What is the difference between having the gene for gluten sensitivity and having the gene for celiac sprue?
I've read Dr. Fine's comments, but I am not sure I understand them correctly. All these genes predispose for gluten sensitivity, the underlying process, but the CS genes mean that it's more likely you will develop villous atrophy, right? If you only have a gene for gluten sensitivty and not CS does it mean you won't develop villous atrophy? The website says only 1% of patients with DQ1 develop villous atrophy.
Are there any other differences?
Dr Fine says that it is known that a person can have every last complication from gluten sensitivity and never have villous atrophy? So it seems having gluten sensitivity can cause the full array of symptoms and problems as CS, just usually without the villous atrophy. Do I have that right?
I need to juice some grapes and pineapple for my hubby and throw some rice cakes into a bag and run back to the surgery center. They want him to eat during his recovery period, but of course he can't eat any of the good they will given him...wheat crackers and juice with sugar.
Aloha for now! Celia
Question on Gluten Intolerance/Celiac Sprue
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Question on Gluten Intolerance/Celiac Sprue
I beleive in magic!
Celia,
I believe you have summed up the essence of the relationship involved with these genes, (and the two diseases). Though the sumptoms can be the same, MC is basically a disease of the colon, whereas CS is a disease of the small intestine, (as far as clinical markers are concerned). My understanding is that MC can affect areas of the small intestine, (primarily the illeum), and while SC theoretically doesn't affect the colon, upstream events obviously cause consequences in the colon, since diarrhea is a primary symptom of CS. I think a primary distinction between diarrhea caused by MC, and diarrhea caused by CS, is the possibility of secretory diarrhea with MC. Unless I am overlooking something, secretory diarrhea is not a symptom of CS.
The damage from CS occurs in the small intestine, primarily in the duodenum, just as you stated, whereas the damage from MC is most notable in the colon, as with the other IBDs. That said, many of us with MC, apparently have residual damage to the small intestine, though it is probably not as significant as the damage caused there by CS, since the villi are not as likely to be seriously affected with MC.
Apparently, though, just as the presence of a gene does not mean that a disease is inevitable, neither does the absence of a gene imply that a disease is impossible. Exceptions apparently occur, which probably means that there are additional, uncataloged genes, involved.
At least that's the way I see it. As always, YMMV.
Tex
I believe you have summed up the essence of the relationship involved with these genes, (and the two diseases). Though the sumptoms can be the same, MC is basically a disease of the colon, whereas CS is a disease of the small intestine, (as far as clinical markers are concerned). My understanding is that MC can affect areas of the small intestine, (primarily the illeum), and while SC theoretically doesn't affect the colon, upstream events obviously cause consequences in the colon, since diarrhea is a primary symptom of CS. I think a primary distinction between diarrhea caused by MC, and diarrhea caused by CS, is the possibility of secretory diarrhea with MC. Unless I am overlooking something, secretory diarrhea is not a symptom of CS.
The damage from CS occurs in the small intestine, primarily in the duodenum, just as you stated, whereas the damage from MC is most notable in the colon, as with the other IBDs. That said, many of us with MC, apparently have residual damage to the small intestine, though it is probably not as significant as the damage caused there by CS, since the villi are not as likely to be seriously affected with MC.
Apparently, though, just as the presence of a gene does not mean that a disease is inevitable, neither does the absence of a gene imply that a disease is impossible. Exceptions apparently occur, which probably means that there are additional, uncataloged genes, involved.
At least that's the way I see it. As always, YMMV.
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.
Thanks. This really helps. I now see where my confusion lies! I had to go back and relook at Dr. Fine's explanation of the genes too.
DQ 2 and 8 are primarily association with CS; DQ1 and DQ3 much less so (less than 1%)
Whereas, DQ1 and DQ3 are associated with microscopic colitis and DQ1 Gluten Ataxia.
In my mind, I was associating all gluten sensitivity with a possible outcome of villous atrophy, but that's not necessarily the case.
But can people simply have gluten sensitivity that doesn't develop into one of these diseases? Like my husband is gluten sensitive but he didn't develop MC, he developed proctitis.
