyunsaturated fatty acids: A possible link in the peroxidant pathogenesis of carcinoma of the gallbladder with cholelithiasis. Proc. UICC XVI International Cancer Congress, Monduzzi Editore, Roma, Italy 1994; 3: 2055-8..  Back to cited text no. 21
22.Shukla VK, Tiwari SC, Roy SK. Biliary bile acids in cholelithiasis and carcinoma of the gall bladder. Eur J Cancer Prev 1993;2:155-60.  Back to cited text no. 22
23.Kaplan EL, Meier P. Nonparametric estimation from incomplete observations. J Am Stat Assoc 1958;53:457-81.  Back to cited text no. 23
24.Silk YN, Dougras HO Jr, Nava HR, Driscoll DL, Tartarian G. Carcinoma of the gall bladder. The Rosewerr Park experience. Ann Surg 1989;210:751-7.  Back to cited text no. 24
25.Pandey M, Pathak AK, Gautam A, Aryya NC, Shukla VK. Digestive diseases and sciences. Dig Dis Sci 2001;46:1145-51.  Back to cited text no. 25
26.Yoshimitsu K, Honda H, Shinozaki K, Aibe H, Kuroiwa T, Irie H, et al. Helical CT of the local spread of carcinoma of the gall bladder: Evaluation of the gall bladder: Evaluation according to the TNM system in patients who underwent surgical resection. AJR Am J Roentgenol 2002;179:423-8.  Back to cited text no. 26
27.Grand D, Horton MK, Fishman EK. CT of the gall bladder: Spectrum of disease. AJR Am J Roentgenol 2004;183:163-70.  Back to cited text no. 27
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29.Fong Y, Wagman L, Gonen M, Crawford J, Reed W, Swanson R, et al. Evidence-based gallbladder cancer staging: Changing cancer staging by analysis of data from the National Cancer Database. Ann Surg 2006;243:767.  Back to cited text no. 29
30.Kiran RP, Pokala N, Dudrick SJ. Incidence pattern and survival for gallbladder cancer over three decades--an analysis of 10301 patients. Ann Surg Oncol 2007;14:827.  Back to cited text no. 30
31.Kapoor VK, Pradeep R, Haribhakti SP, Sikora SS, Kaushik SP. Early carcinoma a of gall bladder: An elusive disease. J Surg Oncol 1996;62:284-7.  Back to cited text no. 31


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