I have been researching and thought I would share this with everyone. I am trying to find and obtain the original article, but this is a reply to the article and then the author's reply. I found it interesting that the pathologist should also be aware of the the possiability for MC.
A letter to the editor is presented in response to the article "A higher diagnostic profile is possible for microscopic colitis."
Alimentary Pharmacology & Therapeutics; Aug2006, Vol. 24 Issue 3, p561-561, 1p
higher diagnostic profile is possible for microscopic colitis
SIRS, We read with interest the review of Nyhlin et al. on microscopic colitis
and agree with the authors that both gastroenterologist and pathologist must
be aware of this diagnosis as possible cause of unexplained chronic diarrhoea.1
However, the diagnosis of microscopic colitis may be missed, principally
because these pathologies tend to be patchy and the gross appearance of the
colonic mucosa is usually normal. Collagen colitis, in particular, may affect
the colon throughout its entire length, but the collagen table thickening is
often non-uniformly distributed among the various colonic segments.1 Because
diagnosis is based almost exclusively on histological findings, it is essential
that biopsy specimens be obtained from the sites of the lesions.2
In our opinion, promising new techniques may overcome the diagnostic limitations
seen with conventional colonscopy. For example, endoscopic ultrasonography
3 and confocal endomicroscopy4 could play a decisive role in the
diagnostic work-up of suspected patients by identifying the areas involved in
order to select the biopsy sites that are ‘more productive’ for the diagnosis.
However, further development in this area is needed before any routine clinical
application.
A higher diagnostic profile is possible for microscopic colitis: authors’
Reply
Alimentary Pharmacology & Therapeutics; Aug2006, Vol. 24 Issue 3, p562-562, 1p
SIRS, We thank Cammarota et al. for their comments and interest in our article.
We agree that efforts to facilitate and improve the diagnosis of collagenous
colitis (CC) are essential. In general, the colonic mucosa is macroscopically
normal in CC, but about 30 % of the patients have minor mucosal abnormalities,
which easily may be overlooked.1 The histopathological changes are most
prominent in the proximal colon and may be absent in the sigmoid or rectum.
2, 3 As Cammarota et al. point out, endoscopic ultrasonography and confocal
endomicroscopy have been applied in CC, though in a limited number of
patients so far. In addition to these new interesting techniques, chromoendoscopy
by vital staining with indigo carmine of the colonic mucosa during colonoscopy
has been used in a few patients with CC to enhance the macroscopic
assessment.4, 5 An uneven and coarse surface with a different staining pattern
has been reported in CC compared with the normal mucosa. Whether this
staining technique or the other mentioned endoscopic techniques would
increase the diagnostic yield of mucosal biopsies in CC remains to be proved.
Until these interesting new techniques have been tested in larger prospective
studies we have to rely on a high clinical awareness of the disorder by the
endoscopist. Currently, a pan-colonoscopy with multiple biopsies throughout
the colon still remains the best diagnostic method.
Kelly
Research
Moderators: Rosie, Stanz, Jean, CAMary, moremuscle, JFR, Dee, xet, Peggy, Matthew, Gabes-Apg, grannyh, Gloria, Mars, starfire, Polly, Joefnh
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Kellyerin222
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Research
Currently waiting results to see exact problem.
Yep, that addresses the chronic problem of failing to discover MC during a diagnostic attempt, simply because you can't find MC, unless you look for it, and, of course, you have to know how to look for it, or you still won't find it.
As expensive as most new high-tech medical equipment is, I'll be very surprised if very many hospitals/clinics rush out to buy the new devices suggested in the letter, in order to improve the diagnostic capabilities of their GI departments. The main problem is that the industry as a whole still considers MC to be a rare disease, and as long as that attitude remains in place, the administrators of most hospitals won't be able to justify such an investment, in view of the questionable payback potential. Most hospitals around here use a lot of what appears to be, at least, fairly antiquated equipment, in their GI departments. It's almost always about money, unfortunately. Still, maybe someone will do the research, and create a little interest.
Thanks for the info.
Tex
As expensive as most new high-tech medical equipment is, I'll be very surprised if very many hospitals/clinics rush out to buy the new devices suggested in the letter, in order to improve the diagnostic capabilities of their GI departments. The main problem is that the industry as a whole still considers MC to be a rare disease, and as long as that attitude remains in place, the administrators of most hospitals won't be able to justify such an investment, in view of the questionable payback potential. Most hospitals around here use a lot of what appears to be, at least, fairly antiquated equipment, in their GI departments. It's almost always about money, unfortunately. Still, maybe someone will do the research, and create a little interest.
Thanks for the info.
Tex
Yep, myself and many others here think that a diagnosis of MC would be much larger if more GI drs took a biopsy when doing a colonoscopy. My Colon was perfect and healthy acording to the Dr, but when the report on the biopsy can back we found otherwise.
In fact I just read a study that was put in pubmed a day or so ago where a diagnosis of Celiac Disease would increase depending on the number of biopsies. 2 at a very minimum, but it increased even more once 4 or more were taken.
Again my theory is that the inflamation found in MC is just a symptom of something else.
Oh and one more thing, various studies have shown that around 50% of folks with MC had constipation. When you read the symptoms of MC I have yet to read any that mention constipation as a symptom. So it's even more diagnosed there as most Drs would probably not take biopsies in folks with constipation. "Luckily" my form had both D and C so I got the biopsies. And FWIW, my last colonocopy showed no inflamation, so I'm either cured or in remission or ??? I still have symptoms every once in a while, but due to the supplements I'm taking I think I keep things in check the majority of the time.
