Authors: Collin P
Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Tampere, Finland
Correspondence: Pekka Collin,
Department: Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital
Address: Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital
City: Tampere
Country: Finland
E-mail: pekka.collin@uta.fi
Manuscript:
Dear Editor,
Leonardi and La Rosa (1) investigated the occurrence of celiac disease in patients with hepatitis B by screening their sera with anti-endomysial and anti-tissue transglutaminase antibodies-both of which are sensitive serological tests for celiac disease. The authors found no one with celiac disease in 60 patients who had contracted hepatitis B infection in childhood. As they admitted, the power of the study was too low to make any definitive conclusions.
Celiac disease is defined as "a permanent intolerance to ingested gluten, the structural protein in wheat rye and barley." The ingestion of gluten results in small bowel mucosal inflammation, crypt hyperplasia and villous atrophy. Typically, patients suffer from diarrhea, abdominal complaints, malaise, and malabsorption with resultant iron deficiency anemia. The histpathology and symptoms resolve on gluten-free diet.
Of note, the condition is often asymptomatic. Extraintestinal manifestations or associated autoimmune conditions may be the sole presentations of celiac disease. Here, I disagree with Leonardi and La Rosa (1) who stated that associated autoimmune diseases are usually found in celiac patients with severe complications: existing autoimmune disorders (e.g., autoimmune hepatitis) may be the only disease manifestation in an otherwise asymptomatic celiac patient (2).
Isolated hypertransaminasemia is common in celiac disease, and conversely, unexplained hypertransaminasemia may be a diagnostic clue in celiac disease. Celiac disease has been reported to occur in patients with primary biliary cirrhosis, autoimmune hepatitis and primary sclerosing cholangitis (3). Untreated celiac disease may exacerbate the associated liver disease, and gluten-free dietary treatment in such cases, may result in a dramatic improvement, even in advanced liver disease (4) .
As to the viral hepatitis, there are more studies on the occurrence of celiac disease in hepatitis C than in hepatitis B. Two large studies comprising 624 (5) and 878 (6) patients with hepatitis C found no increased frequency of celiac disease. The positive associations are mainly based on case reports.
When considering the reports, some facts must be taken into account. Firstly, celiac disease affects more than 1% of people in many countries, which means that the disease associations may be fortuitous. For instance, if we make an estimate that 1% of the population in Italy is infected by hepatitis B virus, it means that 6000 people with hepatitis B will have (mostly undetected) celiac disease; and there would be even more cases with hepatitis C and celiac disease. Secondly, symptoms of celiac disease are variable and subtle. There are case reports where celiac disease has been activated after the commencement of interferon therapy (6). This is yet to be proved, however. Patients treated with interferon are usually kept on careful surveillance, and side-effects of interferon may mimic symptoms of celiac disease (i.e., anemia, depression, and fatigue). It is thus possible that serologic screening will be carried out more easily in patients who have received medical therapy for viral hepatitis than in other patients suffering from similar symptoms. Nevertheless, the development of celiac disease should be kept in mind during interferon therapy, as the drug may activate latent autoimmune diseases.
Evidence suggests that patients with celiac disease have a lower response rate to hepatitis B vaccination than healthy subjects. This failure to respond may increase the risk of hepatitis B in celiac disease (7).
To conclude, at the moment, there is no convincing evidence that patients with viral hepatitis carry an increased risk of celiac disease. The results of Leonardi and La Rosa (1) support this conclusion.
Acknowledgement
Celiac Disease Study Group is financially supported by the Competitive Research Funding of the Pirkanmaa Hospital District, Finland.
References:
1. Leonardi S, La Rosa M. Are Hepatitis B Virus and Celiac Disease Linked?
2. Collin P, Kaukinen K, Valimaki M, Salmi J. Endocrinological disorders and celiac disease. Endocr Rev. 2002;23(4):464-83. [PubMed]
3. Rubio-Tapia A, Murray JA. The liver in celiac disease. Hepatology. 2007;46(5):1650-8. [PubMed]
4. Kaukinen K, Halme L, Collin P, et al. Celiac disease in patients with severe liver disease: gluten-free diet may reverse hepatic failure. Gastroenterology. 2002;122(4):881-8. [PubMed]
5. Thevenot T, Denis J, Jouannaud V, et al. Coeliac disease in chronic hepatitis C: a French multicentre prospective study. Aliment Pharmacol Ther. 2007;26(9):1209-16. [PubMed]
6. Hernandez L, Johnson TC, Naiyer AJ, et al. Chronic hepatitis C virus and celiac disease, is there an association? Dig Dis Sci. 2008;53(1):256-61. [PubMed]
7. Leonardi S, Spina M, Spicuzza L, Rotolo N, La Rosa M. Hepatitis B vaccination failure in celiac disease: is there a need to reassess current immunization strategies? Vaccine. 2009;27(43):6030-3. [PubMed]
Celiac Disease and Viral B Hepatitis: Lessons for Clinical Practice
.
