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Case Reports in Infectious Diseases
Volume 2013, Article ID 407182, 4 pages
http://dx.doi.org/10.1155/2013/407182
Case Report

Acute Acalculous Cholecystitis due to Viral Hepatitis A

1Department of Infectious Disease, Diyarbakir Training and Research Hospital, 21000 Diyarbakir, Turkey
2Department of Hematology, Diyarbakir Training and Research Hospital, 21000 Diyarbakir, Turkey
3Department of General Surgery, Diyarbakir Training and Research Hospital, 21000 Diyarbakir, Turkey
4Department of Gastroenterology, Faculty of Medicine, Bezmialem University, 34000 Istanbul, Turkey
5Department of General Surgery, Faculty of Medicine, Dicle University, 21000 Diyarbakir, Turkey
6Department of Microbiology, Diyarbakir Training and Research Hospital, 21000 Diyarbakir, Turkey
7Department of Radiology, Diyarbakir Training and Research Hospital, 21000 Diyarbakir, Turkey

Received 11 June 2013; Accepted 6 August 2013

Academic Editors: L. M. Bush, M. Ghate, J. Koirala, and A. C. Sena

Copyright © 2013 Safak Kaya et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Inflammation of the gallbladder without evidence of calculi is known as acute acalculous cholecystitis (AAC). AAC is frequently associated with gangrene, perforation, and empyema. Due to these associated complications, AAC can be associated with high morbidity and mortality. Medical or surgical treatments can be chosen according to the general condition of the patient, underlying disease and agent. Particularly in acute acalculous cholecystitis cases, early diagnosis and early medical treatment have a positive effect on the patient and protect them from surgical trauma. ACC is a rare complication of acute viral hepatitis A. Herein, we present an adult patient of acalculous cholecystitis due to acute viral hepatitis A. She responded to the conservative management.

1. Introduction

Hepatitis A is generally an acute, self-limited infection of the liver by an enterically transmitted hepatitis A virus (HAV). Infection may be asymptomatic or result in acute hepatitis, and rarely, fulminant hepatitis can ensue. Recognized complications of hepatitis A include cholestasis, prolonged and relapsing disease, fulminant hepatitis, and triggering of chronic active autoimmune extrahepatic disease [1]. Acute acalculous cholecystitis (ACC) is a rare complication of acute viral hepatitis [2]. Although the origin is obscure, demonstrated invasion of the gallbladder and bile duct epithelium by HAV and cell-mediated immunologic response have been proposed in the pathogenesis of HAV infection induced cholecystitis [3, 4]. Herein, we report a case of acalculous cholecystitis due to acute viral hepatitis A along with the published literature.

2. Case Report

A 31-year-old female patient was admitted to the hematology department because of pancytopenia in February 2013. She had nausea, loss of appetite, back and joint pain, darkening of urine, and abdominal pain for 10 days. Her medical history was unremarkable. There was no history of medication or drug abuse. Physical examination showed body temperature of 37.5°C, heart rate of 92/minute, and blood pressure of 110/60 mmHg. Scleral icterus was present. The right side of the abdomen was tender with painful fullness in the right hypochondrium (a positive Murphy’s sign). Her liver was painful and palpable 3 cm under right costal margin. After examination, she was referred to general surgery with a diagnosis of acute cholecystitis, and surgery was planned. Laboratory investigations revealed microcytic anemia, leukopenia, and thrombocytopenia, elevated levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma glutamyltransferase (GGT), and total serum bilirubin (Table 1). She had iron deficiency anemia (reduced levels of serum iron and serum ferritin with increased total iron binding capacity (TIBC)). Prothrombin time, C-reactive protein, erythrocyte sedimentation rate, and urinalysis were normal. Brucella standard tube agglutination (STA) test was negative. Abdominal ultrasound revealed hydropic gallbladder without calculus, thickened gallbladder wall (14 mm), perivesical liquid accumulation, and hepatosplenomegaly. Serology for viral hepatitis suggested acute hepatitis A infection (anti-HAV IgM (+) and anti-HAV IgG (+)) and was negative for other causes (HBsAg (−), anti-HBcIgM (−), and anti-HCV (−)). The diagnosis was acute viral acalculous cholecystitis. Patient was treated with supportive therapy of intravenous (I.V.) fluid, I.V. metoclopramide, and I.V. ranitidin with low fat and high carbohydrate diet. Her symptoms regressed within four days, and the biochemical markers including serum ALT, AST, and total bilirubin levels decreased (Table 1). The gallbladder wall thickness was regressed to 3.5 mm, and no surgical intervention was required. She was discharged on the 8th day of admission. During the followup, she was in good condition without any complaints with improved biochemical tests in March 2013.

tab1
Table 1: Laboratory findings of the patient during the follow-up period (ALP: alkaline phosphatase; ALT: alanine transaminase; AST: aspartate transaminase; GGT: gamma-glutamyltransferase; Hb: hemoglobin; WBC: white blood cells).