Thanks, for the research.
Mike
In fact I just read a study that was put in pubmed a day or so ago where a diagnosis of Celiac Disease would increase depending on the number of biopsies. 2 at a very minimum, but it increased even more once 4 or more were taken.
Again my theory is that the inflamation found in MC is just a symptom of something else.
Oh and one more thing, various studies have shown that around 50% of folks with MC had constipation. When you read the symptoms of MC I have yet to read any that mention constipation as a symptom. So it's even more diagnosed there as most Drs would probably not take biopsies in folks with constipation. "Luckily" my form had both D and C so I got the biopsies. And FWIW, my last colonocopy showed no inflamation, so I'm either cured or in remission or ??? I still have symptoms every once in a while, but due to the supplements I'm taking I think I keep things in check the majority of the time.
Thanks, for the research.
Mike
Mike,
Another reason why I think that C is seldom/rarely mentioned in medical descriptions of MC, is because not very many people would be likely to pursue a medical remedy all the way to a GI doc's office, unless they have uncontrollable D. I know I damn sure would never have have gone to my doc, and announced that I've got "uncontrollable constipation". LOL.
In my case, it was alternating D and C, and I suspect that is that generally the case with most people who have the "C" phase of MC. The distinction of whether it is labeled as D or C, probably hinges on whether the D is occasionally interrupted by C.
If you have D only, it is often continuous, (that is, numerous BMs per day, every day), whereas those of us with the "C" phase have D for a while, and then our system is flushed out by D, for a few days. After that, C takes over for a while, as the cycle repeats. YMMV, but that's the way I think it works, and that's basically what happened in my case.
Tex
Another reason why I think that C is seldom/rarely mentioned in medical descriptions of MC, is because not very many people would be likely to pursue a medical remedy all the way to a GI doc's office, unless they have uncontrollable D. I know I damn sure would never have have gone to my doc, and announced that I've got "uncontrollable constipation". LOL.
In my case, it was alternating D and C, and I suspect that is that generally the case with most people who have the "C" phase of MC. The distinction of whether it is labeled as D or C, probably hinges on whether the D is occasionally interrupted by C.
If you have D only, it is often continuous, (that is, numerous BMs per day, every day), whereas those of us with the "C" phase have D for a while, and then our system is flushed out by D, for a few days. After that, C takes over for a while, as the cycle repeats. YMMV, but that's the way I think it works, and that's basically what happened in my case.
Tex
Very good point.tex wrote:Mike,
Another reason why I think that C is seldom/rarely mentioned in medical descriptions of MC, is because not very many people would be likely to pursue a medical remedy all the way to a GI doc's office, unless they have uncontrollable D. I know I damn sure would never have have gone to my doc, and announced that I've got "uncontrollable constipation". LOL.
Tex
Oh in case anyone is wondering here's the study I mentioned about on Celiac Disease and number of biopsies.
How many duodenal biopsy specimens are required to make a diagnosis of celiac disease?
http://www.ncbi.nlm.nih.gov/pubmed/18308317
And here's a couple of other recent articles on CD that I found interesting. Seems there is other testing that can be useful. And that again there's a potential link between gut bacteria and disease.
Comparative Usefulness of Deamidated Gliadin Antibodies in the Diagnosis of Celiac Disease.
http://www.ncbi.nlm.nih.gov/pubmed/18304884
Differences in faecal bacterial communities in coeliac and healthy children as detected by PCR and denaturing gradient gel electrophoresis.
http://www.ncbi.nlm.nih.gov/pubmed/17919298
Mike
Mike,
Those are interesting observations. One of the things that makes me feel like Andy Rooney, though, (IOW, one of the things that bugs me), is the way that so many research articles leave out one or more vital pieces of information, and the absence of that info makes the value of the article dubious at best. For example, in the last article for which you provided a link, the authors fail to mention whether or not the celiac cohort was in remission; on a GF diet, but not yet in remission; or untreated. (Unless I'm going blind, and overlooked it). That information matters a great deal, since treated celiacs, whose gut fauna have had sufficient time to develop stable populations, based on their modified diet, (a GF diet), will surely present with a different fauna distribution than members of the general population. We can only guess at what the conditions actually were. Like you, I believe that a distorted bacterial balance plays a part in CD and MC. The question is: "which comes first - the bacterial imbalance or the triggering of the genes that lead to gluten sensitivity?" It may be that in every case, a bacterial imbalance causes the initiation of events that leads to gluten sensitivity, but we certainly can't conclude that from that article - in fact, I'm not sure what to conclude from it, since they stumbled on the first step, by not accurately defining their sample set criteria.
Thanks for the links. I've always suspected that a lot of GI docs don't take enough biopsies. I'll bet that they just don't know any better, and they incorrectly assume that the inflammation is present throughout the colon for most patients, and therefore the markers should show up anywhere they choose to take a sample.
