Hello,
Does there exist a thread or a sticky, describing the difference between the different colities?
I came across an old discussion the other day, where Tex emphasized that CC is a connective tissue disease, and I wonder if some of you could give me a link describing the differences, if such a link or thread exists?
Grateful in beforehand, and hoping you all enjoy a blessed Christmas holiday :-)
Lilja
The difference between CC and other colitis diseases
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The difference between CC and other colitis diseases
Collagenous Colitis diagnosis in 2010
Psoriasis in 1973, symptom free in 2014
GF, CF and SF free since April, 2013
Psoriasis in 1973, symptom free in 2014
GF, CF and SF free since April, 2013
Hi Lilja,
I doubt that such an article exists, because virtually all of the major institutions try to ignore MC when they discuss IBDs. If they mention it at all, they provide very little information on MC (because they typically know very little about it), and much of the posted information about MC is incorrect and based on obsolete references.
Here are the basic differences among the IBDs:
1. Crohn's disease can affect any part of the digestive system, from mouth to anus, and typically causes gross (visible to the naked eye) lesions in the intestines that can penetrate through to every layer of the intestinal walls, including the serosa (the outer surface of the intestines). Crohn's disease commonly causes significant bleeding and occasional perforations, requiring surgical intervenrtion in the form of resections.
2. Ulcerative colitis always begins at the distal end of the colon (the bottom end), or the rectum, or the anus, and progresses upstream, but it usually does not progress upward past the intestines to affect the stomach or any other organ upstream of the duodenum. It is also marked by gross lesions that can penetrate into the mid layers (the lamina propria) of the intestinal wall, but unlike Crohn's disease, UC lesions typically do not completely penetrate the intestinal walls all the way to the serosa. Like Chron's disease, it can cause significant bleeding. UC also frequently causes damage that requires surgical intervention in the form of resections.
There are at least a dozen different types of MC, so I will only describe the 2 most commonly encountered (and these are the only 2 that most GI specialists are familiar with, anyway).
3. Collagenous colitis is marked by thickening of the collagen bands; in the lamina propria (a mid-layer in the intestinal wall) of the colon. There is also typically increased infiltration of lymphocytes into the lamina propria, and sometimes into the mucosal layer of enterocytes, but the lymphocyte count is often below the level that is diagnostic of lymphocytic colitis. Some doctors claim that if a CC patient has both increased collagen band thickness and a lymphocyte count that exceeds 20 per high-power field under a microscope, the diagnosis should include both CC and LC, but others disregard the lymphocyte count and list a diagnosis of CC only (because LC is not marked by increased collagen band thickness, so the existence of increased collagen band thickness is sufficient to distinguish between the 2 types of MC). With CC, the intestinal damage can only be observed under a microscopic, and the interior of the colon appears normal to the unaided eye (or through a colonoscope).
4. Lymphocytic colitis is marked by increased lymphocyte infiltration between the enterocytes of the mucosa of the colon. These lymphocytes are killer T cells, and they are the primary source of inflammation with LC. A count of at least 20 lymphocytes per high-power field of a microscope is diagnostic of LC. Collagen band thickness in the lamina propria is either normal or at least below 10 microns (a thickness in excess of 10 microns is diagnostic of CC). As with CC, the intestinal damage caused by LC can only be observed under a microscopic, and the interior of the colon appears normal to the unaided eye (or through a colonoscope).
The markers of both CC and LC can typically also be found in the small intestine (especially the ileum) of patients diagnosed with the respective diseases. IOW, in CC patients, it is common to find thickened collagen bands in the lamina propria of the small intestine, and sometimes in the stomach or esophagus. With LC, increased lymphocytic infiltration can commonly be found in the mucosa of the small intestine, and sometimes in the stomach or esophagus. Many GI specialists are not even aware of this, unfortunately.
5. Celiac disease is also an IBD. It is marked by (diagnosed by) flattening of the villa of the mucosa in the small intestine. But similar to the other IBDs (and unknown to most GI specialists), celiac disease also causes inflammation in the colon of most celiac patients. The inflammation in both the small intestine and the colon is promoted by the presence of increased numbers of T cells that infiltrate the mucosal layer of the intestines.
IMO, MC does not segue into Crohn's disease or UC, as some sources claim. But having MC does not make us immune to the development of another IBD, either. We have basically the same risk of developing Crohn's disease or UC as anyone else in the general population. However, because of the genetic associations involved with gluten sensitivity, we obviously have an increased risk of developing celiac disease, and in fact there is a significant overlap.