3. Discussion

Inflammation of the gallbladder without evidence of calculi is known as ACC [5]. AAC is frequently associated with gangrene, perforation, and empyema. Due to these associated complications, AAC can be associated with high morbidity and mortality [6]. The pathophysiology of the acalculous cholecystitis during acute viral hepatitis is not clear: hypoalbuminemia, local extension of the hepatic inflammatory process, and elevated portal pressure all could be reflected as the edema of the gallbladder wall [7]. The diagnosis is suspected clinically and then confirmed through ultrasound. The ultrasonographic criteria for diagnosing AAC include (1) gallbladder distention; (2) thickening of the gallbladder wall (>3.5 mm); (3) no acoustic shadow or biliary sludge; (4) perivesical liquid accumulation; and (5) no dilatation of the intra- and extrahepatic bile ducts. The sensitivity of ultrasound for detection of AAC is 88.9%, and the specificity and accuracy are 97.8 and 96.1%, respectively. Treatment is initially conservative, with indications for urgent cholecystectomy in cases of gangrene or perforation of the gallbladder wall [8]. HAV induced AAC has been very rarely reported. Indeed, by searching the MEDLINE database for published articles using the words “acalculous cholecystitis” and “viral hepatitis A,” we identified only 20 reports in the literature, including twenty-two patients with ACC due to acute viral hepatitis A [2, 3, 824] of which fifteen had appropriate information for analysis (Table 2). Four of these publications were in adults [9, 11, 13, 22].

tab2
Table 2: Review of the clinical presentation, ultrasound findings with treatment modalities, and outcomes of patients with acalculous cholecystitis due to viral hepatitis A published in the literature (F: female; M: male; NA: not available; USG: ultrasonography).

Ozaras et al. [11] described two adult patients (28 and 20 years of age) with acute cholecystitis due to HAV infection. Both patients had acute HAV infection documented by biochemical, serologic, and clinical features. Cholecystitis developed during the course of the disease but did not lead to an acute phase response and required neither administration of antibiotics nor surgical intervention. With a close followup, both of the patients had fully recovered. Melero Ferrer and coworkers [14] reported a 39-year-old woman with fever, abdominal pain, and moderately elevated transaminase levels who developed jaundice and peritoneal irritation. Diagnosis of acute cholecystitis was given by abdominal ultrasound and magnetic resonance imaging. The patient underwent surgery. In the postoperative period, positive IgM antibody titers for HAV were obtained, confirming the diagnosis of HAV infection. Black and colleagues [2] reported a 6-year-old child presenting with gangrenous cholecystitis due to HAV infection. Ultrasonography showed a slightly distended gallbladder containing echogenic bile. Laparotomy revealed a distended gallbladder with areas of necrosis. Dalgic et al. [12] presented case had acute HAV infection with acalculous cholecystitis developed during the course of the disease. Surgical intervention was not required in their patient. A repeated imaging with ultrasonographic findings regressed after 4 days of admission. Mourani et al. [9] described a patient with acute cholecystitis due to HAV infection. They detected the HAV antigen immunohistochemically in the gallbladder which was removed by laparoscopy. This patient was operated on considering a diagnosis of cholecystitis with ascending cholangitis. Both ultrasonography and retrograde cholangiopancreatogram showed thickening of the gallbladder wall.

Acute hepatitis A virus (HAV) infection is frequently encountered in developing countries especially in children [11]. In our country, anti-HAV IgG positive rate in adult patients is between 85 and 100% in different studies [25]. Our case is an adult patient. Looking at the literature, majority of the cases are children. Hepatitis A virus infection should be considered as a cause of acute acalculous cholecystitis in adult patients, in countries in which the disease is mainly passed in childhood such as our country.

The treatment of AAC varies depending on the clinical presentation. Most cases are self-limited, and the gallbladder may spontaneously decompress with treatment of the underlying systemic disease within approximately two weeks. Associated complications such as gallbladder perforation and deterioration of abdominal signs have been suggested as indications for surgery [16]. Eleven of fifteen patients that had appropriate information for analysis in previous reports were managed conservatively [8, 1113, 15, 16, 1820] and others with surgical intervention [2, 9, 10, 14].