Tex
Those are interesting observations. One of the things that makes me feel like Andy Rooney, though, (IOW, one of the things that bugs me), is the way that so many research articles leave out one or more vital pieces of information, and the absence of that info makes the value of the article dubious at best. For example, in the last article for which you provided a link, the authors fail to mention whether or not the celiac cohort was in remission; on a GF diet, but not yet in remission; or untreated. (Unless I'm going blind, and overlooked it). That information matters a great deal, since treated celiacs, whose gut fauna have had sufficient time to develop stable populations, based on their modified diet, (a GF diet), will surely present with a different fauna distribution than members of the general population. We can only guess at what the conditions actually were. Like you, I believe that a distorted bacterial balance plays a part in CD and MC. The question is: "which comes first - the bacterial imbalance or the triggering of the genes that lead to gluten sensitivity?" It may be that in every case, a bacterial imbalance causes the initiation of events that leads to gluten sensitivity, but we certainly can't conclude that from that article - in fact, I'm not sure what to conclude from it, since they stumbled on the first step, by not accurately defining their sample set criteria.
Thanks for the links. I've always suspected that a lot of GI docs don't take enough biopsies. I'll bet that they just don't know any better, and they incorrectly assume that the inflammation is present throughout the colon for most patients, and therefore the markers should show up anywhere they choose to take a sample.
Tex
Very interesting discussion...sounds like, "which came first....chicken or egg." I for one, have not had C...just loose stools and D and scattered Normans....constipation sounds like a welcome problem right now!! I have been wondering WHY I developed LC in the first place....thru the years however I have had tons of antibiotics...including amoxyicillon... mostly for bronchitis and sinus infections. Now I have read that the docs are not using the antibiotics for sinus infections as they are not effective....hmmmm.....wonder what Polly would say to that?
Sunny
Sunny
Hi Sunny!
You KNEW I couldn't resist jumping in if you mentioned chronic sinusitis - LOL. I had the infection for almost a year despite various and prolonged antibiotic treatment and 2 surgeries. Five separate cultures showed no growth or "normal flora". I found this article to be especially interesting......the research found that some cases of chronic sinusitis are not due to resistance to antibiotics - rather, they are due to an underlying immune problem:
Weakened Immune System In Chronic Sinusitis Reveals New Treatment Targets
Article Date: 15 Sep 2006 - 7:00 PST
Researchers at Johns Hopkins have evidence that curbed activity from several key chemicals on the inner lining of the nose are linked to chronic sinusitis that fails to respond to the usual current treatments.
An estimated 32 million Americans know the misery of persistent inflammation of the moist tissue that lines the nose and sinus cavities. The result is clogged passages and recurring infections, according to the U.S. Centers for Disease Control and Prevention.
Because nearly one in 10 of those treated see symptoms return within weeks or months after drugs or surgery fail to keep the sinus passages open, scientists have long suspected that these resistant cases had some underlying problem with the immune system contributing to the ailment.
In a study to be described on Sept. 19 at the annual scientific sessions of the American Academy of Otolaryngology, Head and Neck Surgery, the Hopkins team found that in chronic sufferers who failed to respond to treatment, the activity of at least four genes in the body's nasal immune defense system were severely decreased, and their production of two proteins critical to this defense was 20 to 200 times less than normal.
Comparing nasal epithelial cell samples from nine patients who benefited from surgery with nine who did not, the Hopkins team discovered suppressed levels of human beta defensin 2 (HBD2) and mannose binding lectin (MBL) in those whose symptoms returned. The proteins are naturally produced in the nose whenever the immune system detects foreign bacteria or fungi, binding to invading pathogens, inactivating them and making them easily disposed of.
An earlier study published by the same team in the March-April issue of the American Journal of Rhinology also showed that sinus tissue from people with chronic sinusitis that resisted treatment had 30 times lower than normal activity of a so-called toll-like receptor gene, TLR9.
Inside the nose, researchers say, toll-like receptor proteins (TLRs) detect invading bacteria and other pathogens in the air by attaching to their trace byproducts. Once a threat is identified, the receptors stimulate the epithelial cells to produce antibiotic proteins, such as HBD2 and MBL, to fight the invading organisms. This innate response helps prevent airborne bacteria or fungi from settling in the nose and sinus cavities, causing infection.
"Colonization with microorganisms is a common problem in patients with chronic sinusitis and polyps, but the reasons for this are incompletely understood," says Andrew Lane, M.D., an associate professor at The Johns Hopkins University School of Medicine and director of its rhinology and sinus surgery center. "Now we are uncovering new clues as to what might be wrong and perhaps, ultimately, how it might be treated.
"The nose's first line of defense is the epithelium, and when the local innate immune function is curtailed, infections can get a head start, which might serve to worsen the sinus inflammation.
"The potential is there to manipulate these chemical receptors and proteins to see if this makes patients more responsive to conventional therapy," says Lane.
The study, led by Lane, was believed to be the first to determine levels of each TLR - there are 10 - by directly measuring messenger RNA expression in sinusitis patients and those more fortunate to not have it. Scientists have known for more than a year that TLRs were present in both the healthy and sinusitis-wracked nose, but not which receptors or proteins were more important than others in the condition's chronic form. That study involved 30 men and women, mostly from the Baltimore region, who had surgery for chronic sinusitis at Hopkins. (Another 10 had no sinus problem and served as study controls.)
Those who underwent surgery did so after standard therapy using antibiotics, decongestants and steroids had failed to stop their symptoms and keep their infections from coming back. Indeed, 20 participants in the study had developed nasal polyps, which have no known cause and are especially hard to treat, researchers say. They note that polyps must often be surgically removed to allow the sinuses to drain normally.
All patients were monitored for a minimum of six months to see if any symptoms or polyps returned. Thirteen in the surgery group had recurrent inflammation within three months to one year after surgery, while the rest remained symptom free.
