This article is very interesting and the first I've seen mentioning 3 forms of MC.
Also states CC not only affects the colon but also the small intestine and stomach. Talks about bile acid malabsorption among other things...take a look
http://www.bcm.edu/gastro/DDC/grandroun ... 9-DISC.HTM
Love,
Joanna
Three forms of MC?
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
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harvest_table
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Three forms of MC?
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harvest_table
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Heres the full text
UTH Gastroenterology Grand Rounds - Discussion
--------------------------------------------------------------------------------
Final Diagnosis: Collagenous Colitis (Microscopic Colitis)
Important points regarding the History of patients with this condition include:
Microscopic colitis is characterized by chronic watery (secretory) diarrhea without bleeding. It usually occurs in middle aged patients but can affect children. The colon appears normal by colonoscopy or barium enema. The diagnosis is established by biopsy of the colonic mucosa which reveal colitis, but not mucosal ulcerations.
There are three different types of microscopic colitis that have been recognized. These include collagenous colitis without lymphocytic infiltration of the surface epithelium which is characterized by a thickened subepithelial collagenous band in the colonic mucosa that varies in thickness from 7-100 micrometers; lymphocytic colitis which is characterized by a subepithelial lymphocytic infiltrate rather than excess collagen in the colonic mucosa, and a mixed form characterized by both a thickening of the collagen plate and an increased number of intraepithelial lymphocytes. It has been suggested that these disorders may be caused by a single pathogenetic mechanism. Lymphocytic and collagenous colitis affect primarily the colon but can also involve the terminal ileum.
There are limited date regarding the epidemiology of microscopic colitis. One of the largest population based studies from Barcelona, Spain included 23 patients with collagenous colitis and 37 patients with lymphocytic colitis who were identified during a five year period. Both diseases were more common in women than men (4.75 to 1 and 2.7 to 1, for collagenous and lymphocytic colitis respectively).
The pathogenesis of the different forms of microscopic colitis is unknown despite a detailed description of their pathology. It remains uncertain if the two diseases are related. The inflammatory cell response is similar with significant histologic overlap. For example, in one study, colonic biopsy was performed in 30 patients with chronic watery diarrhea and normal radiographic and endoscopic studies: 6 showed lymphocytic colitis alone; 7 collagenous colitis alone; and 17 showed a mixed form with both thickening of the collagenous plate and an increased number of intraepithelial lymphocytes. However, some observations suggest that there are some differences between the two conditions. For example, the histocompatability phenotypes appear to be different. Moreover, long-term follow up usually reveals no transformation from one type to another. However, there has been a case report which described a patient who had collagenous colitis two weeks prior to colectomy and the colectomy specimen revealed loss of the thickened collagen plate with lymphocytic colitis being the predominant finding.
Several theories on the etiology of collagenous colitis have been suggested. It is possible that the underlying causes may differ among patients. Collagenous colitis may represent one clinical presentation of a group of collagenous mucosal inflammatory diseases of the gastrointestinal tract that affect not only the colon but also the small intestine and stomach.
Abnormal collagen metabolism may be responsible for the thick collagen band in collagenous colitis.
An alternative hypothesis is that the inflammation and collagen deposition results from bacterial toxins that cause mucosal injury. This theory was supported in a case report in which treatment with cholestyramine was associated with a resolution in symptoms, normalization of histology, and the reversal of the cytotoxic effects of fecal extracts on an in vitro model. All three parameters worsened when treatment was discontinued, and resolved again upon reinstitution. In addition to binding bacterial toxins, the benefit of bile-acid binding resins may also be related to underlying bile-acid malabsorption, which is common in patients with collagenous colitis. The cause of bile acid malabsorption in patients with microscopic colitis is unclear since morphologic alterations in the terminal ileum are usually absent.
It has also been proposed that NSAIDs are responsible for some cases of watery diarrhea-colitis syndrome. In one study, among the patients with collagenous colitis and NSAID use, diarrhea followed the use of NSAIDs by a mean of 5.5 years. However, in another series, no association was noted between NSAID use and collagenous colitis.
