Celiac Disease: recheck antibodies after successful treatment?

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DrMetal

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If you diagnose an antibody-positive Celiac disease, treat it (with just a gluten free diet), patient returns in 6 months feeling a lot better (essentially asymptomatic, all other deficiencies resolved) . . . .do you recheck the celiac antibodies? (anti transglutaminase, anti gliadin etc). Why would you?

[It was suggested to me that they should be rechecked, to 'confirm' that your intervention, the glutenfree diet, worked. But cant you just assume that clinically if the patient is now asymptomatic and following the diet? The antibodies will always be positive, but is there value in monitoring their titers?]

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I agree what would the point be? They would still need to avoid gluten and the test wont change any management so would just be 100% waste of money so dont do it.
 
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No. That's not cost effective or helpful.
 
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If you diagnose an antibody-positive Celiac disease, treat it (with just a gluten free diet), patient returns in 6 months feeling a lot better (essentially asymptomatic, all other deficiencies resolved) . . . .do you recheck the celiac antibodies? (anti transglutaminase, anti gliadin etc). Why would you?

[It was suggested to me that they should be rechecked, to 'confirm' that your intervention, the glutenfree diet, worked. But cant you just assume that clinically if the patient is now asymptomatic and following the diet? The antibodies will always be positive, but is there value in monitoring their titers?]
Not a gastroenterologist, but I do not think trending the antibodies/titres in Celiac's is a thing.
 
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GI guidelines would say check. Check to make sure there is not low level noncompliance and also check histology to make sure it’s healed. As long as there is chronic inflammation they are at risk of long term complications. Also it’s not expensive to at least check antibodies.
 
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Trending a $250 dollar blood test does not make sense unless the patient continues to be symptomatic and you suspect inadvertent dietary non-adherence. If the patient is not compliant and lies to you, the blood test will not change the outcome.
 
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Trending a $250 dollar blood test does not make sense unless the patient continues to be symptomatic and you suspect inadvertent dietary non-adherence. If the patient is not compliant and lies to you, the blood test will not change the outcome.
If you have ever tried sticking to a true gluten free diet, you’d understand that it has nothing to do with “lying”. Symptoms are not reliable and patients with celiac disease have higher all cause mortality for a reason. Insurance will cover most or all of the cost in a known celiac patient. This is why we have evidence based medicine and not arguments on what feels right to you.
 
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Show me the evidence. Please show me the study that demonstrates that physicians trending celiac antibody panels improve all cause mortality.

Didn’t think so. Thank you.
 
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GI guidelines would say check. Check to make sure there is not low level noncompliance and also check histology to make sure it’s healed. As long as there is chronic inflammation they are at risk of long term complications. Also it’s not expensive to at least check antibodies.

I've seen these guidelines, and this is the source of my confusion. So the patient that f/u in 6 months, endorses following the diet, good resolution of symptoms, good resolution of other deficiencies (say iron is up, vitamin D is good) . . . you would recheck Abs, even re-scope that patient?

that *****ic physicians

Please, let's follow the SDN courtesy rules. Remember to purposely misspell your curse words, for example, mthrfckr, so as to avoid the auto-correction. Is this supposed to be psychic, psychotic ?
 
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I've seen these guidelines, and this is the source of my confusion. So the patient that f/u in 6 months, endorses following the diet, good resolution of symptoms, good resolution of other deficiencies (say iron is up, vitamin D is good) . . . you would recheck Abs, even re-scope that patient?



Please, let's follow the SDN courtesy rules. Remember to purposely misspell your curse words, for example, mthrfckr, so as to avoid the auto-correction. Is this supposed to be psychic, psychotic ?
ACG clinical guidelines give a strong recommendation with a moderate level of evidence to do so. The articles they site for this are actually pretty good. I encourage anyone interested to read it and take a look at figure 3 as a nice summary of how to manage/follow celiac patients. AGA came out with an update on management a couple of years ago that basically said the same thing.