The Hopkins team took samples during surgery of the mucous membrane lining the nose, and using real-time polymerase chain reaction, analyzed the samples for any genetic differences between the groups.
"Surgically treating sinusitis is much like plumbing, in the sense that we try to restore normal sinus cavity drainage pathways," adds study presenter Murugappan Ramanathan Jr., M.D., a resident in otolaryngology - head and neck surgery at Hopkins. "But for the intractable cases, surgery may fail because the problem is not so much about plumbing as it is inflammation, and for this we need research at the molecular level to find a solution."
----------------------------
Article adapted by Medical News Today from original press release.
----------------------------
Funding for this study was provided in part by the National Institutes of Health, including the National Institute on Deafness and Other Communication Disorders, and the National Institute of Allergy and Infectious Diseases, with additional funding coming from the American Rhinologic Society.
Me again:
It seems as if so many health problems are immune-related. Periodontal disease is now thought to be a hyperreactive immune response to normal bacteria in the mouth......similar to what happens in the gut with colitis. Won't it be nice when all of these pieces fit together???
Love,
Polly
You KNEW I couldn't resist jumping in if you mentioned chronic sinusitis - LOL. I had the infection for almost a year despite various and prolonged antibiotic treatment and 2 surgeries. Five separate cultures showed no growth or "normal flora". I found this article to be especially interesting......the research found that some cases of chronic sinusitis are not due to resistance to antibiotics - rather, they are due to an underlying immune problem:
Weakened Immune System In Chronic Sinusitis Reveals New Treatment Targets
Article Date: 15 Sep 2006 - 7:00 PST
Researchers at Johns Hopkins have evidence that curbed activity from several key chemicals on the inner lining of the nose are linked to chronic sinusitis that fails to respond to the usual current treatments.
An estimated 32 million Americans know the misery of persistent inflammation of the moist tissue that lines the nose and sinus cavities. The result is clogged passages and recurring infections, according to the U.S. Centers for Disease Control and Prevention.
Because nearly one in 10 of those treated see symptoms return within weeks or months after drugs or surgery fail to keep the sinus passages open, scientists have long suspected that these resistant cases had some underlying problem with the immune system contributing to the ailment.
In a study to be described on Sept. 19 at the annual scientific sessions of the American Academy of Otolaryngology, Head and Neck Surgery, the Hopkins team found that in chronic sufferers who failed to respond to treatment, the activity of at least four genes in the body's nasal immune defense system were severely decreased, and their production of two proteins critical to this defense was 20 to 200 times less than normal.
Comparing nasal epithelial cell samples from nine patients who benefited from surgery with nine who did not, the Hopkins team discovered suppressed levels of human beta defensin 2 (HBD2) and mannose binding lectin (MBL) in those whose symptoms returned. The proteins are naturally produced in the nose whenever the immune system detects foreign bacteria or fungi, binding to invading pathogens, inactivating them and making them easily disposed of.
An earlier study published by the same team in the March-April issue of the American Journal of Rhinology also showed that sinus tissue from people with chronic sinusitis that resisted treatment had 30 times lower than normal activity of a so-called toll-like receptor gene, TLR9.
Inside the nose, researchers say, toll-like receptor proteins (TLRs) detect invading bacteria and other pathogens in the air by attaching to their trace byproducts. Once a threat is identified, the receptors stimulate the epithelial cells to produce antibiotic proteins, such as HBD2 and MBL, to fight the invading organisms. This innate response helps prevent airborne bacteria or fungi from settling in the nose and sinus cavities, causing infection.
"Colonization with microorganisms is a common problem in patients with chronic sinusitis and polyps, but the reasons for this are incompletely understood," says Andrew Lane, M.D., an associate professor at The Johns Hopkins University School of Medicine and director of its rhinology and sinus surgery center. "Now we are uncovering new clues as to what might be wrong and perhaps, ultimately, how it might be treated.
"The nose's first line of defense is the epithelium, and when the local innate immune function is curtailed, infections can get a head start, which might serve to worsen the sinus inflammation.
"The potential is there to manipulate these chemical receptors and proteins to see if this makes patients more responsive to conventional therapy," says Lane.
The study, led by Lane, was believed to be the first to determine levels of each TLR - there are 10 - by directly measuring messenger RNA expression in sinusitis patients and those more fortunate to not have it. Scientists have known for more than a year that TLRs were present in both the healthy and sinusitis-wracked nose, but not which receptors or proteins were more important than others in the condition's chronic form. That study involved 30 men and women, mostly from the Baltimore region, who had surgery for chronic sinusitis at Hopkins. (Another 10 had no sinus problem and served as study controls.)
Those who underwent surgery did so after standard therapy using antibiotics, decongestants and steroids had failed to stop their symptoms and keep their infections from coming back. Indeed, 20 participants in the study had developed nasal polyps, which have no known cause and are especially hard to treat, researchers say. They note that polyps must often be surgically removed to allow the sinuses to drain normally.
All patients were monitored for a minimum of six months to see if any symptoms or polyps returned. Thirteen in the surgery group had recurrent inflammation within three months to one year after surgery, while the rest remained symptom free.
The Hopkins team took samples during surgery of the mucous membrane lining the nose, and using real-time polymerase chain reaction, analyzed the samples for any genetic differences between the groups.