The case reported here is an adult patient who presented with HAV, which was confirmed serologically, and symptoms suggestive of acute cholecystitis with pancytopenia. Ultrasonographic examination revealed the diagnosis of acalculous cholecystitis which required neither antibiotic treatment nor surgical intervention. The anemia was due to iron deficiency which improved with oral iron supplements, and leukopenia and thrombocytopenia were normalized during the followup (Table 1).

In conclusion, however, ACC is an extremely rare complication of acute viral hepatitis A, and mortality from ACC in patients with viral hepatitis A is extremely low in comparison to ACC of other origins that need urgent surgical intervention. It should be kept in mind that acute viral cholecystitis can develop during the course of acute HAV infection. Hence, conservative therapy may be adequate, so we can avoid unnecessarily invasive procedures.

References

  1. A. Wasley, S. M. Feinstone, and B. P. Bell, “Hepatitis A virus,” in Principles and Practice of Infectious Diseases, G. L. Mandell, J. E. Bennet, and R. Dolin, Eds., pp. 2367–2387, Elsevier Churchill Livingstone, Philadelphia, Pa, USA, 7th edition, 2010. View at Google Scholar
  2. M. M. Black and N. P. Mann, “Gangrenous cholecystitis due to hepatitis A infection,” Journal of Tropical Medicine and Hygiene, vol. 95, no. 1, pp. 73–74, 1992. View at Google Scholar · View at Scopus
  3. P. Casha, H. Rifflet, C. Renou, J.-C. Bulgare, and J.-B. Fieschi, “Acalculous acute cholecystitis and viral hepatitis A,” Gastroenterologie Clinique et Biologique, vol. 24, no. 5, pp. 591–592, 2000. View at Google Scholar · View at Scopus
  4. P. Portincasa, A. Moschetta, A. Di Ciaula et al., “Changes of gallbladder and gastric dynamics in patients with acute hepatitis A,” European Journal of Clinical Investigation, vol. 31, no. 7, pp. 617–622, 2001. View at Publisher · View at Google Scholar · View at Scopus
  5. J. K. Ryu, K. H. Ryu, and K. H. Kim, “Clinical features of acute acalculous cholecystitis,” Journal of Clinical Gastroenterology, vol. 36, no. 2, pp. 166–169, 2003. View at Publisher · View at Google Scholar · View at Scopus
  6. J. A. McChesney, P. G. Northup, and S. J. Bickston, “Acute acalculous cholecystitis associated with systemic sepsis and visceral arterial hypoperfusion: a case series and review of pathophysiology,” Digestive Diseases and Sciences, vol. 48, no. 10, pp. 1960–1967, 2003. View at Publisher · View at Google Scholar · View at Scopus
  7. A. Klar, “Gallbladder and pancreatic involvement in hepatitis A,” Journal of Clinical Gastroenterology, vol. 27, no. 2, pp. 143–145, 1998. View at Publisher · View at Google Scholar · View at Scopus
  8. L. J. de Souza, L. C. Braga, N. D. S. M. Rocha, and R. R. Tavares, “Acute acalculous cholecystitis in a teenager with hepatitis A virus infection—a case report,” Brazilian Journal of Infectious Diseases, vol. 13, no. 1, pp. 74–76, 2009. View at Google Scholar · View at Scopus
  9. S. Mourani, S. M. Dobbs, R. M. Genta, A. K. Tandon, and B. Yoffe, “Hepatitis A virus-associated cholecystitis,” Annals of Internal Medicine, vol. 120, no. 5, pp. 398–400, 1994. View at Google Scholar · View at Scopus
  10. A. O. Ciftci, A. Karnak, and F. C. Tanyel, “The association of hepatitis A virus infection, acalculous cholecystitis, and blunt abdominal trauma: a diagnostic challenge,” Journal of Pediatric Gastroenterology and Nutrition, vol. 32, no. 1, pp. 92–94, 2001. View at Publisher · View at Google Scholar · View at Scopus
  11. R. Ozaras, A. Mert, M. H. Yilmaz et al., “Acute viral cholecystitis due to hepatitis A virus infection,” Journal of Clinical Gastroenterology, vol. 37, no. 1, pp. 79–81, 2003. View at Publisher · View at Google Scholar · View at Scopus