Collagenous colitis has been linked to Simvastatin, Lansoprazole, and Ticlopidine, while Lymphocytic colitis has been linked to Lansoprazole, Ticlopidine, Flutamide, and gold salts.
Thickening of the colonic subepithelial collagen band has been found in some diabetic patients with diarrhea. There was no correlation between collagen thickness, age, and the duration of diabetes.
The severity of diarrhea in microscopic colitis correlates with the inflammatory changes in the lamina propria, NOT with collagen table thickening. Thus, diarrhea is most likely caused by the inflammation.
Clinical Manifestations:
Collagenous and lymphocytic colitis produce a similar clinical picture characterized by nonbloody chronic watery (secretory) diarrhea of up to two liters daily. The clinical course is mainly intermittent, but is sometimes continuous or rarely consists of a single episode. Affected patients usually produce between four and nine watery stools per day. If the colonic mucosa is overlooked, most patients with collagenous colitis would be diagnosed with diarrhea predominant IBS.
The typical patient with collagenous colitis is a middle-aged woman in her sixth decade in otherwise good general condition with female to male ratio up to 15:1. Accompanying symptoms are variable, and are mostly nonspecific and may include nausea, vague abdominal pain, and fecal urgency. Extraintestinal symptoms, such as arthralgia, arthritis, or uveitis can occur. Many patients have temporary periods in which normal bowel function returns.
The long term course of patients with lymphocytic colitis may be more favorable than with collagenous colitis as evidenced by several head to head comparison series.
Lab Findings:
Lab tests are nonspecific. Slight anemia and elevated ESR may be seen. Autoantibodies are found in 50% of patients and may include Rheumatoid Factor, ANA, AMA, and ANCA.
Colonic Biopsies:
Although specimens obtained by flexible sigmoidoscopy are frequently sufficient to establish the diagnosis, the severity of histologic changes declines from the proximal to the distal colon. Therefore, biopsies obtained from the right colon are optimal. Collagenous colitis can be patchy, with normal mucosa being found mainly in specimens from the rectosigmoid. In several reports, rectosigmoid colon biopsies alone would have missed the diagnosis of collagenous colitis in up to 40% of cases. In a retrospective analysis of histologic specimens from 56 patients, the highest diagnostic yield was achieved in biopsies from the transverse colon (83%) and right colon (70%), and lowest in the rectosigmoid (66%). Thus, total colonoscopy is necessary to establish the diagnosis of collagenous colitis and to exclude other inflammatory diseases.
Association with small bowel and other diseases:
Patients with microscopic colitis only rarely have laboratory evidence of small bowel involvement with associated malabsorption or protein losing enteropathy. The simultaneous occurrence of lymphocytic colitis and lymphocytic gastritis has been reported. Focal area of microscopic colitis have also been described in patients with established inflammatory bowel disease.
An association between microscopic colitis and celiac disease has been observed. In fact, collagenous enterocolitis may represent a diffuse manifestation of gluten sensitivity. Therefore, it is reasonable to test patients for celiac disease.
There is also evidence in some patients that collagenous colitis is a systemic disorder. In one report, concomitant autoimmune diseases were more common in collagenous compared with lymphocytic colitis while celiac disease was present in both disorders.
Treatment:
Large randomized controlled trials do not exist for the treatment of collagenous or lymphocytic colitis.
Patients should be reassured since microscopic colitis has not been associated with increased mortality or severe deterioration. Also, the diarrhea may resolve within weeks with or without treatment, although relapses can occur. The histologic response does not seem to parallel the therapeutic response in all cases.
Therapy should consist of stopping NSAIDs and if have concomitant celiac disease, then refrain from gluten in diet, etc.
The first line of treatment should be antidiarrheal therapy with Loperamide.
The second line of treatment can be Budesonide which is given to nonreponders of Loperamide. This is a glucocorticoid which has low systemic activity due to extensive first pass metabolism in the liver. A meta-analysis of three trials estimated that Budesonide significantly decreased stool frequency versus placebo and was well tolerated. It appears that a treatment duration of six weeks appeared to be optimal but a shorter duration of treatment may be sufficient. The long-term benefit of Budesonide remains to be determined.
If both Loperamide and Budesonide both fail, then would try an aminosalicylate or sulfasalazine.