"Surgically treating sinusitis is much like plumbing, in the sense that we try to restore normal sinus cavity drainage pathways," adds study presenter Murugappan Ramanathan Jr., M.D., a resident in otolaryngology - head and neck surgery at Hopkins. "But for the intractable cases, surgery may fail because the problem is not so much about plumbing as it is inflammation, and for this we need research at the molecular level to find a solution."
----------------------------
Article adapted by Medical News Today from original press release.
----------------------------
Funding for this study was provided in part by the National Institutes of Health, including the National Institute on Deafness and Other Communication Disorders, and the National Institute of Allergy and Infectious Diseases, with additional funding coming from the American Rhinologic Society.
Me again:
It seems as if so many health problems are immune-related. Periodontal disease is now thought to be a hyperreactive immune response to normal bacteria in the mouth......similar to what happens in the gut with colitis. Won't it be nice when all of these pieces fit together???
Love,
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
HAH!! I knew you would jump in, Polly. I mentioned to my doc last fall that i thought i had a sinus infection and she said in no uncertain terms would she give me antibiotics...research shows....blah blah....but i told her that i wouldn't take an antibiotic unless i were half dead because of the terrible impact on me. so your article shows a surprising (at least to me) link to underlying immune problem....thanx for the article....very informative!! 
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Kellyerin222
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Tex I do think you are right that most of the research that I have found really states MC as chronic diarrhea and there has only been once that I have read about constipation or C and D alternating.
Polly I have been finding so much information on auto-immune related diseases and how that has been correlated with so many health problems. I went to the Notre Dame library a few weeks back and got a book just on auto-immune diseases and it was very eye opening. The fact that it stated how at one time autoimmune diseases were thought to be very rare and now new studies show that they are in fact a lot more common, but harder to diagnose. One quote from that book I will never forget is it stated "49% of all patients were labeled as hypochondriacs by their physicans when in fact they had an autoimmune disease"-- it's just with an autoimmune disease it is harder to diagnose. I am hoping with more advanced technologies and awareness this will shed new light and help more people who suffer who are not yet dianogsed.
I have been doing some more reasearching and I wish I could post a link to this, but I have access to index of journals being a college student and it would ask you for a password to sign for you to gain access. I did find this one journal article and if I copied and pasted (17 pages worth) you guys might smack me upside the head, lol, so I am going to copy and paste some revelant and intresting things that I found.
ARTICLE: Scandinavian Journal of Gastroenterology; Sep2004, Vol. 39 Issue 9, p837-845, 9p
Clinical characteristics of collagenous and lymphocytic colitis
Diagnostic delay and symptoms
The duration of symptoms before the diagnosis varied
widely in both groups, but there was a trend towards a longer
diagnostic delay in CC than in LC (median 19.5 months,
range 0.5–216 versus 5 months, range 0.5–264; P = 0.087). In
MC patients, the most common indication for primary
colonoscopy had been diarrhea (94%; 79/84). Other or
additional reasons were anemia or fecal blood (3 patients
with CC), abdominal pain (11 patients with LC), changed
bowel habits (2 patients), and obstipation (1 patient with LC).
In the other cases (8 patients), colonoscopy was performed for
varying reasons, such as hemorrhoids, follow-up of adenoma,
or diverticular disease. A comparison of the clinical features
of CC and LC is given in Table III. There were no significant
differences in the symptoms and course of the disease
between LC and CC. The most common symptom was
watery diarrhea associated with nocturnal diarrhea and
incontinence. In addition, about two-thirds of the patients
experienced weight loss and about half fatigue. The stool
frequency at the time of diagnosis was estimated, and median
value was 4 stools per day (range 1–30).
*** This study found symptom as change in bowel habits and obstipation***
Concomitant conditions
The diseases associated with LC and CC are listed in TableIV. All patients with celiac disease (CD) fulfilled the revised
ESPGAN (European Society of Paediatric Gastroenterology
and Nutrition) diagnostic criteria for CD (13). The prevalence
of CD was significantly higher in MC (16.7%; 14/84) than in
the control group (1%; 1/84; P = 0.001). In MC, 9 patients had
had CD for several years before the diagnosis of MC. Two
patients had been on a gluten-free diet for less than one year.
In three patients, CD was diagnosed during the year following
the diagnosis of MC. Two of the patients with CD had
dermatitis herpetiformis (1 with CC, 1 with LC), and three
had IgA deficiency (1 with CC, two with LC). One patient had
refused gastroscopy, but she had negative celiac serology. Celiac serology was positive in three of the four patients with
CD and negative in three of the patients with MC without CD.
As indicated in Table IV, autoimmune conditions were
more common in MC (36%) than in the controls (14%;
P = 0.002) and turned out to be more prevalent in CC (53%)
compared to LC (26%; P = 0.017). Subjects with LC more
often had bronchial asthma (26%) than patients with CC (7%;
P = 0.042), but no significant difference was seen compared
to controls. Nor were statistically significant differences seen
in the prevalence of cardiovascular or other diseases in
comparison with the control group, or between the subgroups
of MC.
The reported patterns of symptoms and the clinical course
in MC are largely similar to our observations, though with
some exceptions. IBS-like symptoms, such as abdominal
pain, flatulence, and abdominal distention, were common in
our patients (about 80%) as also in previous studies (about
30%–70%) (4, 7, 15). In addition to some resemblance in the
pattern of symptoms between IBS and MC, there is evidence
suggesting pathogenetic relatedness. In a recent study of 77
patients meeting the Rome Criteria for diagnosis of IBS (20),
31 had a non-specific microscopic inflammation not fulfilling
the criteria of MC in the bowel, 8 patients had classic LC, and
only 38 patients had histology within the normal limits.
