Questions Regarding Enterolab Results/gene Test

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I've been reading here quite a bit while impatiently awaiting my Enterolab test results. A year and a half ago, I had a negative blood test and biopsy, but that was after 13 months gluten free with only an 8 day gluten challenge. Since I have a son who is gluten sensitive and I've had digestive issues since I was two months old, I was really interested in the Enterolab tests. I feel better on a gluten free diet, but I still have some inflammation and disgestive issues, and Enterolab seemed like a reliable way to at least be pointed in the right direction to start elimination diets. (Other than gluten -- I've been gluten-free since October 2011 other than my 8 day gluten challenge in November 2012. Gluten is absolutely not an option for me)!


Anyway, my results are below. Here are my questions:


1) The gene stuff is really confusing. Although I understand I don't have the celiac genes, I do have two gluten sensitivity genes. I just get confused by the "DQ8" , "DQ2", DQ1, terms I see on this forum. I know I don't have DQ2 or DQ8, but which DQ do I have? In the end, it probably doesn't matter, but I'd like to know so when I hear people talking about a DQ-whatever, I'll know "Oh that's me!" :)


2) Since I don't have DQ2 or DQ8 genes, I can't be celiac right? Because I have elevated Anti-TTG and some major malabsorbtion going on. I thought that those were celiac things. Especially the Anti-TTG which indicates auto-immune reaction. I had read previously that non-celiac gluten intolerance didn't produce auto-immune reactions, but celiac -- and only celiac -- does produce auto-immune reaction to gluten. I'm probably missing something. 


In addition to gluten, I now have to change my diet to eliminate dairy and egg too. (And also walnut and oats, which I find amusing because I've eaten them maybe five times in my life. I hate them both! Not sure how I have been making antibodies to those). 


Anyway, I'd be interested in any thoughts or answers to these questions. Thanks!


A-2) Gluten/Antigenic Food Sensitivity Stool/Gene Panel

Fecal Anti-gliadin IgA      19 Units   (Normal Range is less than 10 Units)

Fecal Anti-casein (cow’s milk) IgA      12 Units   (Normal Range is less than 10 Units)

Fecal Anti-ovalbumin (chicken egg) IgA      10 Units   (Normal Range is less than 10 Units)

Fecal Anti-soy IgA      7 Units   (Normal Range is less than 10 Units)

HLA-DQB1 Molecular analysis, Allele 1      0303   

HLA-DQB1 Molecular analysis, Allele 2      0603   

Serologic equivalent: HLA-DQ   3,1  (Subtype 9,6)

Anti-TissueTransglutaminase Antibody

Fecal Anti-tissue Transglutaminase IgA      13 Units   (Normal Range is less than 10 Units)

C-1) Antigenic Food Sensitivity Stool Panel

Mean Value 11 Antigenic Foods      7 Units   (Normal Range is less than 10 Units)


Within each class of foods to which you displayed multiple reactions, the hierarchy of those reactions detected were as follows:

Grain toward which you displayed the most immunologic reactivity: Oat

Nut toward which you displayed the most immunologic reactivity: Walnut

Fat Malabsorption Stool Test (Fecal Fat)

Quantitative Microscopic Fecal Fat Score      504 Units   (Normal Range is less than 300 Units)

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Even if you don't have celiac, you could have NCGS. There are no reliable tests for this right now. Partly because they aren't sure exactly what causes NCGS. it looks like it may be several different issues so it isn't likely it is 1 problem./ disease.

If eating gluten free makes you feel better, that is probably what you should do. If another food seems to bother you , try eliminating it, too. Unfortunately, there are no good tests for food intolerances, currently.




"These genes are located on 
the HLA-class II complex and are called 
DQ2 and DQ8. Each case of celiac disease 
has been found to show these so-called 
“haplotypes”; therefore, a negative gene 
test indicates that celiac disease cannot 
develop in that individual."
Can I be screened for non-celiac gluten sensitivity?

There are no tests to diagnose non-celiac gluten sensitivity at this time. Which means, no research has been through a scientific, evidence-based, peer-reviewed study that proves what some labs claim as a way to detect non-celiac gluten sensitivity.

Read more about the fallacy of stool tests to diagnose celiac disease and/or non-celiac gluten sensitivity.



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HLA-DQB1 Molecular analysis, Allele 1      0303   

HLA-DQB1 Molecular analysis, Allele 2      0603   

Serologic equivalent: HLA-DQ   3,1  (Subtype 9,6)



Hi there,


It looks like you have HLA-DQ9 as well as HLA-DQ6. The problem with the enterolab genetic tests is that they are not fully comprehensive as they only look for the beta unit (the B1 part) of a particular gene and not the alpha unit, therefore they cannot be used to determine whether celiac can be ruled out on the basis of genetics. In other words, the beta unit and alpha units tend to correspond (beta DQ9 tends to go with alpha DQ9 so on and so forth..), but that is not always the case: one could have beta DQ9 and alpha DQ8 (DQ8 being a 'celiac gene').