You are right in thinking of all the symptoms resolve that it’s unlikely they still have severe inflammation. But many of my patients with CD actually remain on iron and vitamin supplements and so they respond but they are still at higher risk of cancer and so on. It’s just safer and the right thing to do to confirm. And yes, if they had severe atrophy of villi it’s good to see that their Marsh grade has improved to normal.
 
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ACG clinical guidelines give a strong recommendation with a moderate level of evidence to do so. The articles they site for this are actually pretty good. I encourage anyone interested to read it and take a look at figure 3 as a nice summary of how to manage/follow celiac patients. AGA came out with an update on management a couple of years ago that basically said the same thing.

You are right in thinking of all the symptoms resolve that it’s unlikely they still have severe inflammation. But many of my patients with CD actually remain on iron and vitamin supplements and so they respond but they are still at higher risk of cancer and so on. It’s just safer and the right thing to do to confirm. And yes, if they had severe atrophy of villi it’s good to see that their Marsh grade has improved to normal.
Are these the 2013 guidelines? Figure 3 says refer to a dietician (multiple times) and workup further 'if clinically indicated' based on an abnormal blood test. It doesn't say anything about cancer. I half expected it to recommend annual endoscopy if abnormal but this seems pretty vague and of unclear clinical utility to repeat a lab test over and over that, in the absence of symptoms, doesn't 'clinically indicate' further workup or repeated dietician referrals.
 
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You remind me of an arrogant resident who likes to challenge an attending on rounds or an old doc who hasn’t read anything of use in 30 years. Not sure which it is but very prideful and ignorant.

Of course, it couldn’t possibly be that you recommend something that is not evidence based, not proven to be cost effective, not proven to change outcomes. Some metrics you proclaim to care about.

This is the evidence you claim is “actually pretty good”:

”Annual follow-up with serology (TTG IgA) was associated with increasing rate of seroconversion of the TTG antibody (99%) among 2,245 patients who underwent systematic follow-up (58). Until more evidence is available, annual follow-up seems reasonable.”

To summarize: antibody levels decline with gluten-avoidance. That’s the evidence for trending a $250 test in every patient with CD annually? I rest my case.
 
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Of course, it couldn’t possibly be that you recommend something that is not evidence based, not proven to be cost effective, not proven to change outcomes. Some metrics you proclaim to care about.

This is the evidence you claim is “actually pretty good”:

”Annual follow-up with serology (TTG IgA) was associated with increasing rate of seroconversion of the TTG antibody (99%) among 2,245 patients who underwent systematic follow-up (58). Until more evidence is available, annual follow-up seems reasonable.”

To summarize: antibody levels decline with gluten-avoidance. That’s the evidence for trending a $250 test in every patient with CD annually? I rest my case.
Annual follow up is what we do when they are well controlled after some time. I work in a center with a higher amount of CD patients and I assure you this is standard. Do whatever you want, but people like you really make me want to be an expert witness in court one day.
 
Seems like there isn't a clear answer here but recommendations do lean towards testing, if for no other reason than liability. And if not, engaging in share-decision making and documenting that. From UpToDate:

"IgA anti tissue transglutaminase (tTG) or IgA (or IgG) deamidated gliadin peptide (DGP) should be used to monitor the response to gluten-free diet. We perform serologic testing 6 and 12 months after the initial diagnosis of celiac disease and annually thereafter

For whichever assay that will be used, a pretreatment antibody level should be determined at the time of diagnosis. Exclusion of gluten from the diet results in a gradual decline in serum IgA anti-gliadin and IgA tTG levels (half-life of six to eight weeks). A normal baseline value is typically reached within 3 to 12 months depending upon the pre-treatment concentrations. Normal IgA tTG levels do not reliably indicate recovery from villous atrophy. Conversely, if the levels do not fall as anticipated, the patient is usually continuing to ingest gluten either intentionally or inadvertently.

