eMedicine Specialties > Gastroenterology > Biliary

Biliary Disease: Differential Diagnoses & Workup

Author: Annie T Chemmanur, MD, Attending Physician, Metrowest Medical Center and University of Massachusetts Memorial Hospital, Marlborough Campus
Coauthor(s): Jeanette G Smith, MD, Fellow, Department of Gastroenterology-Hepatology, University of Connecticut School of Medicine; George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
Contributor Information and Disclosures

Updated: Aug 29, 2009

Differential Diagnoses

Acalculous Cholecystopathy
Empyema, Gallbladder
Bile Duct Strictures
Fitz-Hugh-Curtis Syndrome
Bile Duct Tumors
Gallbladder Mucocele
Biliary Colic
Gallbladder Tumors
Biliary Obstruction
Gallbladder Volvulus
Biliary Trauma
Gastroesophageal Reflux Disease
Bilirubin, Impaired Conjugation
Hepatic Cysts
Budd-Chiari Syndrome
Hepatitis, Viral
Carcinoma of the Ampulla of Vater
Hyperbilirubinemia, Conjugated
Cholangiocarcinoma
Hyperbilirubinemia, Unconjugated
Cholangitis
Pancreatic Cancer
Cholecystitis
Pancreatic Pseudocysts
Choledochal Cysts
Pancreatitis, Chronic
Choledocholithiasis
Papillary Tumors
Cholelithiasis
Peptic Ulcer Disease
Cirrhosis
Pericholangitis
Clostridial Cholecystitis
Postcholecystectomy Syndrome
Emphysema
Recurrent Pyogenic Cholangitis
Emphysematous Cholecystitis

Other Problems to Be Considered

Biliary cirrhosis

Workup

Laboratory Studies

  • Alkaline phosphatase is a marker of cholestasis, ie, elevation of alkaline phosphatase occurs in more than 90% of patients with cholestasis and suggests a reduction in bile flow. It also is elevated in infiltrative disorders or fungal infections of the liver, often quite strikingly, with levels above 1000 U/L.
    • Because isozymes are found in the liver, bone, placenta, leukocytes, and small intestine, an elevated alkaline phosphatase is not specific for the biliary tract. Although the source can be determined by measuring isozyme subtypes, these electrophoretic tests seldom are available clinically. A biliary source is inferred when the alkaline phosphatase is associated with an elevated gamma-glutamyl transpeptidase (GGT), 5'-nucleotidase, or leucine aminopeptidase.
    • An elevation of the hepatic alkaline phosphatase level involves an enzyme-induced secretory process, ie, it represents enzyme induction and accelerated de novo synthesis of alkaline phosphatase and backup into the circulation, not just a simple mechanical obstruction to flow. For this reason, an elevation of alkaline phosphatase may be delayed in the setting of acute obstruction.
  • Bilirubin is a breakdown product of heme, with 80% coming from senescent red blood cells and 20% coming from cytochromes and myoglobin. Unconjugated bilirubin is hydrophobic and transported in the blood reversibly bound to albumen. It is taken up by the hepatocyte, converted to conjugated bilirubin by glucuronyl transferase, and actively secreted into the biliary canaliculi.
  • Aminotransferases: In addition to the liver, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) are found in cardiac and skeletal muscle and renal and cerebral nerve cells. The ALT is found predominantly in the cytosol of the hepatocyte, and an elevated ALT is more likely to suggest liver injury. The AST has both cytosolic and mitochondrial forms. Elevated aminotransferase levels are observed with hepatocellular injury (eg, viral hepatitis), usually sustained over weeks. A rapid rise and fall may be observed in acute posthepatic biliary obstruction or transient hepatic ischemia.
  • AMA: More than 95% of cases of primary biliary cirrhosis are associated with positive test results for AMA. The antigen that reacts with AMA is part of the 2-oxo-acid dehydrogenase multienzyme complex in the mitochondria, especially the E2 subunit of pyruvate dehydrogenase, located on the inner mitochondrial membrane.
  • Miscellaneous immunologic markers: An emerging role for immune markers in inflammatory bowel disease may have implications in the diagnostic evaluation of cholestatic liver disease. Just as AMA is an immunologic marker of PBC, 2 markers are used in the evaluation of patients with suspected inflammatory bowel disease and PSC. These are antineutrophil cytoplasmic antibody (ANCA) and anti-Saccharomyces cerevisiae antibody (ASCA). ANCA is strongly associated with ulcerative colitis (79%) and PSC (82%). Although ASCA is associated with Crohn disease, currently, no association with PSC exists.