In some studies DQ9 has been found to be associated with celiac in the asian population, but I'm not sure if those studies have been replicated or where they are with it. You might do some googling if you are interested. :)


You are correct that NCGI does not result in an autoimmune reaction (per current knowledge). Unfortunately there is very little known about the role of elevated TTG antibodies in the stool, thus making it hard to draw accurate conclusions from as kareng mentioned above.


Family history can sometimes be helpful in situations where the diagnosis is unclear, particularly if you have other autoimmune diseases or if they run in your family. If you don't care so much about getting the 'right' diagnosis and plan to be 100% gluten free, I'd try eliminating some of those foods and see how you feel. I'd also add a good probiotic if you haven't and maybe think about digestive enzymes. Both of those were tremendously helpful to me along the way!


Best wishes,


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Here's a link to a new study discussing TTG and celiac 



Clin Exp Immunol. 2014 Apr 28. doi: 10.1111/cei.12366. [Epub ahead of print]
In celiac disease intestinal titers of anti-tissue transglutaminase2 antibodies positively correlate with the mucosal damage degree and inversely with the gluten-free diet duration.


Skylark's blog post on the Enterolab tests was one of the more useful things I've read on the topic.




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Thanks for the helpful info, everyone! I am on Day 21 gluten/casein/egg free. I am not feeling much better yet, but I hope to soon. I do have more energy and my "seasonal allergies" have cleared up, but my gut is still pretty messed up. I have switched to gluten-free makeup, shampoos, lotions, etc. I have also eliminated corn for now, as I have the exact same reaction to that as I do to gluten. Honestly, it seems like my gut has gotten worse in the last 3 weeks, so maybe there is an element of "it will get worse before it gets better" in this healing process. For now, I'm following a modified paleo diet and taking probiotics and L-glutamine. Hopefully I'm on the road to recovery!

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I can't say whether Enterolab is going to benefit those with easily diagnosed Celiac Disease...the people that are nearly dying from the symptoms.

Dr. Fine does not seem to be interested in the work that already tests for the A panel of the gene markers for Celiac, or the blood work/endoscopic procedures for determining damage on Celiac Patients. He's is testing for everything that the other doctors are not testing for, or won't test for.

From his own statements, Dr. Fine M.D. is discerning from his tests not the absolute guarantee of Celiac Disease such tests render to only 30% of those tested, but what is making a person feel rotten long before permanent damage is done, in the hope of arresting, or minimizing whatever situation is causing the problem.

As for his credentials...he does not appear to be some medtech scammer out to make all that he can get off the unsuspecting patient who has never been diagnosed with any problems until they get hit with Gluten touchiness.

Dr.Fine owns a Health/Nutrition place, EnteroLab, and has a 501C research facility...which argues for maximising his discoveries.

On the other hand, I've spent 42 years with doctors already that don't what they are doing, but my doctors own the new Hospital I must go to as well as a their own Sports Injury Rehab Center, so I figure that is how Doctors really make money.  They don't get paid much by Insurance Companies these days.

Enterolab will test what I want them to test, rather than tell me to go, and "get used to it.  There is nothing else I can do for you." That was a direct quote from one of my doctors.

EnteroLab is testing for everything that is an immune problem indicator, and all of that for only $1,047.00,
Including Crohn's Disease. That seems cheap to me, after so many years.  My niece had to pay for an extended visit to Mayo Clinic to be diagnosed...I think she still owes them about $24,000.00

I already have two immune system problems, but I don't think it matters all that much to my doctors, especially since it take 17 years for a new discovery to be generally talked about in medical circles, and mine aren't even aware that my symptoms might not be IBS. They accept what the last doctor has said as a given, and then pat me on head as if I were a kindergarten student.

Please don't rule out a test for indicators as the first step towards a diagnosis after your doctors have said there is nothing wrong with you.  And for the other Gene test, there is CyrexLab...who does a complete gluten blood panel, and full gene test, for about $250.00.

At that point you will know enough to get the doctors to do the right things.

Dr. Kenneth Fine

    Medical Director and Director of Operations
    EnteroLab Reference Laboratory Owned by Dr. FIne

    Director of Operations and Director of Medical Research
    Intestinal Health Institute  501C

    Director of Operations and Chief Consultant
    FinerHealth and Nutrition  Owned by Dr. FIne

    Attending Physician and Staff Gastroenterologist
    Department of Internal Medicine, Division of Gastroenterology
    Baylor University Medical Center, Dallas 1992-2002

    Medical Director, Gastrointestinal Physiology Laboratory
    Baylor University Medical Center, Dallas 1996-1999

    Staff Researcher, Division of GI Research
    Baylor University Medical Center, Dallas 1992-2000

    Attending Physician, Staff Gastroenterologist
    Dallas VA Medical Center 1992-1998

    Clinical Assistant Professor
    University of Texas-Southwestern Medical School       1992-2000

    University of Missouri - Kansas City
    Degree: B.A. - Biology

    University of Missouri - Kansas City, School of Medicine
    Degree: M.D.