Although the general patterns above can be helpful, the accuracy of these tests in establishing compliance with a gluten-free diet is unsettled. The value of these tests in monitoring adherence to a gluten-free diet is particularly limited in three respects:

1. The test is useless if antibody levels are not elevated prior to therapy.

2. Inter-assay variations in test results may be substantial and make interpretation difficult. Serial samples should ideally be sent to one laboratory for testing to keep inter-assay variation to a minimum. Minor fluctuations in IgA anti-gliadin or IgA TTG levels are the norm and their importance should not be over interpreted.

3. Persistently high antibody levels usually reflect continued exposure to substantial amounts of dietary gluten. Antibody levels will fall when dietary gluten intake is reduced, however, they are not a sensitive indicator of occasional or minor dietary transgressions. Negative serology in a treated patient is also not a reliable indicator of mucosal healing."
 
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Seems like there isn't a clear answer here but recommendations do lean towards testing, if for no other reason than liability. And if not, engaging in share-decision making and documenting that. From UpToDate:

"IgA anti tissue transglutaminase (tTG) or IgA (or IgG) deamidated gliadin peptide (DGP) should be used to monitor the response to gluten-free diet. We perform serologic testing 6 and 12 months after the initial diagnosis of celiac disease and annually thereafter

For whichever assay that will be used, a pretreatment antibody level should be determined at the time of diagnosis. Exclusion of gluten from the diet results in a gradual decline in serum IgA anti-gliadin and IgA tTG levels (half-life of six to eight weeks). A normal baseline value is typically reached within 3 to 12 months depending upon the pre-treatment concentrations. Normal IgA tTG levels do not reliably indicate recovery from villous atrophy. Conversely, if the levels do not fall as anticipated, the patient is usually continuing to ingest gluten either intentionally or inadvertently.

Although the general patterns above can be helpful, the accuracy of these tests in establishing compliance with a gluten-free diet is unsettled. The value of these tests in monitoring adherence to a gluten-free diet is particularly limited in three respects:

1. The test is useless if antibody levels are not elevated prior to therapy.

2. Inter-assay variations in test results may be substantial and make interpretation difficult. Serial samples should ideally be sent to one laboratory for testing to keep inter-assay variation to a minimum. Minor fluctuations in IgA anti-gliadin or IgA TTG levels are the norm and their importance should not be over interpreted.

3. Persistently high antibody levels usually reflect continued exposure to substantial amounts of dietary gluten. Antibody levels will fall when dietary gluten intake is reduced, however, they are not a sensitive indicator of occasional or minor dietary transgressions. Negative serology in a treated patient is also not a reliable indicator of mucosal healing."
Sounds like the practice is based on no data. Thanks for posting.
 
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Annual follow up is what we do when they are well controlled after some time. I work in a center with a higher amount of CD patients and I assure you this is standard. Do whatever you want, but people like you really make me want to be an expert witness in court one day.
Seriously. Question your practice patterns.
 
I can’t believe this topic is such a hot button issue... Look, the general idea is it’s good to be proactive. If Abs are up it’s late, if they become iron deficient or osteopenic it’s too late, if it’s cancer or actual ulcerative small bowel disease then it’s tragic. At what point someone starts having diarrhea is variable because often people can have other issues that can constipate them. If you capture things earlier it’s the right thing to do. We do this is most of medicine when someone has a chronic disease and if you want to save money, it shouldn’t be on this.
 
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I can’t believe this topic is such a hot button issue... Look, the general idea is it’s good to be proactive. If Abs are up it’s late, if they become iron deficient or osteopenic it’s too late, if it’s cancer or actual ulcerative small bowel disease then it’s tragic. At what point someone starts having diarrhea is variable because often people can have other issues that can constipate them. If you capture things earlier it’s the right thing to do. We do this is most of medicine when someone has a chronic disease and if you want to save money, it shouldn’t be on this.
It’s fine. I just disagree with you. I also disagree with getting a CT head every time someone walks into an ED. I also disagree with rechecking ANA every time a patient is admitted. You do you. I’m only pointing out that there is no good data to support the practice other than eminence in some centers.
 