Imaging Studies

  • Ultrasound uses technology similar to sonar. A 2-dimensional image of echoes is created. Fluid appears black, solid organs appear hypoechoic, and structures with high amounts of fat or minimal water are hyperechoic.
    • Right upper quadrant ultrasound: This is the principal study used to evaluate biliary-type pain and detect gallbladder disease and biliary dilatation. Gallstones appear as a highly echogenic focus with acoustic shadows and move to a dependent portion of the gallbladder. Right upper quadrant ultrasound can detect stones as small as 1-2 mm and has a sensitivity of 95% and a specificity of 97%. The presence of a thickened gallbladder wall, pericholecystic fluid, and a sonographic Murphy sign supports the diagnosis of cholecystitis. Because of interference by bowel gas, ultrasound does not reveal the common bile duct well, and ultrasound may miss 25-40% of bile duct stones.
    • Endoscopic ultrasonography (EUS): By placing a higher-frequency transducer into the gut adjacent to the hepatobiliary tract, endoscopic ultrasound provides more detailed images than a transcutaneous approach. Although no major advantage to examining the gallbladder exists, EUS can be used to detect intraductal stones with a sensitivity of 88-97% and specificity of 97%. It also can be used to assess adjacent structures, such as porta hepatis nodes; malignancy is suggested by the presence of large (>1 cm), round, sharply demarcated hypoechoic nodes. By better defining the local anatomy of ampullary tumors in relation to neighboring structures, information obtained with EUS can help guide the physician's selection of appropriate intervention.
  • Computed abdominal tomography (CAT) scan: This imaging study usually is not very helpful in evaluating the biliary system. It may demonstrate dilated bile ducts and reveal the cause of a biliary obstruction. Recent technologic advances, such as thin-section helical CT scan, have increased the sensitivity for detection of bile duct stones from 60-90%.
  • Cholangiography: Both endoscopic retrograde cholangiopancreatography (ERCP) and magnetic resonance cholangiopancreatography (MRCP) provide images of the biliary ductal system, which has an appearance similar to a deciduous tree in the wintertime. ERCP is an invasive endoscopic procedure in which radiopaque contrast is injected into the biliary ductal system under fluoroscopic guidance. MRCP is a noninvasive procedure that relies on heavily T2-weighted images to create an image of the fluid within the biliary and pancreatic ductal system.
    • Choledocholithiasis: On a cholangiogram, stones within the bile ducts appear as filling defects within the trunk or branches of the biliary tree. Depending on the type of stone and duration of the illness, they may be single or multiple, round or faceted, free-floating or adherent.
    • In PSC, the bile ducts are characterized by strictures and ectatic areas in an irregular, diffuse pattern. In some cases, the duct may resemble a string of beads due to alternating annular bandlike strictures separating areas of cholangiectasia. Diverticular outpouchings occur in 10% of cases and are observed exclusively in PSC, not cholangiocarcinoma. Specific radiologic patterns (ie, diffuse involvement versus intrahepatic versus extrahepatic) are not associated with differences in median survival.

Other Tests

  • Hepatobiliary scintigraphy
    • This test should be ordered when acute cholecystitis is suspected. Nonvisualization of the gallbladder supports the diagnosis of acute calculous cholecystitis with a sensitivity of 92-98% and a specificity of 95-98%. It also is used to confirm the presence of a biliary leak.
    • Although controversial, hepatobiliary scintigraphy occasionally is helpful in diagnosing chronic cholecystitis or gallbladder dyskinesia in patients with biliary-type pain and normal findings on right upper quadrant ultrasound. The test employs a 45-minute infusion of cholecystokinin (CCK) octapeptide to measure the gallbladder ejection fraction; values lower than 35% are considered abnormal. In some patients, an abnormal gallbladder ejection fraction may be associated with sphincter of Oddi dysfunction.