If an aminosalicylate is not effective, a short trial of cholestyramine should be initiated.
If cholestyramine is not effective, then would switch to corticosteroids. Prednisone leads to a reduction in colonic inflammation but not in the thickness of the collagen band. However, it is associated with a greater risk of side-effects compared with Budesonide and relapses often occurs when therapy is tapered or withdrawn.
A number of other regimens have been effective in small case series in patients in whom the diarrhea is resistant to steroids. These include Metronidazole, Octreotide, Methotrexate, Azathioprine, 6-Mercaptopurine, and Verapamil.
Another promising therapy is Bismuth subsalicylate. This treatment improved symptoms as well as colonic histology in some studies.
Natural History after medical treatment:
Few prospective studies have examined the natural history of microscopic colitis in patients who received the medical treatments described above. One of the largest studies included 37 patients with collagenous colitis and 44 patients with lymphocytic colitis who were followed prospectively after diagnosis for an average of 37 months. Patients were treated with a variety of interventions, including withdrawal of implicated medications and the use of the above named medications. These interventions were associated with long-term cessation of diarrhea in approximately 70% of patients, while 25-30% relapsed. Microscopic colitis has not been associated with an increased risk of colorectal cancer.
Surgery:
Surgery has rarely been reported in microscopic colitis. Ileostomy may be the procedure of choice in older patients with resistant disease. In one series of patients with collagenous colitis with severe diarrhea refractory to medical therapy, ileostomy was performed eight patients and sigmoidostomy in one. Postoperatively, the diarrhea ceased in all patients and the collagen layer was reduced to normal throughout the colon following ileostomy and in the excluded colon following sigmoidostomy. The findings suggest that fecal stream diversion eliminates noxious luminal factors which seem to be of pathogenetic importance at least in patients with refractory disease.
--------------------------------------------------------------------------------
--------------------------------------------------------------------------------
Final Diagnosis: Collagenous Colitis (Microscopic Colitis)
Important points regarding the History of patients with this condition include:
Microscopic colitis is characterized by chronic watery (secretory) diarrhea without bleeding. It usually occurs in middle aged patients but can affect children. The colon appears normal by colonoscopy or barium enema. The diagnosis is established by biopsy of the colonic mucosa which reveal colitis, but not mucosal ulcerations.
There are three different types of microscopic colitis that have been recognized. These include collagenous colitis without lymphocytic infiltration of the surface epithelium which is characterized by a thickened subepithelial collagenous band in the colonic mucosa that varies in thickness from 7-100 micrometers; lymphocytic colitis which is characterized by a subepithelial lymphocytic infiltrate rather than excess collagen in the colonic mucosa, and a mixed form characterized by both a thickening of the collagen plate and an increased number of intraepithelial lymphocytes. It has been suggested that these disorders may be caused by a single pathogenetic mechanism. Lymphocytic and collagenous colitis affect primarily the colon but can also involve the terminal ileum.
There are limited date regarding the epidemiology of microscopic colitis. One of the largest population based studies from Barcelona, Spain included 23 patients with collagenous colitis and 37 patients with lymphocytic colitis who were identified during a five year period. Both diseases were more common in women than men (4.75 to 1 and 2.7 to 1, for collagenous and lymphocytic colitis respectively).
The pathogenesis of the different forms of microscopic colitis is unknown despite a detailed description of their pathology. It remains uncertain if the two diseases are related. The inflammatory cell response is similar with significant histologic overlap. For example, in one study, colonic biopsy was performed in 30 patients with chronic watery diarrhea and normal radiographic and endoscopic studies: 6 showed lymphocytic colitis alone; 7 collagenous colitis alone; and 17 showed a mixed form with both thickening of the collagenous plate and an increased number of intraepithelial lymphocytes. However, some observations suggest that there are some differences between the two conditions. For example, the histocompatability phenotypes appear to be different. Moreover, long-term follow up usually reveals no transformation from one type to another. However, there has been a case report which described a patient who had collagenous colitis two weeks prior to colectomy and the colectomy specimen revealed loss of the thickened collagen plate with lymphocytic colitis being the predominant finding.
