Three forms of MC?

[harvest_table]

The subtypes of MC is interesting. I believe most of us have been DX with either collagenous colitis or lymophocytic colitis.

I've found info on 2 other subtypes: in general here's what I've learned so far.

collagenous enterocolitis: very rare, describes possible drug toxicity and gluten sensitivity, giant cells

lymophocytic enterocolitis- very rare, describes sprue like condition with malabsorption, steriod resistant, not responsive to gluten free diet, common among celiacs

Anyone been DX with a subtype?

Love,
Joanna

[mle_ii]

The subtypes of MC is interesting. I believe most of us have been DX with either collagenous colitis or lymophocytic colitis.

I've found info on 2 other subtypes: in general here's what I've learned so far.

collagenous enterocolitis: very rare, describes possible drug toxicity and gluten sensitivity, giant cells

lymophocytic enterocolitis- very rare, describes sprue like condition with malabsorption, steriod resistant, not responsive to gluten free diet, common among celiacs

Anyone been DX with a subtype?

Love,
Joanna

Interesting, where did you find this? I wonder what the difference in diagnosis is.

[harvest_table]

This is an interesting article:

Chang F, Deere H, Vu C.
Department of Histopathology, St. Thomas' Hospital, Guy's & St Thomas' NHS Foundation Trust, London, United Kingdom. fuju.chang@gstt.nhs.uk

Microscopic colitis is defined as a syndrome of chronic watery diarrhea with a chronic inflammatory cell infiltrate in the colonic mucosa but without significant abnormalities at colonoscopy. It encompasses at least two histopathologic entities (ie, collagenous and lymphocytic colitis). The recognition and characterization of microscopic colitis has markedly changed the approach to the evaluation and management of chronic diarrhea. The histologic features of collagenous and lymphocytic colitis are well known to most pathologists. By considering the clinical history and symptoms, the pathologist should be able to reach the correct diagnosis in most cases. However, the spectrum of morphologic changes associated with watery diarrhea syndrome appears to be broader than originally thought. Morphologic changes more often associated with chronic inflammatory bowel disease or even chronic ischemic or infectious colitis have been noted in patients with clinically established microscopic colitis. The data presented in this article suggest that microscopic colitis is a heterogeneous entity, which includes both classic and "atypical" forms. Problems arise when cases do not fit the usual pattern or lack some of the findings that are expected. Pathologists should be aware of the presence of atypical forms of microscopic colitis.

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum

The article link nets to similar articles on the subject

Love,
Joanna

[harvest_table]

Mike, here are a few links

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

Um, maybe more than you wanted. It's all interesting.

Love,
Joanna

[mle_ii]

I should have just googled the term. :)

Here's info:

Enterocolitis
From Wikipedia, the free encyclopedia
Enterocolitis (or "coloenteritis") is an inflammation of both the small and large intestine. However, most conditions are categorized as one or the other of the following:

Enteritis is the inflammation of the small intestine
Colitis is inflammation of the large intestine, especially the colon
One specific type of enterocolitis is necrotizing enterocolitis.

So it appears that you would need an investigation of the small intestine as well. Something that wasn't done for me.

What symtoms warrant this type of investigation I wonder?

Thanks,
Mike

[mle_ii]

Wow, look at this...

Breen et al. noted a celiac proctitis in 11 of 42 patients (8) with histologic descriptions resembling lymphocytic colitis in most cases.

Breen EG, Coughlam G, Connoly CE et al. Coeliac proctitis. Scand J Gastroenterol 1987;22:471-7.

Here's the link if it works...
http://www.jpgn.org/pt/re/jpgn/fulltext ... -00018.htm

[harvest_table]

Mike,

Yes, it's interesting stuff! The following quote intrigues me

The data presented in this article suggest that microscopic colitis is a heterogeneous entity, which includes both classic and "atypical" forms. Problems arise when cases do not fit the usual pattern or lack some of the findings that are expected. Pathologists should be aware of the presence of atypical forms of microscopic colitis

Here's another study that might be of interest . I'm not sure what to make of it all.

ARTICLE LINKS:
Fulltext
Colonic Epithelial Lymphocytosis Without a Thickened Subepithelial Collagen Table: A Clinicopathologic Study of 40 Cases Supporting a Heterogeneous Entity.

