<<Disclaimer: Verify this information before applying it to your situation.>>

To those of you with both Celiac Disease and colitis, I can sympathize with
you because I have gastritis (stomach inflammation), and lymphocytic
gastritis has been implicated in Celiac Disease.  These lymphocytes which
attack our villi are also being found in the colon and stomach.  Although my
Gastroenterologist who is the Chief of his Gastroenterology department
cannot identify whether I have lymphocytic gastritis, he admitted at my
diagnosis meeting that he was more worried about my stomach problems than my
adherence to a GF diet.  I’ve been GF now 7 months and any symptoms I have
due to continued fat malabsorption seem to stem from my stomach.  He
admitted that I have lymphocytes residing in my stomach, waiting for any
ingestion of gluten, and he could not estimate the time frame from which
these lymphocytes would eventually go to sleep (dormant).  Although I’m
strictly gluten-free, I am struggling to gain my entire weight back because
I lose weight when I eat fats and that is ironically why my
Gastroenterologist has prescribed a low fat diet to prevent further
malabsorption contributed by my stomach problems, not only due to gastritis
but my slow stomach emptying rate.   He also has me on a neutral pH food
diet (no acid or alkaline foods) which is ironically part of the treatment
of microscopic colitis, avoidance of acids as is present in caffeine and
alcohol.  He has told me the reason for the neutral pH of the foods is to
prevent slow gastric emptying which allows the bacteria to grow, produce
gases, and disrupt the environment of the stomach and small bowel leading to
further malabsorption.  Acids also exacerbate stomach inflammation and based
upon my medical readings, gastritis can cause slow stomach emptying.  My
Gastroenterologist calls my dilemma a vicious cycle.

The following is from a review article entitled “Microscopic Colitis”,
Peter Tagkalidis et al, Jour. of Gastro. And Hepat. 17:3, 236-243
(www.blackwell-synergy.com):
“Microscopic colitis is an umbrella term that includes two idiopathic forms
of inflammatory bowel disease: lymphocytic colitis and collagenous colitis.
The cardinal clinical manifestation of microscopic colitis is a watery,
non-bloody diarrhea.  The onset of the diarrhea is often sudden, and may in
its early stages be confused with an infective diarrhea. The clinical
course, however, is protracted, with an average of six bowel actions per day
but with more than 20 bowel actions per day not unusual. The long-term
pattern of diarrhea may be chronic and continuous, or intermittent and
relapsing.   Other features that are occasionally present include abdominal
cramping, anorexia, nausea, mild weight loss, urgency, and incontinence.
The presence of nocturnal diarrhea is a distinguishing feature from
irritable bowel syndrome, which is often a differential diagnosis.
Hypokalemia may occur in patients with severe diarrhea.   Malabsorption is
generally not seen in microscopic colitis, although mild steatorrhea and
protein-losing enteropathy have rarely been reported. Symptoms can often be
present for many months to years before the diagnosis is made, but there is
evidence to suggest that the period prior to diagnosis has reduced with
greater clinician awareness of the syndrome.

Celiac disease has been noted in association with lymphocytic and
collagenous colitis by numerous authors.  Only one study has reported a
prospective evaluation of celiac autoantibodies in all patients with
microscopic colitis presenting to their center.  Two out of 53 patients
(3.8%) demonstrated positive anti-endomysial antibodies.  A number of
retrospective studies have reported the diagnostic yield of various
investigations for celiac disease as less than 5% in microscopic colitis
populations.  One large series of 176 patients with collagenous and
lymphocytic colitis reported 10 cases of concomitant celiac disease.  When
the two are associated, the diagnosis of celiac disease often precedes that
of microscopic colitis, which is commonly made once the patient fails to
respond to a gluten-free diet.  HLA-DQ typing of patients with microscopic
colitis has shown an increased incidence of celiac-associated alleles,
including HLA-DQ2, compared to controls.  This study also demonstrated that
a majority of microscopic colitis patients have small bowel mucosal changes
ranging from a mild inflammatory infiltrate to subtotal villous atrophy.
The majority of these small bowel changes are seen in the presence of the
HLA-DQ2 allele, but with the absence of specific celiac autoantibodies.  In
other words, patients with microscopic colitis who do not have celiac
disease on the basis of a lack of autoantibodies and no response to gluten,
can demonstrate small bowel abnormalities similar to celiac disease.
A number of studies have examined colonic histology in patients with newly
diagnosed untreated celiac disease. Approximately 30% of such patients have
been found to harbor changes indistinguishable from lymphocytic colitis. The
incidence of such colonic abnormalities seems to be higher in patients with
refractory celiac disease.  The presence of increased colonic
intraepithelial lymphocytes was likely to be secondary to gluten exposure in
these patients, as improvement on a gluten-free diet was noted in the
majority.
A range of drugs have been associated with the development of lymphocytic
and collagenous colitis including non-steroidal anti-inflammatory agents
(NSAIDs), ticlopidine, ranitidine, carbamazepine, Cyclo 3 Fort, and
flutamide.”

Researchers are continuing to examine the genetic susceptibility and
environmental triggers such as drugs, bile acids, infection, or food antigen
which may be responsible for microscopic colitis.

This is the treatment algorithm I found in the review article “Microscopic
Colitis:  A Review,” Pardi et al, Amer. Jour. of Gastro. 97,4; 793-799) for
those of you with lymphocytic and collagenous colitis:
1) Discontinue NSAIDS, caffeine, dairy products, alcohol
2) Antidiarrheals
3) Bismuth subsalicylate
4) Cholestyramine or Aminosalicylates
5) Steroids
6) Azathioprine/6-mercaptopurine
7) ? octreotide, methotrexate, cyclosporin
8) surgery

I hope this helps.

Laura




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