Several theories on the etiology of collagenous colitis have been suggested. It is possible that the underlying causes may differ among patients. Collagenous colitis may represent one clinical presentation of a group of collagenous mucosal inflammatory diseases of the gastrointestinal tract that affect not only the colon but also the small intestine and stomach.
Abnormal collagen metabolism may be responsible for the thick collagen band in collagenous colitis.
An alternative hypothesis is that the inflammation and collagen deposition results from bacterial toxins that cause mucosal injury. This theory was supported in a case report in which treatment with cholestyramine was associated with a resolution in symptoms, normalization of histology, and the reversal of the cytotoxic effects of fecal extracts on an in vitro model. All three parameters worsened when treatment was discontinued, and resolved again upon reinstitution. In addition to binding bacterial toxins, the benefit of bile-acid binding resins may also be related to underlying bile-acid malabsorption, which is common in patients with collagenous colitis. The cause of bile acid malabsorption in patients with microscopic colitis is unclear since morphologic alterations in the terminal ileum are usually absent.
It has also been proposed that NSAIDs are responsible for some cases of watery diarrhea-colitis syndrome. In one study, among the patients with collagenous colitis and NSAID use, diarrhea followed the use of NSAIDs by a mean of 5.5 years. However, in another series, no association was noted between NSAID use and collagenous colitis.
Collagenous colitis has been linked to Simvastatin, Lansoprazole, and Ticlopidine, while Lymphocytic colitis has been linked to Lansoprazole, Ticlopidine, Flutamide, and gold salts.
Thickening of the colonic subepithelial collagen band has been found in some diabetic patients with diarrhea. There was no correlation between collagen thickness, age, and the duration of diabetes.
The severity of diarrhea in microscopic colitis correlates with the inflammatory changes in the lamina propria, NOT with collagen table thickening. Thus, diarrhea is most likely caused by the inflammation.
Clinical Manifestations:
Collagenous and lymphocytic colitis produce a similar clinical picture characterized by nonbloody chronic watery (secretory) diarrhea of up to two liters daily. The clinical course is mainly intermittent, but is sometimes continuous or rarely consists of a single episode. Affected patients usually produce between four and nine watery stools per day. If the colonic mucosa is overlooked, most patients with collagenous colitis would be diagnosed with diarrhea predominant IBS.
The typical patient with collagenous colitis is a middle-aged woman in her sixth decade in otherwise good general condition with female to male ratio up to 15:1. Accompanying symptoms are variable, and are mostly nonspecific and may include nausea, vague abdominal pain, and fecal urgency. Extraintestinal symptoms, such as arthralgia, arthritis, or uveitis can occur. Many patients have temporary periods in which normal bowel function returns.
The long term course of patients with lymphocytic colitis may be more favorable than with collagenous colitis as evidenced by several head to head comparison series.
Lab Findings:
Lab tests are nonspecific. Slight anemia and elevated ESR may be seen. Autoantibodies are found in 50% of patients and may include Rheumatoid Factor, ANA, AMA, and ANCA.
Colonic Biopsies:
Although specimens obtained by flexible sigmoidoscopy are frequently sufficient to establish the diagnosis, the severity of histologic changes declines from the proximal to the distal colon. Therefore, biopsies obtained from the right colon are optimal. Collagenous colitis can be patchy, with normal mucosa being found mainly in specimens from the rectosigmoid. In several reports, rectosigmoid colon biopsies alone would have missed the diagnosis of collagenous colitis in up to 40% of cases. In a retrospective analysis of histologic specimens from 56 patients, the highest diagnostic yield was achieved in biopsies from the transverse colon (83%) and right colon (70%), and lowest in the rectosigmoid (66%). Thus, total colonoscopy is necessary to establish the diagnosis of collagenous colitis and to exclude other inflammatory diseases.
Association with small bowel and other diseases:
Patients with microscopic colitis only rarely have laboratory evidence of small bowel involvement with associated malabsorption or protein losing enteropathy. The simultaneous occurrence of lymphocytic colitis and lymphocytic gastritis has been reported. Focal area of microscopic colitis have also been described in patients with established inflammatory bowel disease.
