Aha! I Found Evidence of Proof Of Another Of Our Theories

[tex]

Hi All,

Remember a few times when we've seen small intestinal biopsy reports where intraepithelial lymphocytes were found, but celiac disease was not diagnosed? Well the pathologists who make such determinations are apparently using obsolete criteria. The current consensus of opinion is leaning toward the recognition that increased intraepithelial lymphocytes in the proximal small intestine, (the upper small intestine), can sometimes be interpreted as evidence of the early stages of celiac disease. How about that? Note that there are many other possible causes of increased intraepithelial lymphocytes in the small intestine, but the acknowledgment that one of the causes can be gluten-sensitive enteropathy, is a huge step in the right direction.

That gluten sensitivity can be morphologically manifest by intraepithelial lymphocytosis without villus atrophy is increasingly being appreciated by pathologists (Figure 2). The reported prevalence of gluten-sensitive enteropathy (GSE) as the cause of increased IELs in architecturally normal small intestinal biopsies has ranged from 9% to 40%,9,10,18 although for reasons mentioned subsequently the exact prevalence is difficult to determine.

The red emphasis is mine, of course. This suggests that the doctors who insist that both positive serology and villus atrophy must be present in order for a patient to qualify for a celiac diagnosis, are just plain wrong. I have a hunch that this suggests that a fair number of us with MC, would probably qualify for a celiac diagnosis, on that basis.

The pathologists may eventually bring the GI docs to their senses on this issue, given enough time. Of course, this article was written in 2006, and not much has happened yet, but I'm guessing that not many GI docs read pathology publications, as a matter of routine, so it will probably take a while for the word to trickle down.

http://www.archivesofpathology.org/doi/ ... 2.0.CO%3B2

Note that, (IMO, at least), this could possibility be interpreted as official recognition that non-celiac gluten-sensitivity does indeed exist.

Consider this:

Although small intestinal biopsy remains the gold standard for the diagnosis of GSE, it is usually supplemented by serologic tests. The latter includes immunoglobulin (Ig) A antiendomysial antibodies, IgA antitissue transglutaminase (which has largely replaced the IgA antiendomysial antibody test), and IgA and IgG antigliadin antibodies. The first 2 have optimal sensitivity and specificity as well as high positive predictive value.23,24 A positive IgA antiendomysial antibody test or a significantly raised anti–tissue transglutaminase titer helps confirm the diagnosis of GSE even when villus architecture is normal.25 Unfortunately, the likelihood of a positive test correlates with the degree of mucosal injury and GSE cases with intraepithelial lymphocytosis alone can often have antibody titers in the normal range.25–28 Thus, negative serology does not exclude a diagnosis of GSE with a Marsh type 1 pattern.

That admits that the blood tests aren't worth much - they only turn positive after the patient suffers significant intestinal damage. Incidentally, quite a few people with MC, (especially CC), present with at least a Marsh 1 level of small intestinal damage, (if their GI doc bothers to biopsy their small intestine). Consider this quote from the article at the following link:

Coeliac disease was found in four out of the 10 patients with collagenous colitis who had had a small bowel biopsy

http://jcp.bmj.com/content/45/9/784

And in a study of patients with LC,

Moreover, in over 10% of patients who underwent esophagogastroduodenoscopy, duodenal biopsies showed villi alterations classified as Marsh I damage, without clinical and serological data for diagnosis of CD.

http://www.ncbi.nlm.nih.gov/pubmed/20575599

Note that this is exactly the message that that Dr. Fine has been preaching, (though obviously based on a different testing mechanism), for the last 10 years - that people with gluten-sensitivity shouldn't have to wait until their small intestine is severely damaged, before receiving a diagnosis of celiac disease.

Tex

[Polly]

Great find, Tex!

Even if GI docs don't read pathology publications, that's OK because it is the pathologist who can make the diagnosis. Now......... if only all of the pathologists who see lymphocytes in the small intestine biopsy would say "indicative of celiac disease" after they note their findings, that would be a big step forward.

Love,

Polly

[Zizzle]

Very interesting. I've convinced my mother in Guatemala to try a gluten-free diet, despite a recent endoscopy with biopsies NOT showing a Marsh 3 result. She was being eveluated for chronic upper GI pain, belching, indigestion, etc. Can someone help me interpret her results?

Her overall diagnosis from biopsies (translated) is: Moderate chronic active gastritis with regenerative changes +2, moderate glandular atrophy and presence of bacilli compatible with helicobacter pylori, density II, biopsies of the antrum, incisura and body gastric angle. Moderate chronic duodenitis and Moderate chronic esophagitis.

The duodenal biopsy portion read:
Duodenal mucosal biopsies have some tall, thin villi and others enlarged, all lined by simple columnar epithelium with discrete alterations in nuclear polarity and adequate lymphocytes. Gastroesophageal junction biopsies show partial coating non-keratinized stratified squamous epithelium with moderate acanthosis and presence of prominent connective papillae with congestion. In addition to this epithelium is observed cardia type epithelium. With multifocal hyperplasia. In the lamina propria is moderately increased lymphoplasmacytic cellularity. There are no areas of intestinal metaplasia.

Would a good GI doc in this country classify this as possible celiac? Or is this simply inflammatory changes caused by the H.Pylori infection? Her doc said she probably picked up H.Pylori as a child (I guess everyone in Latin America has it), so my question is, what allowed it to reproduce now and cause so much damage? Perhaps a GI system compromised by gluten sensitivity? She is feeling MUCH better on a bland GF diet, including mood, and she hasn't begun the treatment for H.Pylori yet, so I suspect she is gluten-sensitive (and the source of my HLADQ2 gene). But will her doctor tell her she absolutely does not have celiac disease?

This is the assessment from the visual portion of the endoscopy. Sounds like she's a mess! Is a GF diet ever recommended for someone with so much upper GI inflammation, even if they are not celiac?

Esophagitis gastroesophageal reflux grade A
Barrett’s Esophagus Short Segment (0.5 cm)
2 venous pathways in the Middle Esophagus do not reach the distal esophagus (rule out incipient varicose)
Ulcer 0.5 cm in the distal esophagus (with active bleeding), and irregular tissue (rule out Metaplasia)
Congestive gastropathy and widespread erosion
Chronic erosive gastropathy with areas of atrophy in the gastric antrum
Mild Bulboduodenitis
Marked Duodenal-Gastric Bile Reflux
Vestiges of old hemorrhage in gastric chamber.

[tex]

Wow! She definitely has some issues. Unfortunately, I'm already late getting to work, so I'll have to respond to this later. How soon I get back will depend on what's going on at work - hopefully I can get things sorted, and be back here pretty soon.

In the meantime, despite all the damage, I seriously doubt that the average GI doc here in this country would diagnose celiac disease. They are going to insist that villus atrophy is a prerequisite for a celiac disgnosis, whereas she appears to have villus hyperplasia - the opposite of villus atrophy.

Tex