Staging

Hepatobiliary histology has emerged as an objective reference for staging PBC and PSC. In both, 4 stages are identified.

  • In PSC, stage 1 is characterized by portal tracts that are enlarged by edema, increased connective tissue, and proliferation of interlobular bile ducts. Periductal inflammation and fibrosis characterize stage 2. Connective tissue begins to encroach into the periportal parenchyma, and a fibrous-obliterative cholangitis is present. Stage 3 is defined by a discernible loss of interlobular bile ducts, and stage 4 is reached when cirrhosis is present.
  • In PBC, stage 1 is characterized by dramatic evidence of asymmetric destruction of septal and interlobular bile ducts by a mononuclear infiltrate (the typical appearance is referred to as a florid duct lesion). Occasionally, hepatic granulomas are observed. Diffuse periportal inflammation characterizes stage 2 and is accompanied by portal fibrosis, periportal liver cell necrosis, patchy ductopenia, and ductular proliferation. Stage 3 is defined by the presence of bridging fibrosis, and stage 4 is reached when cirrhosis is present.

More on Biliary Disease

Overview: Biliary Disease
Differential Diagnoses & Workup: Biliary Disease
Treatment & Medication: Biliary Disease
Follow-up: Biliary Disease
Multimedia: Biliary Disease
References
Further Reading
[ CLOSE WINDOW ]

References

  1. Yun EJ, Choi CS, Yoon DY, Seo YL, Chang SK, Kim JS, et al. Combination of magnetic resonance cholangiopancreatography and computed tomography for preoperative diagnosis of the Mirizzi syndrome. J Comput Assist Tomogr. Jul-Aug 2009;33(4):636-40. [Medline].

  2. Reynolds BM, Dargan EL. Acute obstructive cholangitis; a distinct clinical syndrome. Ann Surg. Aug 1959;150(2):299-303. [Medline]. [Full Text].

  3. Solis Herruzo JA, Solis Munoz P, Munoz Yague T. The pathogenesis of primary biliary cirrhosis. Rev Esp Enferm Dig. Jun 2009;101(6):413-423. [Medline].

  4. Berg CP, Kannan TR, Klein R, et al. Mycoplasma antigens as a possible trigger for the induction of antimitochondrial antibodies in primary biliary cirrhosis. Liver Int. Jul 2009;29(6):797-809. [Medline].

  5. Cavallaro A, Cavallaro V, Di Vita M, Cappellani A. Main bile duct carcinoma management. Our experience on 38 cases. Ann Ital Chir. Mar-Apr 2009;80(2):107-11. [Medline].

  6. Drebber U, Mueller JJ, Klein E, et al. Liver biopsy in primary biliary cirrhosis: clinicopathological data and stage. Pathol Int. Aug 2009;59(8):546-54. [Medline].

  7. Kageoka M, Watanabe F, Maruyama Y, et al. Long-term prognosis of patients after endoscopic sphincterotomy for choledocholithiasis. Dig Endosc. Jul 2009;21(3):170-5. [Medline].

  8. Ohashi A, Tamada K, Wada S, et al. Risk factors for recurrent bile duct stones after endoscopic papillary balloon dilation: long-term follow-up study. Dig Endosc. Apr 2009;21(2):73-7. [Medline].

  9. Catena F, Ansaloni L, Di Saverio S, et al. Prospective analysis of 101 consecutive cases of laparoscopic cholecystectomy for acute cholecystitis operated with harmonic scalpel. Surg Laparosc Endosc Percutan Tech. Aug 2009;19(4):312-6. [Medline].

  10. Murphy MM, Shah SA, Simons JP, et al. Predicting major complications after laparoscopic cholecystectomy: a simple risk score. J Gastrointest Surg. Aug 12 2009;epub ahead of print. [Medline].

  11. Moody FG, Vecchio R, Calabuig R. Transduodenal sphincteroplasty with transampullary septectomy for stenosing papillitis. Am J Surg. Feb 1991;161(2):213-8. [Medline].

  12. Allison RR, Zervos E, Sibata CH. Cholangiocarcinoma: an emerging indication for photodynamic therapy. Photodiagnosis Photodyn Ther. Jun 2009;6(2):84-92. [Medline].

