Dear Editor,
We read with interest the article by Israeli et al. on Anti-
Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies as
predictors of inflammatory bowel disease as they concluded that ASCA and
pANCA may predict development of inflammatory bowel disease years before
the disease is clinically diagnosed.[1]
Anti-Saccharomyces cerevisiae antibodies (ASCA) are known as specific
markers in Crohn's disease albeit the clinical relevance of these
antibodies to some oligomannose epitope of the Saccharomyces cerevisiae is
not clear. Neither the origin and nor the clinicopathological role are
clarified. It is also known that ASCA positivity correlates principally
with small intestines. Crohn's disease and in these cases both the IgG and
IgA type antibodies are present.[2,3]
Gluten-sensitive enteropathy (GSE) or, as it is more commonly called,
celiac disease, is another immune-mediated enteropathic condition
(specified as an autoimmune inflammatory disease of the small intestine)
that is precipitated by the ingestion of gluten, a component of wheat
protein, in genetically susceptible persons.
In 2003, we examined whether there was ASCA positivity in our patients
with biopsy-confirmed celiac disease in a pilot study and found a
relatively high incidence of ASCA in GSE. Our and other’s results also
foreshadows that ASCA positivity predicts both CD and celiac disease.[4-6]
Both celiac disease and Crohn’s disease are characterized by the presence
of distinct (auto) antibodies. Theoretically and practically it is
thinkable that ASCA positivity is not only a specific marker of Crohn’s
disease but correlates with the (auto-) immune inflammation of the small
intestines. Oligomannosids of Saccharomyces cerevisiae with modification
by ASCA can change their immunopathogenicity and trigger a process that
results in specific inflammation. The antibodies in the sera of the
analyzed ASCA positive cases proved a systemic immune response against
Saccharomyces cerevisiae and suggested the end of the oral tolerance
against the yeast’s antigens.
The diet restriction (elemental diet, total parenteral nutrition, and
faecal diversion) may ameliorate the status of the patients with Crohn’s
disease. It can also be speculated that the yeast-free diet as a part of
the therapy for the ASCA positive patients can be reasonable, moreover the
permanent "forbidding" of the yeast can be an acceptable alternative in
case of getting well.[7]
Reference List
(1) Israeli E, Grotto I, Gilburd B et al. Anti-Saccharomyces
cerevisiae and antineutrophil cytoplasmic antibodies as predictors of
inflammatory bowel disease. Gut 2005;54(9):1232-6.
(2) Bernstein CN, Orr K, Blanchard JF et al. Development of an assay
for antibodies to Saccharomyces cerevisiae: Easy, cheap and specific for
Crohn's disease. Can J Gastroenterol 2001;15(8):499-504.
(3) Quinton JF, Sendid B, Reumaux D et al. Anti-Saccharomyces
cerevisiae mannan antibodies combined with antineutrophil cytoplasmic
autoantibodies in inflammatory bowel disease: prevalence and diagnostic
role. Gut 1998;42(6):788-91.
(4) Barta Z, Csipo I, Szabo GG et al. Seroreactivity against
Saccharomyces cerevisiae in patients with Crohn's disease and celiac
disease. World J Gastroenterol 2003;9(10):2308-12.
(5) Tursi A, Giorgetti GM, Brandimarte G et al. High prevalence of
celiac disease among patients affected by Crohn's disease. Inflammatory
Bowel Diseases 2005;11(7):662-6.
(6) Yang A, Chen Y, Scherl E et al. Inflammatory bowel disease in
patients with celiac disease. Inflammatory Bowel Diseases 2005;11(6):528-
32.
(7) Barclay GR, McKenzie H, Pennington J et al. The effect of
dietary yeast on the activity of stable chronic Crohn's disease. Scand J
Gastroenterol 1992;27(3):196-200.
Dear Editor,
We read with interest the article by Israeli et al. on Anti- Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies as predictors of inflammatory bowel disease as they concluded that ASCA and pANCA may predict development of inflammatory bowel disease years before the disease is clinically diagnosed.[1]
Anti-Saccharomyces cerevisiae antibodies (ASCA) are known as specific markers in Crohn's disease albeit the clinical relevance of these antibodies to some oligomannose epitope of the Saccharomyces cerevisiae is not clear. Neither the origin and nor the clinicopathological role are clarified. It is also known that ASCA positivity correlates principally with small intestines. Crohn's disease and in these cases both the IgG and IgA type antibodies are present.[2,3]
Gluten-sensitive enteropathy (GSE) or, as it is more commonly called, celiac disease, is another immune-mediated enteropathic condition (specified as an autoimmune inflammatory disease of the small intestine) that is precipitated by the ingestion of gluten, a component of wheat protein, in genetically susceptible persons.
In 2003, we examined whether there was ASCA positivity in our patients with biopsy-confirmed celiac disease in a pilot study and found a relatively high incidence of ASCA in GSE. Our and other’s results also foreshadows that ASCA positivity predicts both CD and celiac disease.[4-6]
Both celiac disease and Crohn’s disease are characterized by the presence of distinct (auto) antibodies. Theoretically and practically it is thinkable that ASCA positivity is not only a specific marker of Crohn’s disease but correlates with the (auto-) immune inflammation of the small intestines. Oligomannosids of Saccharomyces cerevisiae with modification by ASCA can change their immunopathogenicity and trigger a process that results in specific inflammation. The antibodies in the sera of the analyzed ASCA positive cases proved a systemic immune response against Saccharomyces cerevisiae and suggested the end of the oral tolerance against the yeast’s antigens.
The diet restriction (elemental diet, total parenteral nutrition, and faecal diversion) may ameliorate the status of the patients with Crohn’s disease. It can also be speculated that the yeast-free diet as a part of the therapy for the ASCA positive patients can be reasonable, moreover the permanent "forbidding" of the yeast can be an acceptable alternative in case of getting well.[7]
Reference List
(1) Israeli E, Grotto I, Gilburd B et al. Anti-Saccharomyces cerevisiae and antineutrophil cytoplasmic antibodies as predictors of inflammatory bowel disease. Gut 2005;54(9):1232-6.
(2) Bernstein CN, Orr K, Blanchard JF et al. Development of an assay for antibodies to Saccharomyces cerevisiae: Easy, cheap and specific for Crohn's disease. Can J Gastroenterol 2001;15(8):499-504.
(3) Quinton JF, Sendid B, Reumaux D et al. Anti-Saccharomyces cerevisiae mannan antibodies combined with antineutrophil cytoplasmic autoantibodies in inflammatory bowel disease: prevalence and diagnostic role. Gut 1998;42(6):788-91.
(4) Barta Z, Csipo I, Szabo GG et al. Seroreactivity against Saccharomyces cerevisiae in patients with Crohn's disease and celiac disease. World J Gastroenterol 2003;9(10):2308-12.
(5) Tursi A, Giorgetti GM, Brandimarte G et al. High prevalence of celiac disease among patients affected by Crohn's disease. Inflammatory Bowel Diseases 2005;11(7):662-6.
(6) Yang A, Chen Y, Scherl E et al. Inflammatory bowel disease in patients with celiac disease. Inflammatory Bowel Diseases 2005;11(6):528- 32.
(7) Barclay GR, McKenzie H, Pennington J et al. The effect of dietary yeast on the activity of stable chronic Crohn's disease. Scand J Gastroenterol 1992;27(3):196-200.