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I can’t believe this topic is such a hot button issue... Look, the general idea is it’s good to be proactive. If Abs are up it’s late, if they become iron deficient or osteopenic it’s too late, if it’s cancer or actual ulcerative small bowel disease then it’s tragic. At what point someone starts having diarrhea is variable because often people can have other issues that can constipate them. If you capture things earlier it’s the right thing to do. We do this is most of medicine when someone has a chronic disease and if you want to save money, it shouldn’t be on this.
The standard of care is to recheck serologies, If physicians wish to deviate outside the standard of care it's their prerogative, and a clear departure from multi-societal guidelines, which unequivocally recommend biochemical and histologic remission in addition to clinical. A refractory sprue patient who develops intestinal lymphoma after years walking around with clinically silent but serologically active disease left unabated is indefensible medically no matter the setting
 
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It is striking to me that you guys like to argue from medico-legal angles and made-up case stories rather than data. You do my job for me. Can we please acknowledge that there is no data to support this silly practice other than the two of you yelling into the ether that you want to testify against me in court? Seriously, are you the same person with two account?

”Unfortunately, although widely used in clinical practice, serologic tests are not very useful in monitoring either adherence to a gluten-free diet or intestinal recovery. An initial drop in any serologic test after initiation of a gluten-free diet is important to ensure adequate gluten avoidance and to pick out patients for whom further education or evaluation is necessary (44). Conversely, a number of studies have documented that normalization of serologies does not predict normalization of intes- tinal histology (45,46). Similarly, it has been shown that neither IgA anti-tTG, EMA, nor anti-DGP is accurate in the assessment of gluten-free diet adherence (47,48), and indeed they are less accurate than simply asking the patient about his or her level of adherence (48,49).
While the utility of routine serologic celiac testing in patients in clinical remission appears to be low, IgA anti-tTG testing is useful in the evaluation of patients with persistent signs and/or symptoms of CD despite apparent adherence to a gluten-free diet, also known as nonresponsive CD. In these patients, elevated IgA anti-tTG titers predict inadvertent gluten exposure, although normal or low positive titers can also be seen in refractory CD and small-intestinal bacterial overgrowth (50). It is clear that a noninvasive marker of CD activity would be of great clinical and research utility. A few tests have been proposed, including intestinal fatty acid-binding protein (I-FABP) (51), fecal fat content (52), and differential carbohydrate absorption test, such as the lactulose-to-mannitol ratio (53). Although, at this time, data are insufficient to recommend any of these tests in clinical practice, continued efforts in this area are warranted.”

 
The standard of care is to recheck serologies, If physicians wish to deviate outside the standard of care it's their prerogative, and a clear departure from multi-societal guidelines, which unequivocally recommend biochemical and histologic remission in addition to clinical. A refractory sprue patient who develops intestinal lymphoma after years walking around with clinically silent but serologically active disease left unabated is indefensible medically no matter the setting
What is the proper approach to clinically silent serologically active disease? Are you going to start that person with no symptoms on immunotherapy? Endoscopies? What if they have a complication related to that therapy is that clinically defensible because they might have have had lymphoma brewing?
 
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What is the proper approach to clinically silent serologically active disease? Are you going to start that person with no symptoms on immunotherapy? Endoscopies? What if they have a complication related to that therapy is that clinically defensible because they might have have had lymphoma brewing?
The proper approach is to identify why the patient has active ongoing disease, are there overlapping or comorbid pathologies ongoing with the sprue?, is your initial presumption mistaken? Is there surreptitious ingestion of offending dietary components? has it deteriorated into a dreaded complication that these patients are at increased risk for? The title of the initial thread is misleading altogether..... If antibody titers are still abnormally elevated, the patient has *not* been successfully treated. A blatant disregard or willful neglect to pursue the accepted satisfactory clinical endpoint for disease control falls short of the standard of care.
 