  13. Belli G, Limongelli P, Fantini C, et al. Laparoscopic and open treatment of hepatocellular carcinoma in patients with cirrhosis. Br J Surg. Sep 2009;96(9):1041-8. [Medline].

  14. Acosta JM, Civantos F, Nardi GL. Fibrosis of the papilla of Vater. Surg Gynecol Obstet. Apr 1967;124(4):787-94. [Medline].

  15. Afdhal NH, Smith BF. Cholesterol crystal nucleation: a decade-long search for the missing link in gallstone pathogenesis. Hepatology. Apr 1990;11(4):699-702. [Medline].

  16. Bennion LJ, Grundy SM. Risk factors for the development of cholelithiasis in man (second of two parts). N Engl J Med. Nov 30 1978;299(22):1221-7. [Medline].

  17. Boey JH, Way LW. Acute cholangitis. Ann Surg. Mar 1980;191(3):264-70. [Medline].

  18. Bohacek L, Pace DE. Advanced laparoscopic training and outcomes in laparoscopic cholecystectomy. Can J Surg. Aug 2009;52(4):291-294. [Medline]. [Full Text].

  19. Bolondi L, Gaiani S, Testa S. Gall bladder sludge formation during prolonged fasting after gastrointestinal tract surgery. Gut. Jul 1985;26(7):734-8. [Medline].

  20. Broome U, Olsson R, Loof L. Natural history and prognostic factors in 305 Swedish patients with primary sclerosing cholangitis. Gut. Apr 1996;38(4):610-5.

  21. Burnstein MJ, Ilson RG, Petrunka CN. Evidence for a potent nucleating factor in the gallbladder bile of patients with cholesterol gallstones. Gastroenterology. Oct 1983;85(4):801-7. [Medline].

  22. Carey MC, Small DM. The physical chemistry of cholesterol solubility in bile. Relationship to gallstone formation and dissolution in man. J Clin Invest. Apr 1978;61(4):998-1026. [Medline].

  23. Castiella A, Iribarren JA, Lopez P. Ursodeoxycholic acid in the treatment of AIDS-associated cholangiopathy. Am J Med. Aug 1997;103(2):170-1.

  24. Csendes A, Burdiles P, Maluenda F. Simultaneous bacteriologic assessment of bile from gallbladder and common bile duct in control subjects and patients with gallstones and common duct stones. Arch Surg. Apr 1996;131(4):389-94.

  25. Denman ST. A review of pruritus. J Am Acad Dermatol. Mar 1986;14(3):375-92. [Medline].

  26. Everhart JE, Khare M, Hill M. Prevalence and ethnic differences in gallbladder disease in the United States. Gastroenterology. Sep 1999;117(3):632-9.

  27. Gallinger S, Taylor RD, Harvey PR. Effect of mucous glycoprotein on nucleation time of human bile. Gastroenterology. Sep 1985;89(3):648-58. [Medline].

  28. Gerecht WB, Henry NK, Hoffman WW. Prospective randomized comparison of mezlocillin therapy alone with combined ampicillin and gentamicin therapy for patients with cholangitis. Arch Intern Med. Jun 1989;149(6):1279-84.

  29. Graziadei IW, Wiesner RH, Batts KP. Recurrence of primary sclerosing cholangitis following liver transplantation. Hepatology. Apr 1999;29(4):1050-6. [Medline].

  30. Harnois DM, Angulo P, Jorgensen RA. High-dose ursodeoxycholic acid as a therapy for patients with primary sclerosing cholangitis. Am J Gastroenterol. May 2001;96(5):1558-62.

  31. Harnois DM, Lindor KD. Primary sclerosing cholangitis: evolving concepts in diagnosis and treatment. Dig Dis. Jan-Apr 1997;15(1-2):23-41.

  32. Heathcote EJ. Management of primary biliary cirrhosis. The American Association for the Study of Liver Diseases practice guidelines. Hepatology. Apr 2000;31(4):1005-13.

  33. Hendrickse MT, Rigney E, Giaffer MH. Low-dose methotrexate is ineffective in primary biliary cirrhosis: long-term results of a placebo-controlled trial. Gastroenterology. Aug 1999;117(2):400-7.