However, even in this group, the number of IELs in the colon
epithelium was higher than in the control group. Patients with
CC were excluded from that study (21). This study suggests
that at least a subset of the patients with IBS may form part of
a continuum with LC, and that immune activation manifesting
as an increased density of intraepithelial lymphocytes could
be an important feature in both IBS and LC.
Diarrhea is usually the main symptom in MC, and some
reports consider chronic diarrhea a necessary diagnostic
criterion of MC (3, 4, 15). In our study, the diagnosis of MC was based on histologic findings of the colon, not on
symptoms. However, there have also been studies of LC
where patients without diarrhea have been diagnosed as
suffering from LC (14, 17) and also one report of CC with
severe constipation (22). One of our LC patients had constipation
and abdominal pain, indicating that the characteristic
histopathology is not always associated with diarrhea in MC.
In the previous case series, up to 40% of patients with MC
have had one or more concomitant autoimmune diseases
along with CC (15), and associated diseases of autoimmune
origin equally common in LC (4, 7). Based on this association,
an autoimmune pathogenic mechanism in MC has been
suggested. In our series, autoimmune conditions were more
often found in MC (36%) than in the control group (14%).
The association was most evident in the CC group, where
about half of the patients had one or more conditions with a
presumed autoimmune origin.
One of the most common diseases with an autoimmune
background in the MC group was CD. According to previous
studies, CD appears to be more frequent in LC (9%–15%)
than in CC (3%–8%) (4, 15, 24). Fine et al. (10) found
inflammation with partial or subtotal villous atrophy in 27%
(10 of 37) of the patients with MC, and only 30% of them had
normal duodenal histology. In our series, the frequency of CD
was higher in CC than in LC (20% versus 14.8%; P = NS), the
overall prevalence of CD in MC (16.7%) clearly exceeding
the reported prevalence of 0.27%–1% in the Finnish population
(25). In the studies of Fine et al. (26), the prevalences of
MC in CD and refractory sprue were 5% and 67%, respectively.
The mechanisms of association between CD and MC
are so far unclear. There have been reports of the celiac
disease associated HLA-DQ2 allele being more frequent in
patients with MC than in the normal population (10),
indicating the possibility of a shared genetic background.
On the other hand, CD has been associated with lymphocytic
gastritis, and it is possible that patients with CD may have a
more widespread increase of intraepithelial lymphocytes in
the gastrointestinal tract due to gluten or some as yet unknown
antigen (27). In our series, only three patients did not have a
gluten-free diet before the diagnosis of MC, and six of our
patients with CD had normal duodenal histology at the time of
the diagnosis of MC. This suggests that gluten is not the
noxious agent associated with celiac disease in MC. In a clinical setting, CD patients with an adequate diet and
improved duodenal histology may still have symptoms, and
colonoscopy in these cases may reveal MC. On the other
hand, when MC is found, CD should be excluded. Because
IgA deficiency is not rare in CD (28) or in CD with MC, as
shown in the present study (21%; 3/14), it advisable not to
rely on IgA-based serological tests.
Kelly
P.S. If anyone wants me to look up or research something don't be afraid to ask I will be glad to!
Polly I have been finding so much information on auto-immune related diseases and how that has been correlated with so many health problems. I went to the Notre Dame library a few weeks back and got a book just on auto-immune diseases and it was very eye opening. The fact that it stated how at one time autoimmune diseases were thought to be very rare and now new studies show that they are in fact a lot more common, but harder to diagnose. One quote from that book I will never forget is it stated "49% of all patients were labeled as hypochondriacs by their physicans when in fact they had an autoimmune disease"-- it's just with an autoimmune disease it is harder to diagnose. I am hoping with more advanced technologies and awareness this will shed new light and help more people who suffer who are not yet dianogsed.
I have been doing some more reasearching and I wish I could post a link to this, but I have access to index of journals being a college student and it would ask you for a password to sign for you to gain access. I did find this one journal article and if I copied and pasted (17 pages worth) you guys might smack me upside the head, lol, so I am going to copy and paste some revelant and intresting things that I found.
ARTICLE: Scandinavian Journal of Gastroenterology; Sep2004, Vol. 39 Issue 9, p837-845, 9p
Clinical characteristics of collagenous and lymphocytic colitis
Diagnostic delay and symptoms
The duration of symptoms before the diagnosis varied
widely in both groups, but there was a trend towards a longer
diagnostic delay in CC than in LC (median 19.5 months,
range 0.5–216 versus 5 months, range 0.5–264; P = 0.087). In
MC patients, the most common indication for primary
colonoscopy had been diarrhea (94%; 79/84). Other or
additional reasons were anemia or fecal blood (3 patients
with CC), abdominal pain (11 patients with LC), changed
bowel habits (2 patients), and obstipation (1 patient with LC).
In the other cases (8 patients), colonoscopy was performed for
varying reasons, such as hemorrhoids, follow-up of adenoma,
or diverticular disease. A comparison of the clinical features
of CC and LC is given in Table III. There were no significant
differences in the symptoms and course of the disease
between LC and CC. The most common symptom was
watery diarrhea associated with nocturnal diarrhea and
incontinence. In addition, about two-thirds of the patients
experienced weight loss and about half fatigue. The stool
frequency at the time of diagnosis was estimated, and median
value was 4 stools per day (range 1–30).
