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• W2308906118 abstract "Question: A 53-year-old man from Martinique (Caribbean Islands) with suspected gallbladder cancer was referred to our department. The patient had been examined with abdominal Doppler ultrasonography after 2 episodes of acute cholecystitis within the previous 5 months. The Doppler ultrasonography results showed almost complete hyperechogenicity of the acalculous gallbladder due to wall thickening. However, there was no ultrasonographic Murphy’s sign (Figure A). Liver function tests were normal. The patient had normal abdominal computed tomography (CT) results 6 months before the first episode of cholecystitis. The scan had been performed after complaints of abdominal discomfort. The patient had no symptoms at the referral examination. However, he reported decreased appetite and recent weight loss of 4 kg. The physical examination was normal. The following laboratory parameters were within normal limits: complete peripheral blood cell count, kidney and liver function tests, and tumor markers (CA 19-9, CEA). The screening results for viruses B, C, and human immunodeficiency virus were negative. The abdominal CT scan showed the gallbladder wall was thickened (12 mm; Figure B), contained punctate calcifications and was disrupted (Figure C) by a lesion protruding into both the gallbladder and the contiguous liver parenchyma (Figure B). The scan also showed there was increased density of the perivesicular fat. Furthermore, 2 hilar lymph nodes were enlarged (7 mm in diameter; Figure B). There were no gallbladder stones and no abnormalities were found. Additionally, the spleen, abdominal vessels, and peritoneum were normal. There was no positron emission tomography-CT examination or magnetic resonance cholangiography performed. What is the diagnosis? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI. Ultrasonography examination showed an acalculous gallbladder with wall thickening (Figure A, thin arrow) with gallbladder lesion protruding into the gallbladder (Figure A, thick arrow). CT scan revealed a tissular gallbladder lesion protruding into both the gallbladder and the contiguous liver parenchyma (Figure B, arrow). Punctuate calcification of the gallbladder wall (Figure C, thin arrow), densified perivesicular fat (Figure C, thick arrow), and an enlarged lymph node (Figure C, interrupted arrow). The clinical and cross-imaging findings suggested the differential diagnosis of gallbladder carcinoma was more probable than cholecystitis and xanthogranulomatous cholecystitis. The initial staging laparoscopy excluded the presence of peritoneal and surface liver metastases. Tense retraction of right colon, duodenum, and omentum to the inferior aspect of the liver hampered the gallbladder exploration. Therefore, the laparoscopy was converted to open surgery. Intraoperative Doppler ultrasound examination of the liver confirmed the preoperative imaging findings, liver vessels patency, and excluded the presence of a deep intrahepatic lesion. Radical cholecystectomy was straightforward and involved en bloc resection of omentum adhesions and lymph node dissection. The surgical specimen pathology ruled out malignancy and revealed combined acute and chronic cholecystitis with dense fibrosis and a mixed inflammatory process consisting of numerous eosinophils (Figure D, encircled), which were positively identified by hematoxylin–eosin–saffron staining. Small and oval structures with a sharp lateral spine that corresponded with Schistosoma eggs (Figure D, arrow) were identified in the gallbladder wall. There were no eggs in the lymph nodes. The bile culture was negative for bacterial or fungal infections. The postoperative course was uneventful, and the patient was discharged on day 5. He received a single dose of 2.4 mg of Praziquantel (Biltricide) 15 days after surgery. There are >207 million people infected with schistosomiasis (85% live in Africa). Additionally, there are an estimated 700 million people at risk of infection in 76 countries where the disease is endemic owing to exposure to infested water. There are 200,000 deaths worldwide attributed to schistosomiasis annually. The majority of these deaths are related to hepatobiliary schistosomiasis1Shaker Y. Samy N. Ashour E. Hepatobiliary schistosomiasis.J Clin Transl Hepatol. 2014; 2: 212-216Crossref PubMed Scopus (31) Google Scholar and rupture of esophageal varices. Since Rappaport reported the first case in 1975, gallstones (the most common cause of cholecystitis) were present in 6 of 9 Schistosoma cholecystitis patients reported so far.2Rappaport I. Albukerk J. Schneider I.J. Schistosomal cholecystitis.Arch Pathol. 1975; 99: 227-228PubMed Google Scholar It remains unclear whether schistosomal eggs deposited in the wall of the gallbladder per se trigger a clinical manifestation of cholecystitis.3Richter J. Evolution of schistosomiasis-induced pathology after therapy and interruption of exposure to schistosomes: a review of ultrasonographic studies.Acta Trop. 2000; 77: 111-131Crossref PubMed Scopus (78) Google Scholar The clinical presentation in our patient, including the lack of gallstones, chronology of events, and pathologic findings, strongly support the association between cholecystitis and schistosomal infection. The recurrence of previously controlled diseases in Western countries is a result of more affordable international travel, global trade and commerce, the export of labor, and population migration. Thus, as in the present case, doctors should determine the travel history of their patients to remember or “relearn” the key aspects of pathogens and include them in the differential diagnosis." @default.
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• W2308906118 date "2016-05-01" @default.
• W2308906118 modified "2023-09-30" @default.
• W2308906118 title "An Unusual Cause of Cholecystitis" @default.
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• W2308906118 doi "https://doi.org/10.1053/j.gastro.2015.12.009" @default.
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