An association between microscopic colitis and celiac disease has been observed. In fact, collagenous enterocolitis may represent a diffuse manifestation of gluten sensitivity. Therefore, it is reasonable to test patients for celiac disease.
There is also evidence in some patients that collagenous colitis is a systemic disorder. In one report, concomitant autoimmune diseases were more common in collagenous compared with lymphocytic colitis while celiac disease was present in both disorders.
Treatment:
Large randomized controlled trials do not exist for the treatment of collagenous or lymphocytic colitis.
Patients should be reassured since microscopic colitis has not been associated with increased mortality or severe deterioration. Also, the diarrhea may resolve within weeks with or without treatment, although relapses can occur. The histologic response does not seem to parallel the therapeutic response in all cases.
Therapy should consist of stopping NSAIDs and if have concomitant celiac disease, then refrain from gluten in diet, etc.
The first line of treatment should be antidiarrheal therapy with Loperamide.
The second line of treatment can be Budesonide which is given to nonreponders of Loperamide. This is a glucocorticoid which has low systemic activity due to extensive first pass metabolism in the liver. A meta-analysis of three trials estimated that Budesonide significantly decreased stool frequency versus placebo and was well tolerated. It appears that a treatment duration of six weeks appeared to be optimal but a shorter duration of treatment may be sufficient. The long-term benefit of Budesonide remains to be determined.
If both Loperamide and Budesonide both fail, then would try an aminosalicylate or sulfasalazine.
If an aminosalicylate is not effective, a short trial of cholestyramine should be initiated.
If cholestyramine is not effective, then would switch to corticosteroids. Prednisone leads to a reduction in colonic inflammation but not in the thickness of the collagen band. However, it is associated with a greater risk of side-effects compared with Budesonide and relapses often occurs when therapy is tapered or withdrawn.
A number of other regimens have been effective in small case series in patients in whom the diarrhea is resistant to steroids. These include Metronidazole, Octreotide, Methotrexate, Azathioprine, 6-Mercaptopurine, and Verapamil.
Another promising therapy is Bismuth subsalicylate. This treatment improved symptoms as well as colonic histology in some studies.
Natural History after medical treatment:
Few prospective studies have examined the natural history of microscopic colitis in patients who received the medical treatments described above. One of the largest studies included 37 patients with collagenous colitis and 44 patients with lymphocytic colitis who were followed prospectively after diagnosis for an average of 37 months. Patients were treated with a variety of interventions, including withdrawal of implicated medications and the use of the above named medications. These interventions were associated with long-term cessation of diarrhea in approximately 70% of patients, while 25-30% relapsed. Microscopic colitis has not been associated with an increased risk of colorectal cancer.
Surgery:
Surgery has rarely been reported in microscopic colitis. Ileostomy may be the procedure of choice in older patients with resistant disease. In one series of patients with collagenous colitis with severe diarrhea refractory to medical therapy, ileostomy was performed eight patients and sigmoidostomy in one. Postoperatively, the diarrhea ceased in all patients and the collagen layer was reduced to normal throughout the colon following ileostomy and in the excluded colon following sigmoidostomy. The findings suggest that fecal stream diversion eliminates noxious luminal factors which seem to be of pathogenetic importance at least in patients with refractory disease.
--------------------------------------------------------------------------------
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barbaranoela
- Emperor Penguin
- Posts: 5394
- Joined: Wed May 25, 2005 6:11 pm
- Location: New York
Joanna----
I like things said plain and simple----and this article is right on the button~~~~
When I first started with this problem I was like
cus my first GI was sooooooooo un-informed himself----
He shows me a passage in a book about MCC --points and says---*see this is what U have*
I stayed with this GI for many years---believing he would get to the *issue* and I never forged ahead to look things up---thats how trusting I was--
Needless to say---I left him cus I was getting worse and headed for New York City and found my *savior*
as I put it--
And he was furious with my *X* GI---
The only course I had to take---was agressive treatment---and that was predisone + Colazal(first tried Asacol--which didnt help)
Most of the things in the article---didnt help me either---
And its very funny cus being my pressure was high I was put on Verapamil, which my GI told me would also be of help~~~~
He told me that many GI's use Verap. as part of their treatment---weird how one med. can help 2 different issues~~~
Well once again thanks for posting that article----I had looked high and low for a simplified version and U did it for me--
U see, I have no patience either----if I dont find it immediately --I QUIT!!