*** This study found symptom as change in bowel habits and obstipation***
Concomitant conditions
The diseases associated with LC and CC are listed in TableIV. All patients with celiac disease (CD) fulfilled the revised
ESPGAN (European Society of Paediatric Gastroenterology
and Nutrition) diagnostic criteria for CD (13). The prevalence
of CD was significantly higher in MC (16.7%; 14/84) than in
the control group (1%; 1/84; P = 0.001). In MC, 9 patients had
had CD for several years before the diagnosis of MC. Two
patients had been on a gluten-free diet for less than one year.
In three patients, CD was diagnosed during the year following
the diagnosis of MC. Two of the patients with CD had
dermatitis herpetiformis (1 with CC, 1 with LC), and three
had IgA deficiency (1 with CC, two with LC). One patient had
refused gastroscopy, but she had negative celiac serology. Celiac serology was positive in three of the four patients with
CD and negative in three of the patients with MC without CD.
As indicated in Table IV, autoimmune conditions were
more common in MC (36%) than in the controls (14%;
P = 0.002) and turned out to be more prevalent in CC (53%)
compared to LC (26%; P = 0.017). Subjects with LC more
often had bronchial asthma (26%) than patients with CC (7%;
P = 0.042), but no significant difference was seen compared
to controls. Nor were statistically significant differences seen
in the prevalence of cardiovascular or other diseases in
comparison with the control group, or between the subgroups
of MC.
The reported patterns of symptoms and the clinical course
in MC are largely similar to our observations, though with
some exceptions. IBS-like symptoms, such as abdominal
pain, flatulence, and abdominal distention, were common in
our patients (about 80%) as also in previous studies (about
30%–70%) (4, 7, 15). In addition to some resemblance in the
pattern of symptoms between IBS and MC, there is evidence
suggesting pathogenetic relatedness. In a recent study of 77
patients meeting the Rome Criteria for diagnosis of IBS (20),
31 had a non-specific microscopic inflammation not fulfilling
the criteria of MC in the bowel, 8 patients had classic LC, and
only 38 patients had histology within the normal limits.
However, even in this group, the number of IELs in the colon
epithelium was higher than in the control group. Patients with
CC were excluded from that study (21). This study suggests
that at least a subset of the patients with IBS may form part of
a continuum with LC, and that immune activation manifesting
as an increased density of intraepithelial lymphocytes could
be an important feature in both IBS and LC.
Diarrhea is usually the main symptom in MC, and some
reports consider chronic diarrhea a necessary diagnostic
criterion of MC (3, 4, 15). In our study, the diagnosis of MC was based on histologic findings of the colon, not on
symptoms. However, there have also been studies of LC
where patients without diarrhea have been diagnosed as
suffering from LC (14, 17) and also one report of CC with
severe constipation (22). One of our LC patients had constipation
and abdominal pain, indicating that the characteristic
histopathology is not always associated with diarrhea in MC.
In the previous case series, up to 40% of patients with MC
have had one or more concomitant autoimmune diseases
along with CC (15), and associated diseases of autoimmune
origin equally common in LC (4, 7). Based on this association,
an autoimmune pathogenic mechanism in MC has been
suggested. In our series, autoimmune conditions were more
often found in MC (36%) than in the control group (14%).
The association was most evident in the CC group, where
about half of the patients had one or more conditions with a
presumed autoimmune origin.
One of the most common diseases with an autoimmune
background in the MC group was CD. According to previous
studies, CD appears to be more frequent in LC (9%–15%)
than in CC (3%–8%) (4, 15, 24). Fine et al. (10) found
inflammation with partial or subtotal villous atrophy in 27%
(10 of 37) of the patients with MC, and only 30% of them had
normal duodenal histology. In our series, the frequency of CD
was higher in CC than in LC (20% versus 14.8%; P = NS), the
overall prevalence of CD in MC (16.7%) clearly exceeding
the reported prevalence of 0.27%–1% in the Finnish population
(25). In the studies of Fine et al. (26), the prevalences of
MC in CD and refractory sprue were 5% and 67%, respectively.
The mechanisms of association between CD and MC
are so far unclear. There have been reports of the celiac
disease associated HLA-DQ2 allele being more frequent in
patients with MC than in the normal population (10),
indicating the possibility of a shared genetic background.
On the other hand, CD has been associated with lymphocytic
gastritis, and it is possible that patients with CD may have a
more widespread increase of intraepithelial lymphocytes in
the gastrointestinal tract due to gluten or some as yet unknown
antigen (27). In our series, only three patients did not have a
gluten-free diet before the diagnosis of MC, and six of our
patients with CD had normal duodenal histology at the time of
the diagnosis of MC. This suggests that gluten is not the
noxious agent associated with celiac disease in MC. In a clinical setting, CD patients with an adequate diet and
improved duodenal histology may still have symptoms, and
colonoscopy in these cases may reveal MC. On the other
hand, when MC is found, CD should be excluded. Because
IgA deficiency is not rare in CD (28) or in CD with MC, as
shown in the present study (21%; 3/14), it advisable not to
rely on IgA-based serological tests.
Kelly
P.S. If anyone wants me to look up or research something don't be afraid to ask I will be glad to!
Currently waiting results to see exact problem.
Hi Kelly!
Interesting and extensive review article - thanks for posting.