  34. Holzbach RT. Recent progress in understanding cholesterol crystal nucleation as a precursor to human gallstone formation. Hepatology. Nov-Dec 1986;6(6):1403-6. [Medline].

  35. Izumi Y, Teramoto K, Ohshima M. Endoscopic resection of duodenal ampulla with a transparent plastic cap. Surgery. Jan 1998;123(1):109-10. [Medline].

  36. Jones DE, Gray JC, Newton J. Perceived fatigue is comparable between different disease groups. QJM. Sep 2009;102(9):617-24. [Medline].

  37. Kaplan MM. Primary biliary cirrhosis. N Engl J Med. Nov 21 1996;335(21):1570-80.

  38. Krishnamurthy GT, Turner FE. Pharmacokinetics and clinical application of technetium 99m-labeled hepatobiliary agents. Semin Nucl Med. Apr 1990;20(2):130-49. [Medline].

  39. Lam SK, Wong KP, Chan PK. Recurrent pyogenic cholangitis: a study by endoscopic retrograde cholangiography. Gastroenterology. Jun 1978;74(6):1196-1203. [Medline].

  40. Levy PF, Smith BF, LaMont JT. Human gallbladder mucin accelerates nucleation of cholesterol in artificial bile. Gastroenterology. Aug 1984;87(2):270-5. [Medline].

  41. Liermann Garcia RF, Evangelista Garcia C, McMaster P. Transplantation for primary biliary cirrhosis: retrospective analysis of 400 patients in a single center. Hepatology. Jan 2001;33(1):22-7. [Medline].

  42. Lim JH. Oriental cholangiohepatitis: pathologic, clinical, and radiologic features. Am J Roentgenol. Jul 1991;157(1):1-8. [Medline].

  43. Mazer NA, Carey MC. Quasi-elastic light-scattering studies of aqueous biliary lipid systems. Cholesterol solubilization and precipitation in model bile solutions. Biochemistry. Jan 18 1983;22(2):426-42. [Medline].

  44. Moody FG. Pathogenesis and treatment of inflammatory lesions of the papilla of Vater. Jpn J Surg. Sep 1985;15(5):341-7. [Medline].

  45. Nijhawan PK, Therneau TM, Dickson ER. Incidence of cancer in primary biliary cirrhosis: the Mayo experience. Hepatology. May 1999;29(5):1396-8.

  46. O'Connor MJ, Schwartz ML, McQuarrie DG, Sumer HW. Acute bacterial cholangitis: an analysis of clinical manifestation. Arch Surg. Apr 1982;117(4):437-41. [Medline].

  47. O'Connor MJ, Sumner HW, Schwartz ML. The clinical and pathologic correlations in mechanical biliary obstruction and acute cholangitis. Ann Surg. Apr 1982;195(4):419-23. [Medline].

  48. Palazzo L, Girollet PP, Salmeron M. Value of endoscopic ultrasonography in the diagnosis of common bile duct stones: comparison with surgical exploration and ERCP. Gastrointest Endosc. Sep 1995;42(3):225-31. [Medline].

  49. Pomeranz IS, Shaffer EA. Abnormal gallbladder emptying in a subgroup of patients with gallstones. Gastroenterology. 1985;88:801. [Medline].

  50. Quirk DM, Rattner DW, Fernandez-del Castillo C. The use of endoscopic ultrasonography to reduce the cost of treating ampullary tumors. Gastrointest Endosc. Oct 1997;46(4):334-7. [Medline].

  51. Ransohoff DF, Gracie WA, Wolfenson LB. Prophylactic cholecystectomy or expectant management for silent gallstones. A decision analysis to assess survival. Ann Intern Med. Aug 1983;99(2):199-204. [Medline].

  52. Ros E, Zambon D. Postcholecystectomy symptoms. A prospective study of gall stone patients before and two years after surgery. Gut. Nov 1987;28(11):1500-4. [Medline].

  53. Ruffolo TA, Sherman S, Lehman GA. Gallbladder ejection fraction and its relationship to sphincter of Oddi dysfunction. Dig Dis Sci. Feb 1994;39(2):289-92. [Medline].