Authors: Tursi A
Gastroenterology Service, ASL BAT, Andria (BAT), Italy
Correspondence:
Antonio Tursi,
Department: Gastroenterology Service, ASL BAT
Address: Servizio di Gastroenterologia Territoriale, DSS No. 4, ASL BAT, Via Torino, 49, 70031 Andria (BAT), Italy
City: Andria (BAT)
Country: Italy
E-mail: antotursi@tiscali.it
Manuscript:
Dear Editor,
Celiac disease (CD) is a chronic inflammatory disease of the gut occurring in genetically susceptible individuals after the ingestion of gluten. It is characterized by a flattened mucosa, villous atrophy, and crypt hyperplasia in the small intestine, by the classic malabsorption syndrome (diarrhea, steatorrhea, weight loss), or by seemingly less severe symptoms such as iron deficiency anemia, osteopenic bone disease, amenorrhea, and infertility (1). The elimination of gluten from the diet generally leads to a return to normality of the morphological changes (2). Intestinal damage is caused by an interaction between the deamidated glutamine residues of gliadin and HLA-DQ2 (DQA1*05/DQB1*2) or DQ8 (DQA1*03/DQB1*0302) molecules (3), with consequent T-cell response and production of autoantibodies against type 2 transglutaminase (anti-tTG2-Ab). HLA phenotype is also considered the most important genetic marker of nonresponders to the hepatitis B (HBV) vaccination. In particular, the immune response to the HBV vaccine is largely determined by the presence of the immunogenetic peptides via the HLA-DR and DQ molecules (4, 5), with the DR3-DQ2 and DR7-DQ2 haplotypes generally having a lower response rate (6-9).
In 2000, the World Health Organization estimated that 2 billion people worldwide had serological evidence of past or present infection with HBV and that 350 million of these people were chronically infected and at risk for HBV-related liver disease (10). HCV infection is endemic to most parts of the world, although there is considerable geographic variation (11). Estimates indicate that 2.2% of the global population is infected with HCV (12). HCV is the most common chronic blood-borne infection in the U.S. and is a major cause of cirrhosis and hepatocellular carcinoma (13). An interesting chapter in clinical practice is the possible association between CD and viral hepatitis. Recently, researchers have hypothesized that nonintestinal inflammatory chronic diseases, such as HBV and HCV, may be the immunologic trigger for the development of CD (14, 15). However, the association between chronic viral hepatitis and the development of CD is still a matter of debate. In a recent study, Leonardi and La Rosa found no cases of CD in a retrospective cohort of patients carrying HBV, and no CD cases appeared during treatment with interferon (16). This study, although limited by the small size of patients studied, is interesting because it may be representative of what has been observed in Italy. HBV prevalence in Italy is higher than in the rest of Europe (17), and a high prevalence of CD is estimated as well (18). A more interesting question is: if it does not seem to be an association between CD and viral hepatitis in Italy, what is happening in other regions of the world that have a high incidence of viral hepatitis (19-21) and an increased incidence of CD (22, 23)? Until further, large, epidemiological studies investigate this question, the answer is still open.
We have more answers about what happens in coeliacs after vaccination. Mass immunization of the population has been recommended by the World Health organization since 1991 (24), and it is generally performed in 12-year-old schoolchildren (25). We know that CD patients have a lower rate of immunization after HBV vaccination (26, 27). We do not know if CD will increase with the actual rate of vaccination. This may be a problem for the public health system because a great deal of young people may be at high risk of contracting HBV due to a lack of immunization. In a fine paper published in 2008, Nemes et al. demonstrated that the response to HBV vaccination in CD patients is related to the response to a gluten-free diet (28). In fact, an adequate vaccine response to HBV was found in coeliacs compliant with (Gluten-Free Diets) GFD, whereas nonresponse was a sign of undiagnosed CD or a lack compliance to GFD (28). Surprisingly, Nemes et al. did not find any association between nonresponse and HLA-DQ2 or DQ8 status (28). These results have been recently confirmed by Ertem et al., who found that response to HBV vaccine in children with CD who are compliant with GFD did not differ from the response in a healthy population (29). Therefore, until new epidemiological data shed light on the possible association between CD and HBV infection, good advices seems to be
1. to screen for CD in schoolchildren before HBV vaccination;
2. to obtain optimal compliance to GFD in CD patients before HBV vaccination to reduce the risk of unresponsiveness;
3. to revaccinate during a well-controlled GFD in order to maintain a high level of immunization.