One of the theories for the increase in autoimmune (AI) diseases is that, although we still have the aggressive immune system of our ancestors from eons ago, there is much less work for it to do. One of the major locations for immune "soldiers" (white cells, etc.) is the gut. Huge numbers of them rush to the gut lining whenever we eat. Nowadays, however, we have such a "pure" food supply for the most part (clean water, refrigerated food, etc.) that there is not as much work for the immune system to do. Not to mention antibiotics, anti-bacterial hand washes and soaps, the ability to bathe daily. So, with a lot less work to do against invading bugs, it makes sense that the immune system would begin attacking "good" tissues in the body or "good" bacteria.
It seems that the most common associated AI problems here on this board are gluten sensitivity/CD/other food intolerances, thyroid disease, DH, and arthritis. At least one had positive tests for lupus and got rid of it with the GF diet, if I remember correctly. One has diabetes type I.
Thanks for your offer to do research. Will let you know.
Have a good day!
Polly
Interesting and extensive review article - thanks for posting.
One of the theories for the increase in autoimmune (AI) diseases is that, although we still have the aggressive immune system of our ancestors from eons ago, there is much less work for it to do. One of the major locations for immune "soldiers" (white cells, etc.) is the gut. Huge numbers of them rush to the gut lining whenever we eat. Nowadays, however, we have such a "pure" food supply for the most part (clean water, refrigerated food, etc.) that there is not as much work for the immune system to do. Not to mention antibiotics, anti-bacterial hand washes and soaps, the ability to bathe daily. So, with a lot less work to do against invading bugs, it makes sense that the immune system would begin attacking "good" tissues in the body or "good" bacteria.
It seems that the most common associated AI problems here on this board are gluten sensitivity/CD/other food intolerances, thyroid disease, DH, and arthritis. At least one had positive tests for lupus and got rid of it with the GF diet, if I remember correctly. One has diabetes type I.
Thanks for your offer to do research. Will let you know.
Have a good day!
Polly
Blessed are they who can laugh at themselves, for they shall never cease to be amused.
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Kellyerin222
- Adélie Penguin
- Posts: 88
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- Contact:
Polly,
What you said makes since about the immune system. Our ancestors did not have the means as we do today; therefore, we are more predisposed to having our immune system on high alert and attack, which causes problems. Also in today’s world we have more pollution and hazards to our health (automobile pollution, chemicals, etc) that we are faced with more than our ancestors were. With everything going on I am more alert to health issues and it seems that now I am able to fit the puzzles pieces together a little more clearly. When I was 2 I was diagnosed with asthma. As a child it was severe to the point I had to be hospitalized several times in a bubble type thing for more oxygen. I now realize in my older years that asthma is associated with the immune system. Every year I would come down with bronchial pneumonia as a child. Luckily now I only notice asthma problems in the fall when I am around burning leaves (so I avoid that type of situation). I have psoriasis--- immune system issue. With all of this new research and information I do ponder the long standing debate of nature vs. nurture (our genetics vs. our environment). Is this brought on and problems arise simply because of my genetics, or is there something environmentally that triggers it and turns on the reaction? I am sure it is a combination of the two-- but I think when research is able to pin point the exact trigger of it a little more, then we will be on our way to taking more steps to help those who suffer these types of issues.
It is a little scary to think that our immune system is a vital part of our health and something that is supposed to be there to help us is actually causing hurt to us. I found your article about the sinus issues and immune system interesting and really never thought there could be a link between the two, but I am finding out so much great information lately. I think what makes it so difficult is our immune system is not so easily visible-- sure you have tests such as C-reactive protein and sedimentation rate, but you have to consider the interpretation results of the pathologist and even at times false results; where, as if you have a problem with your heart a cardiologist can visually see the problem. So I think we have come a long way in technology, but it shows me that we still have a ways to go to really get it down to a science.
Hope your having a great day!
Kel
What you said makes since about the immune system. Our ancestors did not have the means as we do today; therefore, we are more predisposed to having our immune system on high alert and attack, which causes problems. Also in today’s world we have more pollution and hazards to our health (automobile pollution, chemicals, etc) that we are faced with more than our ancestors were. With everything going on I am more alert to health issues and it seems that now I am able to fit the puzzles pieces together a little more clearly. When I was 2 I was diagnosed with asthma. As a child it was severe to the point I had to be hospitalized several times in a bubble type thing for more oxygen. I now realize in my older years that asthma is associated with the immune system. Every year I would come down with bronchial pneumonia as a child. Luckily now I only notice asthma problems in the fall when I am around burning leaves (so I avoid that type of situation). I have psoriasis--- immune system issue. With all of this new research and information I do ponder the long standing debate of nature vs. nurture (our genetics vs. our environment). Is this brought on and problems arise simply because of my genetics, or is there something environmentally that triggers it and turns on the reaction? I am sure it is a combination of the two-- but I think when research is able to pin point the exact trigger of it a little more, then we will be on our way to taking more steps to help those who suffer these types of issues.
It is a little scary to think that our immune system is a vital part of our health and something that is supposed to be there to help us is actually causing hurt to us. I found your article about the sinus issues and immune system interesting and really never thought there could be a link between the two, but I am finding out so much great information lately. I think what makes it so difficult is our immune system is not so easily visible-- sure you have tests such as C-reactive protein and sedimentation rate, but you have to consider the interpretation results of the pathologist and even at times false results; where, as if you have a problem with your heart a cardiologist can visually see the problem. So I think we have come a long way in technology, but it shows me that we still have a ways to go to really get it down to a science.
Hope your having a great day!
Kel
Currently waiting results to see exact problem.