Dr Lewey on Mast Cells

[mle_ii]

Some rather interesting reading about Mast Cells can be found here, seems that testing for increased lymphocytes has a partner in being missed during biopsy analysis.

http://thefooddoc.blogspot.com/2008/02/ ... -i-be.html

Mike

[tex]

Mike,

Great information. I'm gonna make a WAEG that excess mast cells may be the reason why several members here are unable to achieve remission, even though they're using a treatment combination of both diet and meds.

Tex

[mle_ii]

Agreed. And though I haven't read a lot about mast cells besides what he's written I wonder if the same opioid issue exists for mast cells or if it's somehow related.

Ok, I read a bit more about mast cells, so I'll have to reread what Dr Lewey said. But the problem I see with saying it is mast cells is that it involves IgE and what we would consider normal allergy responses. And no the intollerant type responses we see here.

Also, if it were mast cells I would think that those folks would have a great response to antihistamines or other antagonists to the mast cell allergic type response.

Another thing I thought of is perhaps those with more mast cells are more sensitive to lower levels of IgE antigens in the blood. So if they were to be tested for IgE allergies in a blood test it might not show enough of a reaction whereas with the larger number of mast cells ready to be signaled that the smaller numbers improve the chance of a reaction.

Another thought, perhaps due to some environmental trigger the mast cells deeper in the GI tract are more more numerous and thus we don't see the normal "allergic" response as it's not as close to the surface.

Like I said I've got to read more.

Thanks,
Mike

[mle_ii]

Not sure if Dr Lewey mentions this, but perhaps higher levels of Tryptase in the blood would be an indication of high numbers of mast cells.

http://en.wikipedia.org/wiki/Tryptase

[tex]

Well, we're talking about "customized" mast cells here , so to speak, aren't we? If I correctly remember what his article said, mast cells are site specific, IOW, they have special characteristics that are important to the type of tissue present in that particular location. He talks about their possible relationship to food intolerances, IBS, etc., but I don't recall him mentioning anything about the histamine reactions that are typically connected with classic allergy reactions.

More than that, though, I suspect that the main reason why classic histamine reactions are of no concern in the gut is because of the fact that there are at least four distinct types of histamine receptors that are found in various areas of the body. The histamine receptors found in smooth muscle tissue, central nervous system, etc., are type H1, and cause the classic allergy symptoms that you mention. The histamine receptors found in the small intestine, colon, and certain other internal organs, though, contain H4 histamine receptors. These particular receptors have an unknown physiological role.

Look at the "Mechanism of Action" chart at this site - you'll find it quite interesting, I believe.

http://en.wikipedia.org/wiki/Histamine

Remember when we talked about histamines causing the parietal cells in the stomach to increase the production of acid? According to the chart, those are type H2 histamine receptors, (located on the parietal cells).

Tex

[harvest_table]

Hi guys,

Just curious why Dr. Lewey does not mention microscopic colitis in this blog.

Check this out.

Microscopic Colitis: The ever-expanding
morphologic diagnosis
One key area of focus is within the
category of microscopic colitis. Ensure
that you are requesting that your
pathologist rule out all forms of
microscopic colitis. We are all familiar
with the two most widely known and
accepted forms of microscopic colitis:
lymphocytic colitis and collagenous
colitis. However, there is new evidence
that a mast cell form of microscopic
colitis also exists. This form of
microscopic colitis, known as mastocytic
enterocolitis, is characterized by an
increased number of mast cells present
in the patient’s tissue.

http://72.14.205.104/search?q=cache:AU1 ... cd=6&gl=us

This is a mast cell form of microscopic colitis- also.

[tex]

Hi Joanna,

Hmmmmmmm. Good point. Apparently he doesn't realize that mastocytic enterocolitis has been classified as a type of MC, or maybe that classification is not actually official, but simply the suggestion of the authors of the article that you cited. Dr. Lewey even mentions mastocytic enterocolitis in the title of his article, and if you look at the links to the right of his blog, there is another earlier article about it:

http://thefooddoc.blogspot.com/2008/02/ ... demic.html

but I didn't notice any reference to MC in it, either. I'll bet a GF cookie that he's not aware of the connection, or surely he would have at least mentioned it in passing.

Thanks for pointing that out - good observation.

Tex

[mle_ii]

Mucosal mast cells are pivotal elements in inflammatory bowel disease that connect the dots: Stress, intestinal hyperpermeability and inflammation
http://www.wjgnet.com/1007-9327/13/3027.asp

[mle_ii]

Ha, and take a look at this!

http://www.ncbi.nlm.nih.gov/pubmed/16373277
Detection of inflammatory markers in stools from patients with irritable bowel syndrome and collagenous colitis.