References:
1. Rostom A, Murray JA, Kagnoff MF. American Gastroenterological Association (AGA) Institute technical review on the diagnosis and management of celiac disease. Gastroenterology. 2006;131(6):1981-2002. [PubMed]
2. Catassi C. The world map of celiac disease. Acta Gastroenterol Latinoam. 2005;35(1):37-55. [PubMed]
3. Di Sabatino A, Corazza GR. Coeliac disease. Lancet. 2009;373(9673):1480-93. [PubMed]
4. Belloni C, Avanzini MA, De Silvestri A, et al. No evidence of autoimmunity in 6-year-old children immunized at birth with recombinant hepatitis B vaccine. Pediatrics. 2002;110(1 Pt 1):e4. [PubMed]
5. Desombere I, Willems A, Leroux-Roels G. Response to hepatitis B vaccine: multiple HLA genes are involved. Tissue Antigens. 1998;51(6):593-604. [PubMed]
6. Durupinar B, Okten G. HLA tissue types in nonresponders to hepatitis B vaccine. Indian J Pediatr. 1996;63(3):369-73. [PubMed]
7. McDermott AB, Zuckerman JN, Sabin CA, Marsh SG, Madrigal JA. Contribution of human leukocyte antigens to the antibody response to hepatitis B vaccination. Tissue Antigens. 1997;50(1):8-14. [PubMed]
8. Martinetti M, De Silvestri A, Belloni C, et al. Humoral response to recombinant hepatitis B virus vaccine at birth: role of HLA and beyond. Clin Immunol. 2000;97(3):234-40. [PubMed]
9. Godkin A, Davenport M, Hill AV. Molecular analysis of HLA class II associations with hepatitis B virus clearance and vaccine nonresponsiveness. Hepatology. 2005;41(6):1383-90. [PubMed]
10. Hepatitis B vaccines: WHO position paper--recommendations. Vaccine.28(3):589-90. [PubMed]
11. Wasley A, Alter MJ. Epidemiology of hepatitis C: geographic differences and temporal trends. Semin Liver Dis. 2000;20(1):1-16. [Pubmed]
12. Global burden of disease (GBD) for hepatitis C. J Clin Pharmacol. 2004;44(1):20-9. [PubMed]
13. NIH Consensus Statement on Management of Hepatitis C: 2002. NIH Consens State Sci Statements. 2002;19(3):1-46. [PubMed]
14. Fine KD, Ogunji F, Saloum Y, Beharry S, Crippin J, Weinstein J. Celiac sprue: another autoimmune syndrome associated with hepatitis C. Am J Gastroenterol. 2001;96(1):138-45. [Pubmed]
15. Bardella MT, Fraquelli M, Quatrini M, Molteni N, Bianchi P, Conte D. Prevalence of hypertransaminasemia in adult celiac patients and effect of gluten-free diet. Hepatology. 1995;22(3):833-6. [PubMed]
16. Leonardi S, La Rosa M. Are Hepatitis B Virus and Celiac Disease Linked? Hepat Mon.2010;10(3):173-5. [HepatMon]
17. Stroffolini T, Almasio PL, Sagnelli E, Mele A, Gaeta GB. Evolving clinical landscape of chronic hepatitis B: A multicenter Italian study. J Med Virol. 2009;81(12):1999-2006. [PubMed]
18. Gasbarrini G, Miele L, Malandrino N, et al. Celiac disease in the 21st century: issues of under- and over-diagnosis. Int J Immunopathol Pharmacol. 2009;22(1):1-7. [PubMed]
19. Merat S, Rezvan H, Nouraie M, et al. Seroprevalence of hepatitis C virus: the first population-based study from Iran. Int J Infect Dis.2010[Epub ahead of print]. [PubMed]
20. Shalaby S, Kabbash IA, El Saleet G, Mansour N, Omar A, El Nawawy A. Hepatitis B and C viral infection: prevalence, knowledge, attitude and practice among barbers and clients in Gharbia governorate, Egypt. East Mediterr Health J.16(1):10-7. [PubMed]
21. Sa-Nguanmoo P, Tangkijvanich P, Thawornsuk N, et al. Molecular epidemiological study of hepatitis B virus among migrant workers from Cambodia, Laos, and Myanmar to Thailand. J Med Virol.2010;82(8):1341-9. [Pubmed]
22. Cummins AG, Roberts-Thomson IC. Prevalence of celiac disease in the Asia-Pacific region. J Gastroenterol Hepatol. 2009;24(8):1347-51. [PubMed]
23. Abu-Zekry M, Kryszak D, Diab M, Catassi C, Fasano A. Prevalence of celiac disease in Egyptian children disputes the east-west agriculture-dependent spread of the disease. J Pediatr Gastroenterol Nutr. 2008;47(2):136-40. [PubMed]
