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Celiac Disease As a Cause of Abnormal Transaminases in Chronic Hepatitis B Infection

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Celiac Disease As a Cause of Abnormal Transaminases in Chronic Hepatitis B Infection A CASE TO REMEMBER Celiac Disease as a Cause of Abnormal Transaminases in Chronic Hepatitis B Infection by Larry E. Clark and Jorge L. Herrera Extrahepatic causes of transaminase elevation are often overlooked when evaluating patients with chronic liver disease. A 54-year-old woman was referred for the manage- ment of chronic hepatitis B (HBV). Serologic testing showed a pattern of chronic hepatitis B infection with mild transaminase elevation. Further diagnostic testing sug- gested a pattern of quiescent HBV disease. Additional testing revealed no other expla- nation of the abnormal transaminase level and liver biopsy showed no significant pathologic change. She subsequently returned with malabsorption complaints and tested positive for celiac disease antibodies. Duodenal biopsies confirmed the presence of villous atrophy. The celiac disease was therefore the cause of the elevated transami- nases concealed by the finding of a positive HBsAg. Elevated liver enzymes may be the only presenting sign of celiac disease; clinicians should include screening tests for celiac disease in the standard evaluation of patients with chronic liver disease as well as asymptomatic elevated liver enzymes. INTRODUCTION serum transaminases is much more common with eliac disease has long been associated with prevalences of up to 54% in untreated cases (6,7). hepatic diseases including primary sclerosing Hypertransaminasemia has also been reported as the Ccholangitis (1), primary biliary cirrhosis (2), presenting feature of otherwise asymptomatic celiac hepatitis C (3), autoimmune hepatitis (4), and acute disease in several cases (8). fatty liver (5). Its association with simple elevations in We report the case of celiac disease discovered in the evaluation of a patient with a positive HBsAg. This Larry E. Clark, M.D., Fellow and Jorge L. Herrera, case emphasizes the importance of screening for celiac M.D., Attending, Division of Gastroenterology Univer- disease as a cause of hypertransaminasemia in asymp- sity of South Alabama College of Medicine, Mobile, tomatic individuals as well as those with chronic liver AL. disease. 50 PRACTICAL GASTROENTEROLOGY • DECEMBER 2003 Celiac Disease as a Cause of Abnormal Transaminases in Chronic Hepatitis B Infection A CASE TO REMEMBER CASE REPORT DISCUSSION A 54-year-old Caucasian woman was referred for the Celiac disease represents an important cause of ele- management of suspected chronic HBV. She had been vated liver enzymes. While some patients present with diagnosed with chronic HBV after presenting with the classic signs of diarrhea and malabsorption, many mildly elevated transaminases found on routine evalu- asymptomatic celiac cases may only present with ation. She reported no hepatitis risk factors or prior hypertransaminasemia. Bardella, et al reported on 140 episodes of acute hepatitis. Medication history was patients with unexplained elevations in transaminases equally unremarkable. Further complaints included rare and found 9.3% to be positive for IgA anti-endomysial loose stools and a bloating sensation but no obvious and antigliadin antibodies (9). The prevalence of celiac symptoms of malabsorption or weight loss. Past med- disease greatly exceeds that of more commonly ical history was significant only for an unknown thy- screened disorders such as Wilson's disease or alpha-1- roid tumor necessitating thyroidectomy 30 years prior. antitrypsin deficiency yet is routinely ignored as a Family history was significant for a sister with autoim- potential cause of asymptomatic elevations in liver mune vasculitis but no gastrointestinal or liver diseases. enzymes. Physical examination was unremarkable. There The etiology of hypertransaminasemia in celiac were no signs of chronic liver disease or nutritional disease is unclear. Proposed mechanisms include the deficiencies. relation of celiac disease to malnutrition and bacterial Laboratory data revealed an alanine transaminase overgrowth however these seem to be only minor con- ( A LT) of 84 U/L (normal 30–65) and an aspartate tributors (7). Liver enzyme abnormalities probably transaminase (AST) of 58 U/L (normal 15–37). The result due to increased intestinal permeability (10) and bilirubin, albumin, alkaline phosphatase, hematocrit, chronic intestinal inflammation (7). When the disease and prothrombin time levels were within normal limits. is treated with a gluten-free diet liver enzymes levels The HBsAg and HBeAb were positive while the almost universally normalize within six months. HBeAg was negative suggesting either an inactive car- Liver biopsy of confirmed celiac patients with ele- rier state versus active