Original Articles

American Journal of Surgical Pathology. 23(9):1068, September 1999.
Wang, Nancy M.D.; Dumot, John A. D.O.; Achkar, Edgar M.D.; Easley, Kirk A. M.S.; Petras, Robert E. M.D.; Goldblum, John R. M.D.
Abstract:
Lymphocytic colitis (LC) is classically described as a triad of chronic nonbloody, watery diarrhea, normal or nearly normal endoscopy findings, and colonic epithelial lymphocytosis without a thickened subepithelial collagen table (SECT). It is unknown how often patients with colonic epithelial lymphocytosis without a thickened SECT actually present with this classic triad. Cases diagnosed histologically as lymphocytic or microscopic colitis were reviewed. Criteria for inclusion were the presence of at least 15 surface lymphocytes per 100 epithelial cells and the absence of a thickened SECT (<12 [mu]m). Clinical features and course were recorded by chart review and telephone follow-up. Forty patients met the inclusion criteria, including 25 women and 15 men with a mean age of 63.2 years (range, 25-83 years). Twenty-eight patients had the classic triad and were designated as having classic LC. The other 12 patients fulfilled the histologic criteria but not the clinical or endoscopic criteria for classic LC and were classified as having atypical LC (constipation, five patients; macroscopic colitis at endoscopy, five patients; hematochezia, one patient; and incidental finding, one patient). Clinically, patients with classic LC were predominantly women and had a higher incidence of autoimmune disease (p = 0.03) than did those with atypical LC. Histologically, surface eosinophilia was significantly greater in patients with classic LC (p = 0.04). Twenty patients were using nonsteroidal antiinflammatory drugs at the time of their colonic biopsy. Surface epithelial lymphocyte counts were higher in these patients, particularly in the distal sigmoid colon (p = 0.02). Fourteen patients had associated autoimmune disease, including three patients with sprue diagnosed by small bowel biopsy, all of whom responded to gluten withdrawal. Diarrhea present in 25 patients, without documented evidence of celiac sprue, was self-limited in five, resolved with treatment in three, required intermittent treatment in eight, daily treatment in five, and was refractory to treatment in four. All eight patients who experienced spontaneous or treatment-related symptom resolution had classic LC. No histologic feature correlated with clinical course. In conclusion, our study shows that colonic epithelial lymphocytosis without a thickened SECT is a histologic finding seen in a heterogeneous group of patients. Within this heterogeneous group is a distinct subset of patients who have the classic clinicopathologic triad of LC. This subset of patients has striking similarities to patients with collagenous colitis, lending further support to a close relationship between these two entities. Atypical LC comprises a heterogeneous group and includes patients with idiopathic constipation, coexisting LC and inflammatory bowel disease, and possibly infectious colitides. Because of the clinical heterogeneity among our study population, the descriptive term colonic epithelial lymphocytosis may be a more prudent diagnosis than lymphocytic colitis in the absence of adequate clinical information.(C) 1999 Lippincott Williams & Wilkins, Inc.


Love,
Joanna

[mle_ii]

http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract

It appears that the rectal tissue can be affected by gluten, at least I think this is what it's saying:

Gastroenterology. 1989 Jul;97(1):29-37.

Studies of intestinal lymphoid tissue. XII. Epithelial lymphocyte and mucosal responses to rectal gluten challenge in celiac sprue.

Loft DE, Marsh MN, Sandle GI, Crowe PT, Garner V, Gordon D, Baker R.

Department of Medicine, University of Manchester School of Medicine, United Kingdom.

The immunopathologic, structural, and functional changes within rectal mucosa of known celiac sprue subjects were quantitated during local challenge with a peptic-tryptic digest of gluten. In the celiac sprue patients challenged with 2 g of digest, major effects occurred in lamina propria, submucosa, and local microvasculature. The lamina propria swelling was biphasic, starting 1-2 h after challenge with widespread extravascular deposition of fibrinogen, indicative of increased microvascular permeability, receding by 24 h postchallenge. A rapid fall in mast cells together with granule discharge suggested their involvement in this response. The late-phase swelling (48-72 h) was preceded by a rapid influx of neutrophils and basophils, the latter showing evidence of degranulation beyond 72 h. Reestablishment of vessel lumina, a rise in mast cells, and loss of neutrophils indicated tapering of the inflammatory cellular cascade by 96 h. Lymphocytes, first seen to enter the lamina by 2 h postchallenge, increased progressively, thereby resulting in substantial infiltration between 36 and 96 h. A marked rise in epithelial lymphocytes, maximal at 6-8 h, waned by 24 h. Volumes of surface and crypt epithelium remained constant throughout. In another challenge series with 4 g of gluten digest, electrical potential difference across rectal mucosa decreased significantly 12 h postchallenge, but the associated decreases in net sodium and chloride absorptive fluxes were insignificant. It is concluded that rectal mucosa is sensitized to gluten in celiac sprue disease and thus offers a promising and convenient in vivo substrate for investigative and diagnostic purposes.