24. Hou J, Liu Z, Gu F. Epidemiology and Prevention of Hepatitis B Virus Infection. Int J Med Sci. 2005;2(1):50-7. [PubMed]
25. Da Villa G, Picciottoc L, Elia S, Peluso F, Montanaro F, Maisto T. Hepatitis B vaccination: universal vaccination of newborn babies and children at 12 years of age versus high risk groups. A comparison in the field. Vaccine. 1995;13(13):1240-3. [Pubmed]
26. Noh KW, Poland GA, Murray JA. Hepatitis B vaccine nonresponse and celiac disease. Am J Gastroenterol. 2003;98(10):2289-92. [PubMed]
27. Park SD, Markowitz J, Pettei M, et al. Failure to respond to hepatitis B vaccine in children with celiac disease. J Pediatr Gastroenterol Nutr. 2007;44(4):431-5. [PubMed]
28. Nemes E, Lefler E, Szegedi L, et al. Gluten intake interferes with the humoral immune response to recombinant hepatitis B vaccine in patients with celiac disease. Pediatrics. 2008;121(6):e1570-6. [PubMed]
29. Ertem D, Gonen I, Tanidir C, et al. The response to hepatitis B vaccine: does it differ in celiac disease? Eur J Gastroenterol Hepatol.22(7):787-93. [PubMed]
The Controversial Link between Hepatitis B Virus and Celiac Disease
Authors:
Burgos A
Hospital Universitario La Paz, Servicio de Aparato Digestivo, Madrid, Spain
Bermejo P
Hospital Universitario Puerta de Hierro, Servicio de Neurología, Madrid, Spain
Correspondence:
Pedro Emilio Bermejo,
Department: Hospital Universitario Puerta de Hierro, Servicio de Neurología
Address: Hospital Universitario Puerta de Hierro. Servicio de Neurología, Calle Manuel de Falla 1, 28222, Majadahonda, Madrid
City: Madrid
Country: Spain
E-mail: pedro_bermejo@hotmail.com
Manuscript:
Dear Editor,
Celiac disease (CD) is an autoimmune disease resulting in inflammatory destruction of small intestinal mucosa after the ingestion of gluten in genetically susceptible individuals. The study of Leonardi and La Rosa (1) tries to establish a possible link between hepatitis B virus (HBV) infection and celiac disease. This is really interesting because only few cases have been described so far in the literature. However, there are two controversial points to be discussed in more detail-the development of CD after HBV infection or after treatment of chronic hepatitis with interferon, and an inadequate response to hepatitis B immunization in patients with CD.
In the first case, several triggers developing an immunologic intolerance to gluten in susceptible patients have already been described including HBV infection, natural interferon released in response to infection or exogenous interferon used for treatment of viral hepatitis (2, 3). However, we cannot establish definitive conclusions about the relationship between these two entities-HBV and CD. For this reason, in this study (1), the authors think that it is not mandatory to check for specific CD antibodies before beginning the treatment or during the follow-up; but this is still a point for discussion and other studies have proposed that these antibodies should be checked (3).
In the second case, data regarding the response to HBV vaccine in CD suggest that non-response to vaccine is higher in CD patients than in control subjects (67.5% vs 85.2%) (4). The majority of these studies included adult celiac patients; it has been shown that younger subjects have a better response. Apart from the age, this poor response has been particularly associated with the major histocompatibility complex (HLA) DQ2, DR3 and DR7 which are closely associated with CD as well. Another study (5), demonstrated a correlation between the disease activity (by measuring serum titers of anti-transglutaminase) and the development of an antibody response to HBV vaccine. A gluten-free diet might have a primary role and these authors suggested that HLA DQ2 per se, was not a good indicator for poor response to HBV vaccine.
