Hepat Mon. 2010; 10(4): 311-312
Celiac Disease and Viral B Hepatitis: Lessons for Clinical Practice
Gastroenterology Service, ASL BAT, Andria (BAT), Italy
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
eliac disease (CD) is a chronic inflammatory
disease of the gut occurring in genetically
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.
Dr. Antonio Tursi, Servizio di Gastroenterologia Territoriale,
DSS No. 4, ASL BAT, Via Torino, 49, 70031 Andria (BAT),
Received: 02 Aug 2010 Revised: 15 Aug 2010
Accepted: 25 Aug 2010
Hepat Mon. 2010; 10 (4): 311-312
Archive of SID
Hepat Mon. 2010; 10(4): 311-312
Celiac Disease and HBV: Lessons for Clinical Practice
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
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.
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