The connective tissue association is simply due to the fact that CC is marked by increased collagen band thickness, and collagen is connective tissue. The body uses collagen to create matrices that hold all the individual cells into the proper shape. Without collagen, our cells would collapse into a pile on the floor, because there would be nothing to hold them together.
I hope this helps.
Tex
I doubt that such an article exists, because virtually all of the major institutions try to ignore MC when they discuss IBDs. If they mention it at all, they provide very little information on MC (because they typically know very little about it), and much of the posted information about MC is incorrect and based on obsolete references.
Here are the basic differences among the IBDs:
1. Crohn's disease can affect any part of the digestive system, from mouth to anus, and typically causes gross (visible to the naked eye) lesions in the intestines that can penetrate through to every layer of the intestinal walls, including the serosa (the outer surface of the intestines). Crohn's disease commonly causes significant bleeding and occasional perforations, requiring surgical intervenrtion in the form of resections.
2. Ulcerative colitis always begins at the distal end of the colon (the bottom end), or the rectum, or the anus, and progresses upstream, but it usually does not progress upward past the intestines to affect the stomach or any other organ upstream of the duodenum. It is also marked by gross lesions that can penetrate into the mid layers (the lamina propria) of the intestinal wall, but unlike Crohn's disease, UC lesions typically do not completely penetrate the intestinal walls all the way to the serosa. Like Chron's disease, it can cause significant bleeding. UC also frequently causes damage that requires surgical intervention in the form of resections.
There are at least a dozen different types of MC, so I will only describe the 2 most commonly encountered (and these are the only 2 that most GI specialists are familiar with, anyway).
3. Collagenous colitis is marked by thickening of the collagen bands; in the lamina propria (a mid-layer in the intestinal wall) of the colon. There is also typically increased infiltration of lymphocytes into the lamina propria, and sometimes into the mucosal layer of enterocytes, but the lymphocyte count is often below the level that is diagnostic of lymphocytic colitis. Some doctors claim that if a CC patient has both increased collagen band thickness and a lymphocyte count that exceeds 20 per high-power field under a microscope, the diagnosis should include both CC and LC, but others disregard the lymphocyte count and list a diagnosis of CC only (because LC is not marked by increased collagen band thickness, so the existence of increased collagen band thickness is sufficient to distinguish between the 2 types of MC). With CC, the intestinal damage can only be observed under a microscopic, and the interior of the colon appears normal to the unaided eye (or through a colonoscope).
4. Lymphocytic colitis is marked by increased lymphocyte infiltration between the enterocytes of the mucosa of the colon. These lymphocytes are killer T cells, and they are the primary source of inflammation with LC. A count of at least 20 lymphocytes per high-power field of a microscope is diagnostic of LC. Collagen band thickness in the lamina propria is either normal or at least below 10 microns (a thickness in excess of 10 microns is diagnostic of CC). As with CC, the intestinal damage caused by LC can only be observed under a microscopic, and the interior of the colon appears normal to the unaided eye (or through a colonoscope).
The markers of both CC and LC can typically also be found in the small intestine (especially the ileum) of patients diagnosed with the respective diseases. IOW, in CC patients, it is common to find thickened collagen bands in the lamina propria of the small intestine, and sometimes in the stomach or esophagus. With LC, increased lymphocytic infiltration can commonly be found in the mucosa of the small intestine, and sometimes in the stomach or esophagus. Many GI specialists are not even aware of this, unfortunately.
5. Celiac disease is also an IBD. It is marked by (diagnosed by) flattening of the villa of the mucosa in the small intestine. But similar to the other IBDs (and unknown to most GI specialists), celiac disease also causes inflammation in the colon of most celiac patients. The inflammation in both the small intestine and the colon is promoted by the presence of increased numbers of T cells that infiltrate the mucosal layer of the intestines.
IMO, MC does not segue into Crohn's disease or UC, as some sources claim. But having MC does not make us immune to the development of another IBD, either. We have basically the same risk of developing Crohn's disease or UC as anyone else in the general population. However, because of the genetic associations involved with gluten sensitivity, we obviously have an increased risk of developing celiac disease, and in fact there is a significant overlap.
The connective tissue association is simply due to the fact that CC is marked by increased collagen band thickness, and collagen is connective tissue. The body uses collagen to create matrices that hold all the individual cells into the proper shape. Without collagen, our cells would collapse into a pile on the floor, because there would be nothing to hold them together.
I hope this helps.
Tex
It is suspected that some of the hardest material known to science can be found in the skulls of GI specialists who insist that diet has nothing to do with the treatment of microscopic colitis.