  54. Sampliner RE, Bennett PH, Comess LJ. Gallbladder disease in Pima Indians. Demonstration of high prevalence and early onset by cholecystography. N Engl J Med. Dec 17 1970;283(25):1358-64. [Medline].

  55. Schoenfield LJ, Carey MC, Marks JW. Gallstones: an update. Am J Gastroenterol. Sep 1989;84(9):999-1007. [Medline].

  56. Sievers MS, Marquis JR. The Southwest American Indian's burden: biliary disease. Journal of the American Medical Association. 1962;182:570-572.

  57. Strauch GO. Primary carcinoma of the gallbladder: presentation of seventy cases from the Rhode Island Hospital and a cumulative review of the last ten years. American Literature of Surgery. 1960;47:368.

  58. Strom BL, Soloway RD, Rios-Dalenz JL. Risk factors for gallbladder cancer. An international collaborative case-control study. Cancer. Nov 15 1995;76(10):1747-56.

  59. Thistle JL, Cleary PA, Lachin JM. The natural history of cholelithiasis: the National Cooperative Gallstone Study. Ann Intern Med. Aug 1984;101(2):171-5.

  60. Wienser RH, Porayko MK, LaRusso NF, et al. In: Schiff L, Schiff ER, eds. Diseases of the Liver. 7th ed. Philadelphia, Pa:. JB Lippincott;1993:411-426.

  61. Wolfhagen FH, Sternieri E, Hop WC. Oral naltrexone treatment for cholestatic pruritus: a double-blind, placebo-controlled study. Gastroenterology. Oct 1997;113(4):1264-9. [Medline].

  62. Yap L, Wycherley AG, Morphett AD. Acalculous biliary pain: cholecystectomy alleviates symptoms in patients with abnormal cholescintigraphy. Gastroenterology. Sep 1991;101(3):786-93. [Medline].

  63. Yoshida J, Chijuwa K. Practical classification of the branching types of the biliary tree: an analysis of 1094 consecutive direct cholangiograms. J Am Coll Surg. 1997;185:274-82. [Medline].

  64. Zeman RK. Cholelithiasis and cholecystitis. In: Gore RM, Levine MS, Laufer I, eds. Text of Gastrointestinal Radiology. Philadelphia, Pa:. WB Saunders;1994:1654-55.

[ CLOSE WINDOW ]

Further Reading

Related eMedicine Topics

Clinical Trials
National Guideline Clearinghouse 

[ CLOSE WINDOW ]

Keywords

biliary disease, abnormal bile composition, abnormal biliary anatomy, abnormal biliary function, gallstones, gall stones, gallbladder disease, cirrhosis, primary biliary cirrhosis, PBC, liver disease, primary sclerosing cholangitis, PSC, acute cholecystitis, cholecystectomy, cholestasis, steatorrhea, cholelithiasis, papillary stenosis, pancreatitis, cholangiocarcinoma, postcholecystectomy syndrome, sphincter of Oddi dyskinesia, vanishing bile duct syndrome

[ CLOSE WINDOW ]

Contributor Information and Disclosures

Author

Annie T Chemmanur, MD, Attending Physician, Metrowest Medical Center and University of Massachusetts Memorial Hospital, Marlborough Campus
Annie T Chemmanur, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Medical Association, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Coauthor(s)

Jeanette G Smith, MD, Fellow, Department of Gastroenterology-Hepatology, University of Connecticut School of Medicine
Jeanette G Smith, MD is a member of the following medical societies: American College of Physicians, American Gastroenterological Association, and American Public Health Association
Disclosure: Nothing to disclose.

George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians
Disclosure: Humana Press Consulting fee Consulting; Novartis Consulting fee Review panel membership

Medical Editor

Ronnie Fass, MD, Director of GI Motility Laboratory, Tucson VA Medical Center, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of Arizona School of Medicine
Ronnie Fass, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians-American Society of Internal Medicine, American Gastroenterological Association, American Motility Society, American Society for Gastrointestinal Endoscopy, and Israel Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

James L Achord, MD, Professor Emeritus, Department of Medicine, Division of Digestive Diseases, University of Mississippi School of Medicine
James L Achord, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Mississippi State Medical Association, New York Academy of Sciences, Sigma Xi, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.