<<Disclaimer: Verify this information before applying it to your situation.>>
 
The duodenum is the first part of the small intestine after you leave the
stomach.  It is exposed to acid and stomach digestive enzymes.  It has a
built-in defense against these corrosive materials.  In many diseases the
duodenum becomes inflammed.  In duodenal ulcer disease, a bacterium,
Helicobacter pylori damages alters the amount of acid the stomach produces
and reduces the defense against the acid resulting in damage of the duodenum
and ulcers.  This is way and far the most common inflammation of the
duodenum.
 
However there are other things that inflame the duodenum and one of those is
celiac disease.  Celiac disease affects the first part of the small intestine
( duodenum more than any other part) the damage may get less furhter douwn
the intestine.  The extent of small intestine involved by the celiac damage
may determine which symptoms the patient gets.  If a lot of the small
intestine is involved then diarrhea and malabsorption is more likely.
However if only a short portion of the intestine is involved then there may
be no diarrhea.  The major consequence may be the result of the inflammation
of the duodenum with pain bloating nausea and vomiting, that may be the same
symptoms as those of the much more common peptic ulcer disease.  Indeed some
patients may even have ulcers that look like the peptic ulcers further
confusing the picture and misleading the physician.  Many patients biopsies
taken by the endoscopists may have been called "non specific duodenitis " in
the past where the pathologist may have assumed that the inflammation was
caused by aicd damage and peptic ulcer disease.
 
There some things that can be done to clarify this.
 
1. Have a high index of suspicion for CD, especially if the patient does not
have helicobacter, or is not on large doses of anti-arthritis drugs.
 
2. Take biopsies in the duodenum past the area that have ulcers or obvious
inflammation (the findings of celiac disease inflammation is more widespread
than the damage with peptic ulcer disease which is usually located tio the
spots whre the ulcers is.
 
3. The pathologist needs to look for intraepithelial lymphocytosis and the
chronic inflammatory cells in the lamina propria( deeper layer)  And draw the
attention of the clinician to the alternate possibility.
 
4. Antibody tests may be helpful in differentiating the 2 conditions.
 
The above represents a new approach to this problem and would not have been
common or usual practise even 3-4 years ago.
 
This is not medical advice and should not be used as such.  It is intended to
be general information and is part of the educational mission of the Univ of
Iowa.
 
Joe Murray MD
Univ of Iowa