Oh, sorry--once I did find an article on MCC--and I was so proud of *me* that I copied and saved it---
A good week to U
luve--Barbara
I like things said plain and simple----and this article is right on the button~~~~
When I first started with this problem I was like
cus my first GI was sooooooooo un-informed himself----He shows me a passage in a book about MCC --points and says---*see this is what U have*
I stayed with this GI for many years---believing he would get to the *issue* and I never forged ahead to look things up---thats how trusting I was--
Needless to say---I left him cus I was getting worse and headed for New York City and found my *savior*
as I put it--And he was furious with my *X* GI---
The only course I had to take---was agressive treatment---and that was predisone + Colazal(first tried Asacol--which didnt help)
Most of the things in the article---didnt help me either---
And its very funny cus being my pressure was high I was put on Verapamil, which my GI told me would also be of help~~~~
He told me that many GI's use Verap. as part of their treatment---weird how one med. can help 2 different issues~~~
Well once again thanks for posting that article----I had looked high and low for a simplified version and U did it for me--
U see, I have no patience either----if I dont find it immediately --I QUIT!!
Oh, sorry--once I did find an article on MCC--and I was so proud of *me* that I copied and saved it---
A good week to U
luve--Barbara
the fruit of the spirit is love, joy, peace, patience, kindness, goodness, faithfulness and self-control
Joanna,
Actually, I believe there are five different types of MC that have been described, though virtually everyone in the medical profession is unaware of more than three, and most doctors apparently believe only two types exist. I can't remember what the fifth type is called, and I can't find a reference right now, but here is a reference on the fourth type:
http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
I posted about all five types on the old board, but unfortunately I didn't save my posts, and the bookmarks to those reference sites are on one of my "retired" computers, that I seldom use now, so it would take a while to track them down. The fifth type is pretty rare, (which is a mouthful, since evern CC, LC, and ordinary MC are rather rare). Maybe I'll remember how I found that reference, one of these days, and I'll locate it again.
Love,
Tex
Actually, I believe there are five different types of MC that have been described, though virtually everyone in the medical profession is unaware of more than three, and most doctors apparently believe only two types exist. I can't remember what the fifth type is called, and I can't find a reference right now, but here is a reference on the fourth type:
http://www.ncbi.nlm.nih.gov/entrez/quer ... t=Abstract
I posted about all five types on the old board, but unfortunately I didn't save my posts, and the bookmarks to those reference sites are on one of my "retired" computers, that I seldom use now, so it would take a while to track them down. The fifth type is pretty rare, (which is a mouthful, since evern CC, LC, and ordinary MC are rather rare). Maybe I'll remember how I found that reference, one of these days, and I'll locate it again.
Love,
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.
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harvest_table
- Rockhopper Penguin
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So, Mrs. Columbo this article hit home for you ? I know what you mean, we all banter back and forth about MC, medications, diet and what have you. Thank you for your input.
Tex, I missed the conversations about there being 3-5 subtypes of MC. This is interesting since our GI's know little about MC and most of us have been DX with either CC or LC- some of us may fall into the sub groups? I wonder what that means in relations to treatment options, if one falls into the sub group catagory.
Love,
Joanna
Tex, I missed the conversations about there being 3-5 subtypes of MC. This is interesting since our GI's know little about MC and most of us have been DX with either CC or LC- some of us may fall into the sub groups? I wonder what that means in relations to treatment options, if one falls into the sub group catagory.
Love,
Joanna
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Liz
- Rockhopper Penguin
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Interesting about the bile acids. Many years ago,more than 30, I was told that one of the reasons that I had a type of colitis was that I over produced bile acids. That was, I think, before MC was even thought of. My GI doctor told me after I was diagnosed with CC that what I had before was not CC. I wonder????
Very interesting article Joanna.
Love
Liz
Very interesting article Joanna.