  12. N. Dalgic, E. Ince, E. Cifti et al., “Acute viral acalculous cholecystitis due to viral hepatitis A,” Journal of Ankara University Faculty of Medicine, vol. 58, no. 2, pp. 78–80, 2005. View at Google Scholar
  13. U. Kayabas, Y. Bayındır, and M. K. Okuyan, “An unusual complication due to acute viral hepatitis A: acute cholecystitis,” Viral Hepatit Dergisi, vol. 12, no. 3, pp. 133–136, 2007 (Turkish). View at Google Scholar
  14. J. L. Melero Ferrer, J. Ortuño Cortés, A. Nevárez Heredia, M. Yago Baenas, and M. Berenguer, “Acute acalculous cholecystitis associated with acute hepatitis A virus infection,” Gastroenterologia y Hepatologia, vol. 31, no. 7, pp. 433–435, 2008 (Spanish). View at Publisher · View at Google Scholar · View at Scopus
  15. M. Arroud, S. Benmiloud, B. Oudghiri, M. A. Afifi, M. Hida, and Y. Bouabdallah, “Acute acalculous cholecystitis revealing hepatitis A virus infection in children,” Saudi Journal of Gastroenterology, vol. 15, no. 4, p. 277, 2009. View at Publisher · View at Google Scholar · View at Scopus
  16. D. R. Suresh, R. Srikrishna, S. K. Nanda, V. Annam, K. Sunil, and B. Arjun, “Acalculous gallbladder distension in a young child due to HAV infection: diagnostic dilemma,” Indian Journal of Clinical Biochemistry, vol. 24, no. 3, pp. 316–318, 2009. View at Publisher · View at Google Scholar · View at Scopus
  17. R. Arcana and O. Frisancho, “Acute pancreatitis and acalculous cholecystitis associated with viral hepatitis A,” Revista de Gastroenterología del Perú, vol. 31, no. 2, pp. 178–182, 2011 (Spanish). View at Google Scholar · View at Scopus
  18. M. Hasosah, K. Althobaiti, H. Ghandourah, and S. Al-Amir, “Acute Hepatitis A Virus (HAV) infection associated with acalculous cholecystitis,” Journal of Pediatric Infectious Diseases, vol. 6, no. 1, pp. 79–81, 2011. View at Publisher · View at Google Scholar · View at Scopus
  19. Ö. Herek, N. Çördük, D. Herek, and Ş. Baǧci, “Acute acalculous cholecystitis due to hepatitis A infection in a child: a rare cause of acute abdomen,” Annals of African Medicine, vol. 10, no. 2, pp. 193–195, 2011. View at Publisher · View at Google Scholar · View at Scopus
  20. G. P. Prashanth, B. H. Angadi, S. N. Joshi, P. S. Bagalkot, and M. B. Maralihalli, “Unusual cause of abdominal pain in pediatric emergency medicine,” Pediatric Emergency Care, vol. 28, no. 6, pp. 560–561, 2012. View at Publisher · View at Google Scholar
  21. M. Fuoti, M. Pinotti, V. Miceli et al., “Acute acalculous cholecystitis as a complication of hepatitis A: report of 2 pediatric cases,” La Pediatria Medica e Chirurgica, vol. 30, no. 2, pp. 102–105, 2008. View at Google Scholar · View at Scopus
  22. O. Bouyahia, I. Khelifi, F. Bouafif et al., “Hepatitis A: a rare cause of acalculous cholecystitis in children,” Medecine et Maladies Infectieuses, vol. 38, no. 1, pp. 34–35, 2008. View at Publisher · View at Google Scholar · View at Scopus
  23. O. Başar, B. Kisacik, E. Bozdogan, O. F. Yolcu, I. Ertugrul, and S. Köklü, “An unusual cause of acalculous cholecystitis during pregnancy: hepatitis A virus,” Digestive Diseases and Sciences, vol. 50, no. 8, p. 1532, 2005. View at Publisher · View at Google Scholar
  24. J. Friberg, R. Sonstabo, G. Tjick Joe, E. Goes, and M. Osteaux, “Acalculous cholecystitis as a complication of hepatitis,” European Journal of Radiology, vol. 7, no. 2, p. 153, 1987. View at Google Scholar · View at Scopus
  25. İ. Dökmetaş, “Epidemiology and pathogenesis of HAV infection,” in Viral Hepatitis, F. Tabak, İ. Balık, and E. Tekeli, Eds., pp. 52–60, Viral Hepatitle Savaşım Derneği, 2007. View at Google Scholar