And what does 0501 and 0502 mean? Is the gluten sensitivity related to the DQ part or the 4 digit number that follows?
Hope I am not driving you nuts with the question. Celia
DQ 2 and 8 are primarily association with CS; DQ1 and DQ3 much less so (less than 1%)
Whereas, DQ1 and DQ3 are associated with microscopic colitis and DQ1 Gluten Ataxia.
In my mind, I was associating all gluten sensitivity with a possible outcome of villous atrophy, but that's not necessarily the case.
But can people simply have gluten sensitivity that doesn't develop into one of these diseases? Like my husband is gluten sensitive but he didn't develop MC, he developed proctitis.
And what does 0501 and 0502 mean? Is the gluten sensitivity related to the DQ part or the 4 digit number that follows?
Hope I am not driving you nuts with the question. Celia
I beleive in magic!
You wrote:
A food intolerance, by definition, will result in an immume system reaction in the gut. The gluten sensitivity tests are based on the production of antibodies, so by definition, it should be impossible to get a positive test result for gluten sensitivity, unless a reaction is taking place, somewhere in the digestive system. Presumably, all possible food intolerance reactions correlate to a known GI disease. IOW, there is no possibility for an undefined reaction that could produce the antibodies required for a positive test result. Do you see what I'm saying? I may not be eloquent enough to convey this so that it illustrates my point.
Concerning a gene molecular test result of HLA-DQB1*501,502. The serologic equivalent of this is HLA-DQ1,1 -subtype 5,5
I know very little about this stuff, but my understanding is that the DQ part specifies that gluten is the allergen, and the 0501 and 0502 codes are the two alleles of a gene occupying the same position on matching chromosomes, presumably one from each parent. IOW, an indivitual normally has two alleles for each trait.
This is getting pretty deep. LOL.
Tex
P S Now I'm curious. Did your husband have biopsies taken, and if so, were they examined under the microscope, by a pathologist who was aware of the possibility of MC? IOW, did the pathologist specificically rule out MC, and/or any other IBD, or just rubber stamp the GI's suggested diagnosis of proctitis?
That's a good question. It would appear at first glance to be possible, but frankly I can't envision a way that this might happen. For one thing, there are numerous asymptomatic celiacs in this world, but they all show villous atrophy, even though they show no outward signs of having the disease. MC is defined as a certain type of microscopic inflammation pattern in the colon, and an abnormal thickening of the subepithelial collagenous plate, in the case of CC. If the inflammation is present, then the disease is present and active. Without looking up proctitis, as I recall, it involves inflammation in the colon, basically below the sigmoid colon.But can people simply have gluten sensitivity that doesn't develop into one of these diseases? Like my husband is gluten sensitive but he didn't develop MC, he developed proctitis..
A food intolerance, by definition, will result in an immume system reaction in the gut. The gluten sensitivity tests are based on the production of antibodies, so by definition, it should be impossible to get a positive test result for gluten sensitivity, unless a reaction is taking place, somewhere in the digestive system. Presumably, all possible food intolerance reactions correlate to a known GI disease. IOW, there is no possibility for an undefined reaction that could produce the antibodies required for a positive test result. Do you see what I'm saying? I may not be eloquent enough to convey this so that it illustrates my point.
Concerning a gene molecular test result of HLA-DQB1*501,502. The serologic equivalent of this is HLA-DQ1,1 -subtype 5,5
I know very little about this stuff, but my understanding is that the DQ part specifies that gluten is the allergen, and the 0501 and 0502 codes are the two alleles of a gene occupying the same position on matching chromosomes, presumably one from each parent. IOW, an indivitual normally has two alleles for each trait.
This is getting pretty deep. LOL.
Tex
P S Now I'm curious. Did your husband have biopsies taken, and if so, were they examined under the microscope, by a pathologist who was aware of the possibility of MC? IOW, did the pathologist specificically rule out MC, and/or any other IBD, or just rubber stamp the GI's suggested diagnosis of proctitis?
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.
Celia,
i wouldn't worry about learning the subtypes which are what those four digit numbers represent. For the purposes of our disease, the old nomenclature (before the subtypes were broken down further), of HLA DQ 1, for example, are adequate because the relevent parts of the proteins are functionally the same.