disease with an HBV precore vated liver enzymes is only recommended if there is mutant strain. HBV DNA by PCR was undetectable persistent transaminase elevation despite several supporting the diagnosis of an inactive carrier state. months of treatment with a gluten-free diet or if eleva- Further testing for other chronic viral infection, autoim- tions in serum bilirubin are present (7,8). Liver test mune disease, hemochromatosis, Wilson's disease, and abnormalities in celiac disease generally include mild alpha-1-antitrypsin deficiency were all negative. elevations in AST and ALT values with normal alka- A liver biopsy was obtained due to the unexplained line phosphatase and bilirubin levels. Liver biopsy elevated liver enzymes which showed essentially nor- findings are nonspecific and not helpful in the diagno- mal findings. Specifically there was no substantial evi- sis or treatment of the disease (8,11). In our case the dence of inflammation, fibrosis, or steatosis. biopsy was performed for the confounding factor of Subsequently the patient returned to clinic with HBsAg positivity coupled with elevated enzymes and complaints of worsening diarrhea and weight loss of 10 undetectable HBV DNA. pounds over a two month period. At this time a malab- We feel the association of HBV in this case was sorption evaluation was pursued revealing 42 grams of coincidental and effectively delayed the diagnosis of fecal fat/day and positive titers for Ig-A antigliadin, celiac disease. Celiac disease has been associated with antiendomysial, and tissue transglutaminase antibodies. primary biliary cirrhosis (2), primary sclerosing Enteroscopy with small bowel biopsy revealed cholangitis (1), hepatitis C (3), autoimmune hepatitis severe villous atrophy, crypt hyperplasia, and intra- (4), and fatty liver (5) but the association with HBV is epithelial lymphocytosis consistent with the diagnosis less clear. Volta, et al found no increased prevalence of of celiac disease. The patient was subsequently started IgA antigliadin antibodies in 30 HBsAg positive on a gluten-free diet with symptomatic improvement and normalization of the transaminases. (continued on page 63) PRACTICAL GASTROENTEROLOGY • DECEMBER 2003 51 Celiac Disease A CASE TO REMEMBER (continued from page 51) patients (4). However in the Bardella series of 158 patients with small intestinal biopsy proven celiac dis- ease, twice the normal prevalence of HBsAg was found although the authors admitted the association could merely be due to chance (7). Given the importance of early treatment of celiac disease to prevent complications such as loss of bone mineral density, clinicians should be aware of celiac disease as a cause of elevated liver enzymes. Screen- ing for celiac disease should be part of the evaluation of patients with known chronic liver disease as well as those with unexplained elevations in liver enzymes. ■ References 1. Hay JE, Wiesner RH, Shorter RG, et al. Primary sclerosing cholangitis and coeliac disease: a novel association. Ann Intern Med, 1988;109:713-717. 2. Olsson R, Kagevi I, Rydberg L. On the occurrence of primary biliary cirrhosis and intestinal villous atrophy. Scand J Gastroen - terol, 1982;17:625-628. 3. Fine KD, Ogunji F, Saloum Y, et al. Celiac sprue: Another autoimmune syndrome associated with hepatitis C. Am J Gas - troenterol, 2001;96:138-145. 4. Volta U, Franchesi L, Molinaro N, et al. Frequency and signifi- cance of anti-gliadin and anti-endomysial antibodies in autoim- mune hepatitis. Dig Dis Sci, 1998;43:2190-2195. 5. Lynch DA, Thorton JR, Axon AT. Acute fatty liver complicating coeliac disease. Eur J Gastroenterol Hepatol, 1994;6:745-747. 6. Bonamico M, Pitzalis G, Culasso F. Hepatic damage during coeliac disease in childhood. Minerva Pediatr, 1986;38:959-962. 7. Bardella MT, Fraquelli M, Quatrini M, et al. Prevalence of hypertransaminasemia in adult celiac patients and effect of gluten-free diet. Hepatology, 1995;22:833-836. 8. Gonzalez-Abraldes J, Sanchez-Fueyo A, Bessa X, et al. Persis- tent hypertransaminasemia as the presenting feature of celiac dis- ease. Am J Gastroenterol, 1999;94:1095-1097. 9. Bardella MT, Vecchi M, Conte D, et al. Chronic unexplained hypertransaminasemia may be caused by occult celiac disease. Hepatology,1999;29:654-657. 10. van Elburg RM, Uil JJ, Mulder CJJ, et al. Intestinal permeability in patients with coeliac disease and relatives of patients with coeliac disease. Gut, 1993;34:354-357. 11. Jacobsen MB, Fausa O, Elgjo K, et al. Hepatic lesions in adult coeliac disease. Scand J Gastroenterol. 1990;25:656-662. There isn’t a physician who hasn’t at least one “Case to Remember” in his career. Share that case with your fellow gastroenterologists. Send it to Editor: Practical Gastroenterology, 99B Main Street Westhampton Beach, NY 11978. Include any appropriate illustrations. Also, include a photo of yourself..
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