Love
Liz
A smile is a light in the window of your face that shows that your heart is at home
Hi all,
I noticed that Dr. Fine's Pepto treatment was the one that had some histological response whereas the other non-dietary ones didn't.
Still, it didn't look as though even that was 100 percent, and not complete in the individuals it did help.
This would lend credence to the pathogen theory which is the one that Fine and probably lots of others think is underlying since Pepto has a sort of antibiotic effect.
I was always chicken to take the stuff due to side effects.
After my gall bladder was removed, there was some concern about possible bile malabsorption. Frankly, I believe the same disease that messed up the rest of my gut messed up the gall bladder as well.
I assume that they are just including major damage to the small bowel like the classical celiac diagnosis in their comments about the overlap with gluten sensitive individuals.
Joanna, did you happen to see who the first author of this review was?
It would probably be easy for me to contact him about our groups' experience in terms of gluten sensitivity that flies beneath the radar in folks with MC without the so-called gold standard diagnostic results.
I might even be able to arrange a face to face visit with him/her if this person is interested, or could arrange a visit with one of the other authors.
Thanks Joanna. This is certainly a lot more comprehensive than many of the other articles we've seen!
Yours, Luce
I noticed that Dr. Fine's Pepto treatment was the one that had some histological response whereas the other non-dietary ones didn't.
Still, it didn't look as though even that was 100 percent, and not complete in the individuals it did help.
This would lend credence to the pathogen theory which is the one that Fine and probably lots of others think is underlying since Pepto has a sort of antibiotic effect.
I was always chicken to take the stuff due to side effects.
After my gall bladder was removed, there was some concern about possible bile malabsorption. Frankly, I believe the same disease that messed up the rest of my gut messed up the gall bladder as well.
I assume that they are just including major damage to the small bowel like the classical celiac diagnosis in their comments about the overlap with gluten sensitive individuals.
Joanna, did you happen to see who the first author of this review was?
It would probably be easy for me to contact him about our groups' experience in terms of gluten sensitivity that flies beneath the radar in folks with MC without the so-called gold standard diagnostic results.
I might even be able to arrange a face to face visit with him/her if this person is interested, or could arrange a visit with one of the other authors.
Thanks Joanna. This is certainly a lot more comprehensive than many of the other articles we've seen!
Yours, Luce
-
harvest_table
- Rockhopper Penguin
- Posts: 1509
- Joined: Wed May 25, 2005 6:29 pm
- Location: Fergus Falls, Minnesota
Luce, here is a reference page
http://www.bcm.edu/gastro/DDC/grandroun ... 11-REF.HTM
I found this googling physicans discussions on microscopic colitis.
If you haven't already looked at the link in my first post please do, and scroll back to the very beginning of this discussion and read it through to the end. It's interesting. They mention gluten sensitivity as last resort in case medications do not work.
I'm curious about the 5 types of MC, 3 are very rare from what I've read. A DX of Collangenous Entercolitis seems to apply to one at least.
Anyone DX with Microscopic Colitis other than CC or LC? We are a indeed a quandry group!
Love,
Joanna
http://www.bcm.edu/gastro/DDC/grandroun ... 11-REF.HTM
I found this googling physicans discussions on microscopic colitis.
If you haven't already looked at the link in my first post please do, and scroll back to the very beginning of this discussion and read it through to the end. It's interesting. They mention gluten sensitivity as last resort in case medications do not work.
I'm curious about the 5 types of MC, 3 are very rare from what I've read. A DX of Collangenous Entercolitis seems to apply to one at least.
Anyone DX with Microscopic Colitis other than CC or LC? We are a indeed a quandry group!
Love,
Joanna
THE GLUTEN FILES
http://jccglutenfree.googlepages.com/
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Joanna,
I am so glad that I backed up to the "Take Homes" page of the last link you posted. I hadn't seen the part about the damage that didn't show up on the gold standard celiac tests. Looks like people are starting to "get it."
I would have no problem with Take Home # 3 if the only meds prescribed prior to a dietary trial were the ones with fewer and less serious side effects, and the patients weren't kept on them indefinitely.
Probably the author never intended for anyone to interpret his point that way, but you know that somewhere, someday, somebody's going to see it that way, and prescribe the whole nine yards of meds before suggesting a gf trial.