For example, my sister and I have two different subtypes of DQ1 to go with the CD2 that each of us acquired from our mom.
However, the results are exactly the same. One way that we can tell is because we have the exact same proven foods we have delayed reactions to.
Again, the relevant part of the human leukocyte antibody for our purposes is the same, regardless of the subtype. This is because not tall of it's protein is involved in the particular response that we can do anything about.
By the way, Rita, a member here, has the EXACT same geneotype as I have, subtypes and all, and she has the exact same foods that she reacts to.
One thing that is interesting is the fact that having a double HLA DQ 1 gene is even more highly productive of so-called "gluten ataxia" than having just one. I just had one, and experienced an apparent problem with balance when walking in a dark or partially darkened hallway at night -- wall would just seem as though it had fallen into my upper arm, when in fact, I was actually leaning into it without even being aware I was leaning.
That went way once I began the "allergen"-free diet.
Like Wayne, I can't see any way that one could have gluten sensitivity without at least SOME involvement of the gut as that's where the antibodies are formed, right??
Still, it looks as though when biopsies are done, at least WHERE they're done in the research studies, the combinations can be all over the map. For instance, it just may be with GS that neuro symptoms are the most common symptom rather than GI symptoms.
However, with the types of biopsies and pathology that has been done on them in studies thus far, it seems as though there's not a definite correlation between the amount of damage to these villi and the symptoms.
Another thing that's interesting is that regardless of one's genotype, it just may be that anyone who's not descended from deep in the heart of China or else Subsaharan Africa may have the genetic predisposition to gluten sensitivity, just not diagnosed the traditional ways or perhaps even mostly UNdiagnosed as yet. However, since those two groups of peoples haven't really been exposed to this type of gluten for all that long, it may be that they will eventually prove to be just as susceptible given enough exposure over time. That would mean the stuff's probably not good for anyone, at least in it's present form.
Hope this helps. Luce
i wouldn't worry about learning the subtypes which are what those four digit numbers represent. For the purposes of our disease, the old nomenclature (before the subtypes were broken down further), of HLA DQ 1, for example, are adequate because the relevent parts of the proteins are functionally the same.
For example, my sister and I have two different subtypes of DQ1 to go with the CD2 that each of us acquired from our mom.
However, the results are exactly the same. One way that we can tell is because we have the exact same proven foods we have delayed reactions to.
Again, the relevant part of the human leukocyte antibody for our purposes is the same, regardless of the subtype. This is because not tall of it's protein is involved in the particular response that we can do anything about.
By the way, Rita, a member here, has the EXACT same geneotype as I have, subtypes and all, and she has the exact same foods that she reacts to.
One thing that is interesting is the fact that having a double HLA DQ 1 gene is even more highly productive of so-called "gluten ataxia" than having just one. I just had one, and experienced an apparent problem with balance when walking in a dark or partially darkened hallway at night -- wall would just seem as though it had fallen into my upper arm, when in fact, I was actually leaning into it without even being aware I was leaning.
That went way once I began the "allergen"-free diet.
Like Wayne, I can't see any way that one could have gluten sensitivity without at least SOME involvement of the gut as that's where the antibodies are formed, right??
Still, it looks as though when biopsies are done, at least WHERE they're done in the research studies, the combinations can be all over the map. For instance, it just may be with GS that neuro symptoms are the most common symptom rather than GI symptoms.
However, with the types of biopsies and pathology that has been done on them in studies thus far, it seems as though there's not a definite correlation between the amount of damage to these villi and the symptoms.
Another thing that's interesting is that regardless of one's genotype, it just may be that anyone who's not descended from deep in the heart of China or else Subsaharan Africa may have the genetic predisposition to gluten sensitivity, just not diagnosed the traditional ways or perhaps even mostly UNdiagnosed as yet. However, since those two groups of peoples haven't really been exposed to this type of gluten for all that long, it may be that they will eventually prove to be just as susceptible given enough exposure over time. That would mean the stuff's probably not good for anyone, at least in it's present form.