In conclusion, we think that checking for specific CD antibodies should be recommended before beginning of the treatment with interferon or during the follow-up, although it is not mandatory since it is still a controversial issue. Finally, gluten-free diet may ameliorate the immune response to HBV vaccine in celiac patients; assessment of this response should be routinely considered in children newly diagnosed with CD.
References:
1. Leonardi S, La Rosa M. Are Hepatitis B Virus and Celiac Disease Linked? Hepat Mon.2010;10(3):173-5. [PubMed]
2. Soto Iglesias S, Vazquez Rodriguez S, Ulla Rocha JL, et al. [Onset of celiac disease after acute hepatitis B infection]. Gastroenterol Hepatol.2010;33(1):17-20. [PubMed]
3. Narváez R, Jiménez J. Hepatitis B virus and celiac disease. Gastroenterol hepatol.2010;33(8):617. [PubMed]
4. Ertem D, Gonen I, Tanidir C, et al. The response to hepatitis B vaccine: does it differ in celiac disease? Eur J Gastroenterol Hepatol.2010;22(7):787-93. [PubMed]
5. Nemes E, Lefler E, Szegedi L, et al. Gluten intake interferes with the humoral immune response to recombinant hepatitis B vaccine in patients with celiac disease. Pediatrics. 2008;121(6):e1570-6. [PubMed]
Relationship between Hepatitis B Virus Infection and Celiac Disease
Authors:
.
Ouakaa-Kchaou A Department of Gastroenterology and Hepatology,
Habib Thameur Hospital, Tunis, Tunisia
Gargouri D Department of Gastroenterology and Hepatology, Habib Thameur Hospital, Tunis, Tunisia
Kharrat J Department of Gastroenterology and Hepatology, Habib Thameur Hospital, Tunis, Tunisia
Ghorbel A Department of Gastroenterology and Hepatology, Habib Thameur Hospital, Tunis, Tunisia
Correspondence:
Asma Ouakaa-Kchaou,
Department: Department of Gastroenterology and Hepatology, Habib Thameur Hospital
Address: Department of Gastroenterology and Hepatology, Habib Thameur Hospital, Tunis-Tunisia
City: Tunis
Country: Tunisia
E-mail: asma.kchaou@rns.tn
Manuscript:
Dear Editor,
We read with great interest the article entitled "are hepatitis B virus and celiac disease linked?" by Leonardi, et al, (1) published in Hepatitis Monthly. Celiac disease (CD), also known as gluten-sensitive enteropathy and non-tropical sprue, is a prevalent autoimmune disorder. The balance of evidence suggests that the celiac immunopathology involves a complex individualized interplay of many pathophysiological variables on a genetic background (2). CD develops as a consequence of the encounter between an environmental trigger (i.e., derivatives of gluten from wheat, rye, and barley), immunologic factors, and a genetically predisposed host, with the possible participation of other environmental cofactors. In particular, intestinal infections might cause a transient rise in small-bowel permeability that could lead to up-regulation and release of tissue transglutaminase which in turn, enhances gluten immunogenicity. Rod-shaped bacteria have been identified in the intestinal epithelium in children with CD, although this colonization could just be coincidental (3).
Rotavirus infections could also raise the risk of CD in genetically predisposed children. The homology between the rotavirus-neutralizing protein VP-7 and tissue transglutaminase might explain how rotavirus infection is implicated in the development of CD (3). It has also been hypothesized that hepatitis B virus (HBV) and hepatitis C virus (HCV) may trigger immunologic gluten intolerance (4, 5). Although the association between CD and several liver disorders has long been documented, no definitive evidence is available about the association between HBV or HCV and CD. The role of HCV infection is better documented and several studies have described the relationship between HCV infection and the development of CD (4). However, little data exist on the relationship between HBV and CD and it seems that no such relation is found concerning HBV immunization.
The main finding of the study of Leonardi (1) is the absence of any relationship between CD and HBV. However, the sample size was small, the studied group was heterogeneous including those with ongoing and resolved HBV infection, there was no control group, endoscopy and duodenal biopsy were not performed in patients who tested positive for either IgA or IgG anti-gliadin antibodies (Ig AGA) in whom symptoms of CD may be lacking. Activation of silent CD during the antiviral treatment with interferon-α has also been reported. Nevertheless, we agree with Leonardi, et al, that it is not mandatory to check for specific CD antibodies before beginning treatment with interferon and during follow-up.
