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Reading a post by Ant, about a supposedly rare disease known as "collagenous sprue", brought to mind something that I've been rolling around in my mind for a long time. Consider the description of collagenous sprue:
The red emphasis is mine, of course. That quote is from:Collagenous sprue (CS) is a rare disease of the small bowel that was first described in 1947 and histologically confirmed in 1970.1,2 This disease is characterized by complete atrophy of mucosal villi and excessive subepithelial collagen deposition that may replace the crypts. Other features that are distinctive, but not pathognomonic of CS, are the expansion of the lamina propria by subcryptal inflammation and a mucosa that appears thin.3 Some authors who doubt the existence and clinical significance of CS as a distinctive histologic picture have confused the prominent basement membrane seen in some patients with celiac disease (CD) with CS, but the degree of subepithelial collagen deposition is distinguishable from that of CD.3 That the subepithelial collagenous thickening can be variable and patchy along the small bowel also makes the diagnosis difficult.2,4,5 Aiding in the distinction between CS and CD is the response to gluten-free diet. As a general rule, the collagenous deposits in CD regress under gluten-free diet, whereas those of CS usually do not.6 This, however, is not true in all cases. Patients may or may not initially respond to a gluten-free diet.2,4 Thus far, the etiology of CS is not clear.
http://www.clinicaladvances.com/article ... 6-xiao.pdf
If you read the article, you will see that they tried the GF diet on one patient, for 2 whole weeks. WOW! No wonder they make the ridiculous statement that, "Patients may or may not initially respond to a gluten-free diet."
Anyway, what does the description of that disease sound like? Right! It sounds like a cross between collagenous colitis, and celiac sprue, (even the name sounds like a cross between the two. LOL). But, of course, it can't be a hybrid of those two, because we all know that collagenous colitis is confined to the colon, (by definition, not by actual physiological characteristics).
The next to last sentence in that quote above, "Patients may or may not initially respond to a gluten-free diet.", sure sounds a lot like collagenous colitis, doesn't it - IOW, I'll bet a GF cookie that the reason for that is due to additional food intolerances.Look at the first marker described, "complete atrophy of mucosal villi". What does that sound like a description of? Right you are! It sounds like mature celiac disease, in which the damage to the villi of the small intestine, has progressed as far as it can go - they're totally destroyed, at that point. And, the second marker, of course, "excessive subepithelial collagen deposition", is pretty much of a perfect match with the primary marker, (in the colon), for collagenous colitis.
It's also interesting that the diagnosis can only be made by examining biopsy samples under the microscope, (just as with CC), to search for the collagen deposits. The "spotty" distribution of those collagen bands, (in the small intestine), also matches the pattern of collagen band distribution, in the colon, when CC is diagnosed. Yep, for all practical purposes, the only significant difference between CS and CC, is the fact that CS occurs in the small intestine, whereas CC occurs, (by definition), in the colon.
At the risk of being accused of oversimplification, I'd like to point out that this is not exactly rocket science. Whatta ya wanna bet that if small intestinal biopsy samples from some of us, (who have CC), were scrutinized under a microscope, a significant percentage of samples would also show thickened collagen bands, (similar to the markers of collagenous sprue)?
So what am I leading up to? IMO, collagenous sprue is just another version of microscopic colitis, and I believe that CS will respond to the same treatment as MC. Entocort EC will probably not be a very effective treatment, (since it activates too far downstream, in the GI tract), but a method of delivery for budesonide that activates immediately downstream of the pyloric valve, (the valve between the stomach and the small intestine), and the diet that works for MC, of course, should work well for CS.
I am implying, of course, that someone with CS also has celiac disease, but that should be so obvious that it's hardly worthy of mention, and it's irrelevant, anyway, since the fact that it's a form of CC, will trump the treatment, and in most cases, that will make the GF diet, (alone), inadequate for achieving remisson, (IOW, additional allergenic proteins will have to be eliminated from the diet, for successful treament by diet alone).
More than that, though, I personally believe that this entire spectrum of diseases have a common link, namely food intolerances, and some day, medical science will become sophisticated enough to be able to revise the descriptions of various diseases, and update the textbooks, to reflect the fact that all of these diseases, (celiac sprue, CS, MC, CC, LC, etc.,) are not diseases at all, but symptoms of food sensitivities. I'm not holding my breath until that happens, but I truly believe that at some point, in the distant future, it will happen.
I'll go one step better than that - I'll predict that some day, all autoimmune diseases will be added to this collection, (IOW, they will no longer be called diseases, (at least, not correctly), but will be classified as symptoms of food sensitivities). I'm not claiming that food sensitivities will be shown to be the only requirement, for some of these "diseases/symptoms", but food sensitivities will be the primary prerequisite, which predisposes for the issues, (secondary to genetics, of course). I believe that some of these issues, such as Crohn's disease, and UC, for example, (and possibly MC), will require the involvement of a second trigger, such as mycobacterium avium subspecies paratuberculosis, (MAP), in order to develop. I'm not ruling out the possibility that the presence of MAP might be a necessary condition for the development of other, (possibility all), autoimmune diseases, but food sensitivities will be the primary prerequisite, I believe.
The time frame for the description of the first autoimmune diseases, and the first description of MAP, might, at first glance, suggest a conflict, but I believe that there is enough flexibility in the way that medical issues were first described back in those days, to allow my theory as a viable possibility. One of the first autoimmune diseases to be described, is hemolytic anemia, which was described in 1872. Of course, when it was first described, it may not have had autoimmune origins. Johne's disease, (caused by MAP), in ruminant livestock, was first described in 1908. Of course, just because it wasn't described until 1908, doesn't mean that it didn't exist before then. After all, it took medical researchers 23 years, (from 1947 until 1970), to histologically, (IOW, actually identify under a microscope), confirm the existence of collagenous sprue.
At least, that's how I see it. Of course, I could be all wet. If/when this actually happens, though, (probably somewhere between about 30 to 60 years from now), remember that you read it here, first.
Tex