What is also interesting is to not the time frames. Given that it takes some time to get to the rectum via the GI and given the times until reaction and reactions are over, no wonder it's so difficult to pinpoint where gluten is getting in.

Mike

[mle_ii]

Anyone have info on GI transit times for foods?

[mle_ii]

Well no wonder I've got proctitis. Given the transit time (estimated/average) the gluten I might ingest and react to is in the colon a long time. Here's some info:

it is difficult to state with any precision how long ingesta remains in the stomach, small intestine and large intestine. Nonetheless, there have been many studies on GI transit, and the table below presents rough estimates for transit times in healthy humans following ingestion of a standard meal (i.e. solid, mixed foods).

50% of stomach contents emptied 2.5 to 3 hours
Total emptying of the stomach 4 to 5 hours
50% emptying of the small intestine 2.5 to 3 hours
Transit through the colon 30 to 40 hours
Remember that these are estimtes of average transit times, and there is a great deal of variability among individuals and in the small person at different times and after different meals.

http://www.vivo.colostate.edu/hbooks/pa ... ansit.html

[tex]

Mike,

I believe those experiments are referring to data gathered after introducing a gluten challenge by way of the rectum, (your second and third posts back). There is no transport time involved--only reaction time.

A rectal challenge means that the test medium used for the challenge is introduced directly into the rectum. This is used to accurately measure inflammation response times, and possibly other effects.

Tex

[mle_ii]

Mike,

I believe those experiments are referring to data gathered after introducing a gluten challenge by way of the rectum. There is no transport time involved--only reaction time.

A rectal challenge means that the test medium used for the challenge is intrtoduced directly into the rectum. This is used to accurately measure inflammation response times, and possibly other effects.

Tex

Yes I understood that, but since gluten isn't digested (or is it) or perhaps not totally digested wouldn't it make it's way to the colon and rectum?

Perhaps not in the quantities, but definitly has the potential given that we have compromised GI systems and the already don't digest everything correctly.

[mle_ii]

It also appears that refined sugars slow down transit time, I would have thought the opposite though.

http://gut.bmjjournals.com/cgi/content/ ... t/32/4/367

Gut, Vol 32, 367-371, Copyright © 1991 by BMJ Publishing Group

Effect of diets low and high in refined sugars on gut transit, bile acid metabolism, and bacterial fermentation
W Kruis, G Forstmaier, C Scheurlen and F Stellaard
Medizinische Klinik I, Albertus-Magnus-Universitat, Kolin.

Increasing consumption of refined sugar has been implicated in many gastrointestinal disorders on epidemiological grounds. Nine volunteers agreed to participate in a study comparing the effects of a diet containing 165 g refined sugar/day with a diet of only 60 g/day on gut transit, bile acid metabolism, and fermentative activity of the intestinal flora. The wet and dry weight, pH, and water content of the stools were similar on the two diets. On the high sugar diet mouth-to- anus transit time was significantly prolonged, despite a shortened mouth-to-caecum transit time. The faecal concentration of total bile acids and the faecal concentration of secondary bile acids increased significantly. Diet affected neither the serum bile acid pattern nor the concentration. Breath hydrogen tests showed significantly enhanced H2 production on the high sugar diet. We conclude that the quantity of refined sugar in the diet can significantly influence gut function and the composition of bowel contents.

[tex]

I'm not sure what you're getting at, but yes, the gluten eventually travels all the way through the GI system. The toxic gliadins in gluten are what we react to in the small intestine and colon.

Tex

P S Yes, those gliadins are undigestible proteins. They pass through a "normal" digestive system without effect, but in our digestive systems, they cause inflammation.

[mle_ii]

What I'm getting at is that my proctitis and could be related to gluten. This is something I've wondered about and now it makes sense. What am I missing that has you confused?

Given that the colon isn't very long and associated with a longer transit time than the small intestines it has more potential for reactions to gluten due to being in contact with gluten longer over a smaller area.

I wonder what the number of folks diagnosed with Celiac also have some form of colitis.

I'm curious, let's say that the antibodies are first produced at orginal contact with gluten, the doudonem (sp), do these antibodies then get produced all over the GI or the body or are they only local to the area of orginal contact. Though other areas would, I suspect, also produce antibodies with continual contact.