Hope this helps. Luce
Celia,
I found a site that describes a study of non-celiac patients who presented with symptoms typical of gluten sensitive enteropathy, but did not meet the criteria for a diagnosis of CS. Presumably, the reseachers ruled out other related diseases, but I didn't notice that specificially mentioned in the article. Here is a quote:
"Interestingly, in clinical practice we have recognized a subgroup of patients who seem to be sensitive to gluten, according to symptoms and signs of gluten-dependent malabsorption, but in whom the SIB revealed only a Marsh II lesion, which does not strictly meet the criteria for the diagnosis of celiac disease. However, the condition of these patients responds to a gluten-free diet, according to symptomatology, malabsorption, and histology parameters." SIB, presumably stands for Small Intestine Biopsy, as I'm sure you're aware.
In my opinion, the primary problem here, is the rather arbitrarity, (and in my opinion, archaic), definition of celiac disease. Is it unreasonable to suggest that those patients were simply in the early stages of disease, and would ultimately have been diagnosed with CS or possibly MC, if allowed to proceed without treatment? That quote comes from this site:
http://www.medscape.com/viewarticle/440971_4
Be aware that you can only access that site once, without registering for membership.
That site also makes a rather interesting observation about the amount of time required to reach remission with celiac disease.
"Histologic recovery profiles of 158 patients with celiac disease in our hospital revealed that only 65.0% of the patients reached histologic remission within 2 years. Moreover, within 5 years, 85.3% were in remission, and in long-term follow-up, 89.9% showed normalization of villous architecture."
Presumably, the problem here is a failure to diagnose the disease and initiate treatment in a timely manner. The more damage that acrues, the longer it takes to heal.
Here's another site, that Luce sent to me, that points out how responsive such patients are to the GF diet:
http://tinyurl.com/nelag
So, to sum it up, I would have to say that in view of this information, by strict definition, it is certainly possibly to be gluten sensitive, and not have a related disease. In my opinion, though, that situation is only made possible by the medical profession's apparent reluctance to appropriately define the diagnostic criteria for certain diseases.
Tex
I found a site that describes a study of non-celiac patients who presented with symptoms typical of gluten sensitive enteropathy, but did not meet the criteria for a diagnosis of CS. Presumably, the reseachers ruled out other related diseases, but I didn't notice that specificially mentioned in the article. Here is a quote:
"Interestingly, in clinical practice we have recognized a subgroup of patients who seem to be sensitive to gluten, according to symptoms and signs of gluten-dependent malabsorption, but in whom the SIB revealed only a Marsh II lesion, which does not strictly meet the criteria for the diagnosis of celiac disease. However, the condition of these patients responds to a gluten-free diet, according to symptomatology, malabsorption, and histology parameters." SIB, presumably stands for Small Intestine Biopsy, as I'm sure you're aware.
In my opinion, the primary problem here, is the rather arbitrarity, (and in my opinion, archaic), definition of celiac disease. Is it unreasonable to suggest that those patients were simply in the early stages of disease, and would ultimately have been diagnosed with CS or possibly MC, if allowed to proceed without treatment? That quote comes from this site:
http://www.medscape.com/viewarticle/440971_4
Be aware that you can only access that site once, without registering for membership.
That site also makes a rather interesting observation about the amount of time required to reach remission with celiac disease.
"Histologic recovery profiles of 158 patients with celiac disease in our hospital revealed that only 65.0% of the patients reached histologic remission within 2 years. Moreover, within 5 years, 85.3% were in remission, and in long-term follow-up, 89.9% showed normalization of villous architecture."
Presumably, the problem here is a failure to diagnose the disease and initiate treatment in a timely manner. The more damage that acrues, the longer it takes to heal.
Here's another site, that Luce sent to me, that points out how responsive such patients are to the GF diet:
http://tinyurl.com/nelag
So, to sum it up, I would have to say that in view of this information, by strict definition, it is certainly possibly to be gluten sensitive, and not have a related disease. In my opinion, though, that situation is only made possible by the medical profession's apparent reluctance to appropriately define the diagnostic criteria for certain diseases.
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.
Lucy and Tex, very interesting information. Thanks. Lucy, I had lots of balance and coordination problems when I first got sick, but they disappeared after I stopped eating wheat.