OBJECTIVE: Irritable bowel syndrome (IBS) and collagenous colitis (CC) share chronically recurring symptoms of altered bowel habits associated with abdominal pain or discomfort. The aims of the present study were to investigate whether inflammatory markers could be detected in faeces from patients with IBS and CC, and to elucidate whether such analyses could be used as non-invasive tools to distinguish between these disorders. MATERIAL AND METHODS: Stool samples were obtained from 18 patients with CC, 46 patients with IBS and 20 healthy controls (HC). Eosinophil protein X (EPX), myeloperoxidase (MPO), tryptase, interleukin-1 beta (IL-1beta) and tumour necrosis factor alpha (TNFalpha) were measured in supernatants from processed faeces using immunoassays. RESULTS: EPX levels were enhanced in faeces from CC patients (median 3.8 microg/g (0.47-16.2)) compared to patients with IBS (0.44 microg/g (0.25-1.8)), p<0.001, and HC (0.46 microg/g (0.21-1.3)), p<0.001. In addition, MPO was increased in CC patients (11.7 microg/g (2.0-124)) compared to IBS patients (1.7 microg/g (0.81-5.2)), p<0.01, and HC (2.5 microg/g (1.1-6.3)), p<0.05. Tryptase was found in 9/18 patients with CC, 6/46 with IBS and 1/19 HC. IL-1beta was only enhanced in 2/11 CC patients and TNFalpha was not detected in any sample. CONCLUSIONS: Increased levels of EPX, MPO and tryptase were observed in stools from collagenous colitis patients, whereas the levels in IBS patients did not differ from healthy controls. Our data suggest that faecal markers could be used as part of the clinical work-up to determine which patients should be biopsied and evaluated for collagenous colitis.

[mle_ii]

And this article, though I'm not sure about their conclusion of CC being a TH2 response given more recent information saying otherwise.

Different distribution of mast cells and macrophages in colonic mucosa of patients with collagenous colitis and inflammatory bowel disease.
http://www.ncbi.nlm.nih.gov/pubmed/12063968

BACKGROUND/AIMS: Chronic inflammatory cells in colonic mucosa is a histopathologic feature in patients with collagenous colitis and inflammatory bowel disease. The aim of this study was to compare the distribution of mast cells and macrophages in the colonic mucosa of patients with collagenous colitis, Crohn's disease, and ulcerative colitis. METHODOLOGY: Patients with histologically confirmed collagenous colitis (n = 13), Crohn's disease (n = 20) or ulcerative colitis (n = 20) and normal control patients (n = 20) were included in this study. Biopsy specimens were obtained from the sigmoid colon of each patient, and immunostained using antibodies to tryptase (AA1) and CD68. The number of mast cells and macrophages located in upper and lower part of the lamina propria was determined. RESULTS: The number of mast cells in the upper part of lamina propria in patients with collagenous colitis (286 +/- 89/mm2, mean +/- SD), Crohn's disease (330 +/- 84/mm2) and ulcerative colitis (355 +/- 90/mm2), was higher than normal controls (201 +/- 44/mm2). The number of mast cells in the lower part of lamina propria in patients with Crohn's disease (345 +/- 87/mm2) and ulcerative colitis (363 +/- 86/mm2) was higher than collagenous colitis (266 +/- 63/mm2) and normal controls (309 +/- 60/mm2). The number of macrophages in the lower part of lamina propria in patients with Crohn's disease (330 +/- 63/mm2) and ulcerative colitis (301 +/- 60/mm2) was higher than in collagenous colitis (247 +/- 46/mm2) and normal controls (242 +/- 52/mm2), although there were no significant differences in the number of macrophages present in the upper part of the lamina propria among the four groups. CONCLUSIONS: Our data showed the presence of a different distribution of mast cells and macrophages in collagenous colitis and inflammatory bowel disease, and these suggest that because mucosal mast cells have been implicated in the development of Th2 response collagenous colitis is more of a Th2 type reaction rather than Th1.

[mle_ii]

And these...

Collagenous colitis and eosinophilic gastritis in a 4-year old girl: a case report and review of the literature.
http://www.ncbi.nlm.nih.gov/pubmed/17718794

Collagenous colitis (CC), a form of microscopic colitis, is characterized by a thick subepithelial collagen layer in the colon in the presence of chronic nonbloody watery diarrhoea and macroscopically normal-appearing colonic mucosa. Typically affecting elderly adults, CC is rare in children with only 12 cases previously reported in the literature. We report the case of a 4-year-old girl with CC associated with eosinophilic gastritis, which was clinically responsive to treatment with ketotifen, a benzocycloheptathiophene derivative, and H(1) class of antihistamine that stabilizes mast cells and potentially impairs eosinophil migration to target organs. We review the published cases of paediatric-onset CC and summarize the links between eosinophils and CC in the clinical and basic science literature. CONCLUSION: CC is a rare cause of chronic diarrhoea in children and may relate to mast cell and eosinophil activity.

Enhanced histamine metabolism: a comparative analysis of collagenous colitis and food allergy with respect to the role of diet and NSAID use.
http://www.ncbi.nlm.nih.gov/pubmed/12755379

Increased colonic mucosal mast cells associated with severe watery diarrhea and microscopic colitis.
http://www.ncbi.nlm.nih.gov/pubmed/2766913

A patient with microscopic colitis, clearly identifiable by its histologic characteristics, is presented in whom the histology also revealed large numbers of mast cells. The patient was treated with H1 antagonists with prompt resolution of the diarrhea. The histologic and therapeutic findings in this case suggest the diarrhea and inflammation of microscopic colitis may be mediated by the degranulation of excessive numbers of mast cells in the colon and small bowel.

A novel enteropathy with partial villous atrophy, microscopic colitis, and pemphigoid change.
http://www.ncbi.nlm.nih.gov/pubmed/2661662

Microscopic colitis associated with gluten-resistant partial villous atrophy was documented in a 21-year-old woman with chronic nonbloody diarrhea. Electron microscopic examination of the colonic and duodenal biopsies showed focal separations of basal lamina from cryptal epithelial cells forming subepithelial blebs in which were mast cells and fibroblasts. These morphologic features have not been previously described in any inflammatory bowel disease and are reminiscent of bullous pemphigoid of the skin. The findings suggest that not all cases of microscopic colitis lie within the spectrum of collagenous colitis.