The proper approach is to identify why the patient has active ongoing disease, are there overlapping or comorbid pathologies ongoing with the sprue?, is your initial presumption mistaken? Is there surreptitious ingestion of offending dietary components? has it deteriorated into a dreaded complication that these patients are at increased risk for? The title of the initial thread is misleading altogether..... If antibody titers are still abnormally elevated, the patient has *not* been successfully treated. A blatant disregard or willful neglect to pursue the accepted satisfactory clinical endpoint for disease control falls short of the standard of care.
So how do I know I dont have any of that? I have no symptoms but I havent had my antibody levels checked either.
 
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The concept of serological activity for autoimmune diseases is very flawed and seems to be a celiac-specific construct. You extrapolate from autoantibodies to T cell responses (unmeasured), to gut inflammation, to risk of consequences of gut inflammation, to worst-case scenarios. All without having proven that making a treatment decision based on autoantibodies leads to reduced risk of the latter. You just postulate it as common sense and claim it is standard of care. It is bad medicine. It's wasteful. You have no established clinical endpoint, you treat to a lab variable that you have convinced yourself is relevant. Almost all rheumatic disease patients in clinical remission still have persistent autoantibodies. Are they serologically active? Should they all be started on cyclophosphamide because they could develop a lymphoma down the line. I mean, sure, but I'm probably going to kill them first due to side effects of my interventions. How about thyroid disease, asymptomatic, normal TSH, but anti-TPO serologically active. Better take out the thyroid? How about your patient with ulcerative colitis that is serologically active? Do you increase immunosuppression? If so, based on what data? Claiming something is "standard of care" is not data. Mercury and leeches used to be standard of care.
 
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So how do I know I dont have any of that? I have no symptoms but I havent had my antibody levels checked either.
You would not know without *screening* for it, screening is recommended for high risk individuals such as those with first degree relatives affected or type 1 diabetes
 
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The concept of serological activity for autoimmune diseases is very flawed and seems to be a celiac-specific construct. You extrapolate from autoantibodies to T cell responses (unmeasured), to gut inflammation, to risk of consequences of gut inflammation, to worst-case scenarios. All without having proven that making a treatment decision based on autoantibodies leads to reduced risk of the latter. You just postulate it as common sense and claim it is standard of care. It is bad medicine. It's wasteful. You have no established clinical endpoint, you treat to a lab variable that you have convinced yourself is relevant. Almost all rheumatic disease patients in clinical remission still have persistent autoantibodies. Are they serologically active? Should they all be started on cyclophosphamide because they could develop a lymphoma down the line. I mean, sure, but I'm probably going to kill them first due to side effects of my interventions. How about thyroid disease, asymptomatic, normal TSH, but anti-TPO serologically active. Better take out the thyroid? How about your patient with ulcerative colitis that is serologically active? Do you increase immunosuppression? If so, based on what data? Claiming something is "standard of care" is not data. Mercury and leeches used to be standard of care.
Yes, the answer to your question concerning titration of medical therapy in inflammatory bowel disease is yes, We use biomarkers that act as surrogates of disease activity as well as documenting histologic as well as endoscopic remission of luminal disease, It is the standard of care and a paradigm in GI medicine called "treat to target", The target you are treating for is the biomarker ( for celiac, antibody titers, UC possibly fecal cal/CRP) or luminal healing such as histology (marsh grade or colon crypt distortion for UC). The reason we treat to these targets is because persons with enteropathy and colopathy can walk around feeling great for many years when internally their gastrointestinal tract appears like a bomb went off inside of them, And they already had unacceptably high risk for the natural history of this unfettered disease activity to become irreversible and have end-stage complications which we work to avoid. This is accomplished by having the disease in adequate remission as indicated by accepted biomarkers such as serology/antibody titers. That is the mark of quality care. The American gastroenterological Association and American College of Gastroenterology unanimously agrees. Advocating for departure from the standard of care does no service to the original poster nor the patient population they wish to serve.
 