In conclusion, we suggest that the findings of this study should be open to a more conservative interpretation. Therefore, large follow-up studies, including a sample size that is more representative of the prevalence of CD, are needed to clarify how HBV infection may affect the development of this condition and to identify primary prevention strategies.
References:
1. Leonardi S, La Rosa M. Are Hepatitis B Virus and Celiac Disease Linked? Hepat Mon.2010;10(3):173-5. [HepatMon]
2. Brandtzaeg P. The changing immunological paradigm in coeliac disease. Immunol Lett. 2006;105(2):127-39. [PubMed]
3. Di Sabatino A, Corazza GR. Coeliac disease. Lancet. 2009;373(9673):1480-93. [PubMed]
4. Plot L, Amital H. Infectious associations of Celiac disease. Autoimmun Rev. 2009;8(4):316-9. [PubMed]
5. Soto Iglesias S, Vazquez Rodriguez S, Ulla Rocha JL, et al. [Onset of celiac disease after acute hepatitis B infection]. Gastroenterol Hepatol.2010;33(1):17-20. [PubMed]
.
Hepatitis B and Celiac Disease
.
Authors: Freeman HJ
University of British Columbia, Vancouver, BC, Canada
Correspondence:
Hugh James Freeman,
Department: University of British Columbia
Address: MD, FRCPC, FACP Professor of Medicine (Gastroenterology)
City: Vancouver, BC
Country: Canada
E-mail: hugfree@shaw.ca
Manuscript:
Dear Editor,
vidence suggests a linkage between different environmental agents and the development of celiac disease-an immune-mediated disorder-in those with a specific genetic predisposition (HLA-DQ2, HLA-DQ8) who exposed to gluten-a major storage protein in wheat and other grains. Infections, particularly viral agents, have been hypothesized to induce or exacerbate immune-mediated disorders, possibly through a mechanism of molecular mimicry (1, 2). Others have suggested that treatment of chronic viral infections (i.e., with α-interferon) or vaccines administered for prevention may be further triggers the process (1). In celiac disease, a host of chronic immunologically-based liver disorders may occur (3). Some early studies noted a relatively high frequency of hypertransaminasemia in celiac disease that usually resolved with a gluten-free diet (4). Failure of raised transaminase values to fall with a gluten-free diet led to eventual detection of chronic infection with hepatitis B or C viruses leading to the hypothesis that infection with hepatitis B or C viruses may trigger or "unmask" the underlying celiac disease.
In the study conducted by Leonardi and Rosa (5), serological testing for celiac disease antibodies was performed in 60 patients with chronic hepatitis B carrier state or a prior, but recovered, hepatitis B infection. Some of the carriers were treated for 12 months with α-interferon. Selective IgA deficiency was not present. In all 60 patients, IgA endomysial antibodies (EMA)-using a monkey esophagus immunofluorescence assay-and IgA tissue transglutaminase antibodies (tTGA)-using a commercial ELISA assay-were negative.
In summary, a linkage between hepatitis B infection and serologically-defined celiac disease could not be established. Moreover, there was no evidence that α-interferon could activate celiac disease. Although the investigators acknowledge the limited sample size of their hepatitis B cohort, the study still provides intriguing data. Future studies might also need to directly examine intestinal biopsies, not only for histological evidence of celiac disease, but for evidence of prior viral "footprints" (6), including identification of specific viral sequences.
References:
1. Molina V, Shoenfeld Y. Infection, vaccines and other environmental triggers of autoimmunity. Autoimmunity. 2005;38(3):235-45. [PubMed]
2. Plot L, Amital H. Infectious associations of Celiac disease. Autoimmun Rev. 2009;8(4):316-9. [PubMed]
3. Freeman H. Hepatic manifestations of celiac disease. Clinical and Experimental Gastroenterology.2010:3:23-39. [Link]
4. Bardella MT, Fraquelli M, Quatrini M, Molteni N, Bianchi P, Conte D. Prevalence of hypertransaminasemia in adult celiac patients and effect of gluten-free diet. Hepatology. 1995;22(3):833-6. [PubMed]
5. Leonardi S, La Rosa M. Are Hepatitis B Virus and Celiac Disease Linked? Hepat Mon.2010;10(3):173-5. [HepatMon]
6. Schattner A, Rager-Zisman B. Virus-induced autoimmunity. Reviews of infectious diseases. 1990;12(2):204-22. [PubMed]
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