Tex, my husband has had two colonoscopies (with two different doctors) and a sigmoidoscopy (with a third doctor) as a follow up.
The first one indicated proctitis, which is in the signmoid colon I believe. He doesn't have the biopsy report from the first one.
During the second colonoscopy, there was little inflammation seen by the naked eye, perhaps a bit in the illeum area, but the biopsy report indicated only showed active proctitis microscopically and nothing else in the rest of the colon.
The final sigmoidoscopy with a third doctor (my doctor) showed that the proctitis was completely healed and the biopsy was fine too. That was after he had done the Guts and Glory and SCD program for six months.
When I asked that same doctor if there was any chance that my husband had MC too, she really didn't think so (although she didn't have his file at hand). She said that the pathologists are training to look for these different diseases and they would had indicated if they saw mc micropsocopically. She's the one that found my mc, but she did note possible mc on the instructions to the pathologists. I don't recall D. every being a problem for my husband either. He had a problem with C.
He is having another colonoscopy in May by my doctor again so we can definitely ask her to be sure to ask them to check for MC. However, if the MC is patchy, as it probably is in my case, its possible for random biopsies to miss it.
He definitely has food intolerances too, but food allergies are also implicated in other types of colitis and chron's, I beleive. Last night he had itching in his face which he gets after eating gluten. I beleive the pain pills he took yesterday probably has corn starch as a filler.
I suppose there is also the period between when the gluten intolerance is triggered and the disease (CS or MC or gluten ataxia) actually appears too. He had more GERD type symptoms and also strong fatigue. It would probably be interesting for him to get the gene test done to see which way he might be pre-disposed.
Thanks for your thoughts on this. Celia
Tex, my husband has had two colonoscopies (with two different doctors) and a sigmoidoscopy (with a third doctor) as a follow up.
The first one indicated proctitis, which is in the signmoid colon I believe. He doesn't have the biopsy report from the first one.
During the second colonoscopy, there was little inflammation seen by the naked eye, perhaps a bit in the illeum area, but the biopsy report indicated only showed active proctitis microscopically and nothing else in the rest of the colon.
The final sigmoidoscopy with a third doctor (my doctor) showed that the proctitis was completely healed and the biopsy was fine too. That was after he had done the Guts and Glory and SCD program for six months.
When I asked that same doctor if there was any chance that my husband had MC too, she really didn't think so (although she didn't have his file at hand). She said that the pathologists are training to look for these different diseases and they would had indicated if they saw mc micropsocopically. She's the one that found my mc, but she did note possible mc on the instructions to the pathologists. I don't recall D. every being a problem for my husband either. He had a problem with C.
He is having another colonoscopy in May by my doctor again so we can definitely ask her to be sure to ask them to check for MC. However, if the MC is patchy, as it probably is in my case, its possible for random biopsies to miss it.
He definitely has food intolerances too, but food allergies are also implicated in other types of colitis and chron's, I beleive. Last night he had itching in his face which he gets after eating gluten. I beleive the pain pills he took yesterday probably has corn starch as a filler.
I suppose there is also the period between when the gluten intolerance is triggered and the disease (CS or MC or gluten ataxia) actually appears too. He had more GERD type symptoms and also strong fatigue. It would probably be interesting for him to get the gene test done to see which way he might be pre-disposed.
Thanks for your thoughts on this. Celia
I beleive in magic!
Thanks for all the info. Considering all that, it's very unlikely that your husband has MC, and it has just been overlooked. Also, after he has been on the GF diet for so long, I would be very surprised if a biopsy from his next exam would show any indication of the markers of MC. Even if he had MC, the markers should be gone, (or at least greatly diminished), by then.
Proctitis, by the way, refers to inflammation of the rectal mucosa, which is below the sigmoid section, of course.
I hope that he can get his diet fine tuned, and preempt any diseases that might have otherwise developed without such atttention to detail in diet.
Tex
Proctitis, by the way, refers to inflammation of the rectal mucosa, which is below the sigmoid section, of course.
I hope that he can get his diet fine tuned, and preempt any diseases that might have otherwise developed without such atttention to detail in diet.
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.