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This is a really interesting discussion. The question we are trying to answer is whether regular serologic testing for celiac disease is helpful. There are several ways to look at this.

The first is theoretical -- does it make scientific sense that this would be helpful? In general, testing autoatibodies for levels in autoimmune syndromes is not helpful. RA and SLE, the two "classic" autoimmune diseases are good examples. Although RF/anti-CCP and ANA/Anti-dsDNA might be helpful in diagnosis, they are not helpful to follow disease activity. The example above of CRP for IBD is not relevant - CRP is not an autoantibody and is a direct measure of disease activity. But TTG is celiac is notably different than RF -- we assume RF (and certainly anti-dsDNA) are antibodies to naturally present antigens in the body. TTG on the other hand is an antibody to an external antigen. If that antigen is removed, one would expect that TTG levels would fall, much like antibody titers fall after vaccinations over time. Hence, it does make some theoretical sense that TTG might behave differently than other autoantibodies and might track with disease activity.

The second is practical -- do we have evidence that TTG (or other) antibodies track with disease activity? There is one study with 2000+ patients that suggests that it does: Five year time course of celiac disease serology during gluten free diet: results of a community based "CD-Watch" program - PubMed (nih.gov) But looking at the study closely, it's not so clear. A small group of patients who were very non-compliant with the diet had persistently elevated TTG levels. Those who were better at the diet had a lower rate of TTG positivity, but because there so many more of them they make up the bulk of the positives. And what happens to these patients -- do they have an increased risk of bad outcomes? -- is unclear. There are studies in children showing that TTG levels don't match biopsy findings. So it's very tempting to think that following TTG levels might be helpful, but we have no clear evidence of such.

The third is legal / guidelines. Many GI orgs have published guidelines which suggest following antibody titers. They quote these same studies, and then recommend testing. Sadly, often in cases like this the person pushing for the tests is the one that developed the test and has a patent on it, hence generates income from the recommendation. I have no idea if that's the case here. This becomes hard to defend against in court -- how could you be smarter than the GI experts whom are publishing this? Yet their recommendations seem flawed. Suggesting that "it can't hurt" isn't true -- a patient with negative symptoms but a positive antibody is going to get more testing, if that testing shows they have active disease then they have been helped, but if nothing is found then they have been harmed by additional testing.

Like many other areas of medicine, the guidelines and evidence are a bit of a mess. Given how long we've had TTG testing, one would think that there might be long term follow up data on whether these patients with persistently elevated TTG are actually at higher risk of bad outcomes or not.
 
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Given how long we've had TTG testing, one would think that there might be long term follow up data on whether these patients with persistently elevated TTG are actually at higher risk of bad outcomes or not.

I'm surprised that there isn't. It's very frustrating, both as a student and a teacher of medicine, when we try to teach 'cost conscious care' and 'choosing wisely' and in some instances we blast patients with labs (even if they're asymptomatic), in other cases we don't! "Which is it?! Do you want me to check stuff, or not?!"

I guess that's the "art of medicine" <-- I hate this phrase so much! Medicine is not supposed to be an art. Art is art. Medicine is supposed to be a science. If it looks like art, it's b/c we haven't figured out the science yet and we don't know what we're doing.
 