Do you suppose that some docs might consider heavy duty chemo or Prednisone to be tried prior to a
the dietary trial?
I'm so glad that this review is out there. This is definitely a big step in the right direction.
Yours, Luce
I am so glad that I backed up to the "Take Homes" page of the last link you posted. I hadn't seen the part about the damage that didn't show up on the gold standard celiac tests. Looks like people are starting to "get it."
I would have no problem with Take Home # 3 if the only meds prescribed prior to a dietary trial were the ones with fewer and less serious side effects, and the patients weren't kept on them indefinitely.
Probably the author never intended for anyone to interpret his point that way, but you know that somewhere, someday, somebody's going to see it that way, and prescribe the whole nine yards of meds before suggesting a gf trial.
Do you suppose that some docs might consider heavy duty chemo or Prednisone to be tried prior to a
the dietary trial?
I'm so glad that this review is out there. This is definitely a big step in the right direction.
Yours, Luce
Joanna,
By the way, would you believe that the only diagnosis I'm aware of is that path report came back with M.C. on it. This was what was called to me after the colonoscopy, and I was supposed to have gone in for a follow-up visit with the GI, but couldn't make it back in to do that.
Besides, at that point in time, I wouldn't have known to ask which type it was.
Recently, when I got an exam at my primary care person's, I signed a release to hopefully get a report from the hospital, but hospital referred me back to the doc's office stating that they didn't have it. (Could be that pathology is totally separate from the hospital).
I sure hope that the GI's got something in my records from the pathologist to establish which type I had, particularly since I just read the comment in the link about the other AI diseases being more common with the one type.
Oh well, I don't plan on having anymore of them anyway, and we're not supposed to get anymore once gf, so hope that's correct. This osteoporosis has me concerned enough as it is!
This has been one of our most interesting threads! Thanks again, Joanna!
I'm going to assume that the review was from University of Texas here in Houston. We're only a few minutes from there as it's in the Texas Medical Center.
Yours, Luce
By the way, would you believe that the only diagnosis I'm aware of is that path report came back with M.C. on it. This was what was called to me after the colonoscopy, and I was supposed to have gone in for a follow-up visit with the GI, but couldn't make it back in to do that.
Besides, at that point in time, I wouldn't have known to ask which type it was.
Recently, when I got an exam at my primary care person's, I signed a release to hopefully get a report from the hospital, but hospital referred me back to the doc's office stating that they didn't have it. (Could be that pathology is totally separate from the hospital).
I sure hope that the GI's got something in my records from the pathologist to establish which type I had, particularly since I just read the comment in the link about the other AI diseases being more common with the one type.
Oh well, I don't plan on having anymore of them anyway, and we're not supposed to get anymore once gf, so hope that's correct. This osteoporosis has me concerned enough as it is!
This has been one of our most interesting threads! Thanks again, Joanna!
I'm going to assume that the review was from University of Texas here in Houston. We're only a few minutes from there as it's in the Texas Medical Center.
Yours, Luce
Luce,
You may have to deal directly with the records release department of the hospital, to get the records you want. That endoscopy report should definitely be in their files, if the exam was done while you were a patient there. You may have to specify the date it was done, though.
Apparently the people in the records release department have a fair amount of leeway in the way they handle things. IOW, the person you deal with in the records release dept can make it very easy for you to obtain a copy of any report, if they choose to do so, or they can require you to "go through channels", probably depending on whether or not you make a favorable impression on them when they first lay eyes on you. FWIW, I have found it incredibly easy to get copies of the records I wanted from Scott & White.
Tex
You may have to deal directly with the records release department of the hospital, to get the records you want. That endoscopy report should definitely be in their files, if the exam was done while you were a patient there. You may have to specify the date it was done, though.
Apparently the people in the records release department have a fair amount of leeway in the way they handle things. IOW, the person you deal with in the records release dept can make it very easy for you to obtain a copy of any report, if they choose to do so, or they can require you to "go through channels", probably depending on whether or not you make a favorable impression on them when they first lay eyes on you. FWIW, I have found it incredibly easy to get copies of the records I wanted from Scott & White.
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.