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Printable Handouts
Navigable Slide Index
- Introduction
- Disclosures
- The celiac affection
- Celiac disease is common (1)
- Small intestinal biopsy capsule
- Celiac disease is common (2)
- Prevalence of celiac disease in the US
- Recent increase in celiac disease diagnosis
- Celiac disease (CD) - then and now
- The spectrum of gluten sensitivity
- Celiac disease: age of presentation
- Celiac disease: diagnostic algorithm (1)
- The clinical manifestations of celiac disease
- 27 year old woman with severe pneumonia
- Celiac disease and irritable bowel syndrome
- Celiac disease: diagnostic algorithm (2)
- Celiac disease: diagnostic criteria
- Serum IgA tTG test
- Serum antibody tests for untreated CD
- Anti-DGP: "new and improved" AGA test
- DGP serology for diagnosis of celiac disease
- Endoscopic features of celiac disease
- Villous atrophy in celiac disease
- Endoscopic markers of celiac disease
- The endoscopic markers are not sensitive
- Enteropathy in celiac disease
- Celiac disease: histology
- Is small intestinal biopsy necessary for diagnosis
- Celiac disease: diagnostic algorithm (3)
- IgA tTG positive - normal biopsy
- The spectrum of gluten sensitivity
- Celiac disease: diagnostic algorithm (4)
- IgA tTG negative - abnormal biopsy
- Celiac disease: diagnostic algorithm (5)
- Treatment of celiac disease
- Management of celiac disease
- Celiac enteropathy usually heals on the GFD
- Non-responsive CD and refractory CD
- "Non-responsive" celiac disease
- Non-responsive celiac disease: etiology
- Predicting cause of non-responsive CD
- IgA tTG and response to GFD
- Celiac disease: response to GFD
- Celiac disease adherence tool (CDAT)
- Non responsive CD: diagnostic algorithm (1)
- Non responsive CD: diagnostic algorithm (2)
- Refractory celiac disease
- Abnormal IELs in refractory sprue
- Abnormal IEL is associated to decreased survival
- Treatment of refractory sprue
- Celiac disease - summary
Topics Covered
- Changing estimates of disease prevalence
- Clinical spectrum of celiac disease
- Approach to diagnosis
- Serology testing
- Histopathology in diagnosis
- Management
- Non-responsive celiac disease
- Refractory celiac disease types I and II
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Kelly, C. (2022, April 12). Celiac disease [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 10, 2024, from https://doi.org/10.69645/EKTY1625.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. Ciaran Kelly has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
A selection of talks on Clinical Practice
Transcript
Please wait while the transcript is being prepared...
0:00
Hello, my name is Ciaran Kelly and
I'm the medical director of
the Celiac center at
Beth Israel Deaconess Medical Center,
which is an affiliate of Harvard
Medical School in Boston Massachusetts,
0:18
and I'll be speaking on celiac disease.
0:22
The first descriptions of celiac
disease in the medical literature have
been attributed to Aretaeus
who worked in Cappadocia and
in 50AD wrote a narrative describing the
clinical manifestations of celiac disease.
In 1888, Samuel Gee, who worked in London,
wrote his treaties on
the celiac affection and
described many of the classical and
atypical features of celiac disease,
including descriptions of the disease
presenting in children and in adults.
He also made the very astute observation
that if the disease is to be cured at all,
it must be by means of diet.
However, his dietary recommendations were
somewhat off key in that he recommended
bread toasted on both sides as a treatment
for celiac disease and as we know,
toasting bread does not inactivate
the toxic gluten moieties of wheat.
In 1950, a major breakthrough was
made when a Dutch pediatrician
identified wheat gluten as a toxic
factor for children with celiac disease.
Based on at the clinical observation that
his patients with celiac disease improved
during rationing that occur during the
Second World War when, of course, wheat
was less available whereas the rest of
his population the rest of his practice,
was becoming less well nourished,
those with celiac disease thrived.
Based on this observation, he hypothesized
that celiac disease was caused by
something that was less available
during Second World War rationing.
And this led him ultimately to
the identification of wheat, barley, and
rye as the toxic factors
in celiac disease.
In 1997 doctor Schuppan and
his colleagues working in Germany
identified tissue transglutaminase as
an autoantigen in celiac disease and
this has led to a number of major
advances in celiac disease.
The most evident being in the way
in which we diagnose celiac disease
using tissue transglutaminase
antibody testing.
However, tissue transglutaminase also
has a role in disease pathogenesis,
which I'll touch upon later.
And has also changed our understanding
of the epidemiology of celiac disease,
which I'll also discuss later.