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Yes, the answer to your question concerning titration of medical therapy in inflammatory bowel disease is yes, We use biomarkers that act as surrogates of disease activity as well as documenting histologic as well as endoscopic remission of luminal disease, It is the standard of care and a paradigm in GI medicine called "treat to target", The target you are treating for is the biomarker ( for celiac, antibody titers, UC possibly fecal cal/CRP) or luminal healing such as histology (marsh grade or colon crypt distortion for UC). The reason we treat to these targets is because persons with enteropathy and colopathy can walk around feeling great for many years when internally their gastrointestinal tract appears like a bomb went off inside of them, And they already had unacceptably high risk for the natural history of this unfettered disease activity to become irreversible and have end-stage complications which we work to avoid. This is accomplished by having the disease in adequate remission as indicated by accepted biomarkers such as serology/antibody titers. That is the mark of quality care. The American gastroenterological Association and American College of Gastroenterology unanimously agrees. Advocating for departure from the standard of care does no service to the original poster nor the patient population they wish to serve.
So it sounds like you're saying the standard of care is to check serologies in a newly remittent patient to confirm that being clinically asymptomatic actually means disease resolution. If serologies are good there is no further immediate investigation. If serologies are abnormal, you would consider further investigation to confirm the absence of disease activity (ie diet review, endoscopy, biopsy, etc.). If further investigation is normal you have confirmed disease remission and if abnormal you would exacerbate treatment. Is that accurate?

That approach would seem analogous to using PSA, CA 19-9, CEA, CA 125, etc. to monitor disease activity vs. a patient's baseline. Using serologies in combination with symptoms to guide potential further investigation seems reasonable even in the absence of significant evidence showing improved clinical outcomes. Using serologies to guide treatment directly does seem unreasonable.

Just trying to learn from this discussion.
 
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So it sounds like you're saying the standard of care is to check serologies in a newly remittent patient to confirm that being clinically asymptomatic actually means disease resolution. If serologies are good there is no further immediate investigation. If serologies are abnormal, you would consider further investigation to confirm the absence of disease activity (ie diet review, endoscopy, biopsy, etc.). If further investigation is normal you have confirmed disease remission and if abnormal you would exacerbate treatment. Is that accurate?

That approach would seem analogous to using PSA, CA 19-9, CEA, CA 125, etc. to monitor disease activity vs. a patient's baseline. Using serologies in combination with symptoms to guide potential further investigation seems reasonable even in the absence of significant evidence showing improved clinical outcomes. Using serologies to guide treatment directly does seem unreasonable.

Just trying to learn from this discussion.

That's my take away, good discussion, it has changed my mind, I shall re-check antibodies (and if we're that concerned, re-biopsying would make more sense than checking Abs . .. at least with histology you get more ground truth).

@Professional Student , as an aside, I'm tripping out over your profile picture and your 'medical student' status. Is that a real picture of you?
 
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That's my take away, good discussion, it has changed my mind, I shall re-check antibodies (and if we're that concerned, re-biopsying would make more sense than checking Abs . .. at least with histology you get more ground truth).

@Professional Student , as an aside, I'm tripping out over your profile picture and your 'medical student' status. Is that a real picture of you?
Nah that's Francis Collins, MD Ph.D., NIH director, author, musician, and all-around cool dude. I highly recommend watching a couple of his songs on youtube.
- "Somewhere Past the Pandemic"
- VCU Graduation Song
 
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So it sounds like you're saying the standard of care is to check serologies in a newly remittent patient to confirm that being clinically asymptomatic actually means disease resolution. If serologies are good there is no further immediate investigation. If serologies are abnormal, you would consider further investigation to confirm the absence of disease activity (ie diet review, endoscopy, biopsy, etc.). If further investigation is normal you have confirmed disease remission and if abnormal you would exacerbate treatment. Is that accurate?

That approach would seem analogous to using PSA, CA 19-9, CEA, CA 125, etc. to monitor disease activity vs. a patient's baseline. Using serologies in combination with symptoms to guide potential further investigation seems reasonable even in the absence of significant evidence showing improved clinical outcomes. Using serologies to guide treatment directly does seem unreasonable.

Just trying to learn from this discussion.
No, that's not accurate, that's incomplete, if patient is asymptomatic, and they have achieved normalized serologies, the standard of care is to demonstrate mucosal healing with histology by Endoscopic sampling.
 
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