    Internal Medicine Internship And Residency: 7/1/86 - 6/30/89
    Baylor University Medical Center, Dallas
    Gastroenterology - Research And Clinical Fellowship: 7/1/89 - 6/30/92
    Baylor University Medical Center, Dallas


        Issued - August 1986


        Issued - July 1987

    National Board of Medical Examiners

        Part I 1983
        Part II 1985

    Federal Licensure Examination 1987

    Texas Medical Jurisprudence Exam 1987

    American Board of Internal Medicine

        Internal Medicine 1989
        Gastroenterology 1993

    1990 Biomedical Research Support Grant - National Institutes of Health
    1994 Smith Kline Beecham Clinical Research Award -
    American Gastroenterological Association Foundation
    1997 National Institutes of Health RO3 - Treatment of Microscopic Colitis

    Peptide Therapy: Index and Reviews 1997 - present

    Baylor University Medical Center Proceedings 1996 - 2000

    Religious Singing for Local Synagogues 1993-present

    Medical Advisor to Local CSA Celiac Sprue Support Group 1994-present

    Email correspondence with online Microscopic Colitis Newsletter Support Group 1999-present

    Organized and run a neighborhood organic produce co-op 2000-present



    Zarabi CM, Huntrakoon M, Fine KD. Disseminated rhabdomyosarcoma of the urinary bladder in an adult. Southern Med J 1987;80:526-529.
    Fine KD. Arthritis in the elderly, is it degenerative or rheumatoid? Baylor University Medical Center Proc 1988;1:25-34.
    Hammer HF, Fine KD, Santa Ana CA, Porter JL, Schiller LR, Fordtran JS. Carbohydrate malabsorption. Its measurement and its contribution to diarrhea. J Clin Invest 1990;86:1936-1944.
    Fine KD. Benzodiazepine withdrawal. Baylor University Medical Center Proc 1991;4:27-30.
    Fine KD, Santa Ana CA, Fordtran JS. Diagnosis of magnesium-induced diarrhea. N Engl J Med 1991;324:1012-1017.
    Fine KD, Santa Ana CA, Porter JL, Fordtran JS. Intestinal absorption of magnesium from food and supplements. J Clin Invest 1991;88:396-402.
    Fine KD, Fordtran JS. The effect of diarrhea on fecal fat excretion. Gastroenterology 1992;102:1936-1939.
    Fine KD, Santa Ana CA, Porter JL, Fordtran JS. Effect of D-glucose on intestinal permeability and its passive absorption in the human small intestine in vivo. Gastroenterology 1993;105:1117-1125.
    Fine KD, Santa Ana CA, Porter JL, Fordtran JS. Mechanism by which glucose stimulates the passive absorption of small solutes by the human jejunum in vivo. Gastroenterology 1994;107:389-395.
    Emmett M, Hootkins RE, Fine KD, Santa Ana CA, Porter JS, Fordtran JS. Effect of three laxatives and a cation exchange resin on fecal sodium and potassium excretion. Gastroenterology 1995;108:752-760.
    Fine KD, Solano M, Polter DE, Tillery GW. Malignant histiocytosis in a patient with hepatic dysfunction and peliosis hepatis. Am J Gastroenterol 1995;90:485-488.
    Fine KD, Santa Ana CA, Porter JL, Fordtran JS. Effect of changing intestinal flow rate on a measurement of intestinal permeability. Gastroenterology 1995;108:983-989.
    Wenzl HH, Fine KD, Schiller LR, Fordtran JS. Determinants of decreased fecal consistency in diarrhea. Gastroenterology 1995;108:1729-1738.
    Fine KD. The prevalence of occult gastrointestinal bleeding in celiac sprue. N Engl J Med 1996;334:1163-1167.
    Wenzl HH, Fine KD, Santa Ana CA, Porter JL, Fordtran JS. Effect of fludrocortisone and spironolactone on sodium and potassium losses in secretory diarrhea. Dig Dis Sci 1997;42:119-128.
    Fine KD, Byrd TD, Stone MJ. Successful treatment of chronic severe neutropenia with weekly granulocyte-colony stimulating factor. Br J Haematol 1997; 97:175-178.
    Fine KD, Meyer RL, Lee EL. The prevalence and causes of chronic diarrhea in treated celiac sprue. Gastroenterology 1997; 112:1830-1837.
    Fine KD, Lee EL. Efficacy of open-label bismuth subsalicylate for the treatment of microscopic colitis. Gastroenterology. 1998; 114:29-36.
    Fine KD, Sarles HE, Cryer, B. Investigation of diarrhea caused by mesalamine in a patient with chronic non-granulomatous enterocolitis. N Engl J Med. 1998;338:923-925.
    Fine KD, Ogunji F, George J, Niehaus MD, Guerrant RL. Utility of a rapid fecal latex agglutination test detecting the neutrophil protein, lactoferrin, for diagnosing inflammatory causes of chronic diarrhea. Am J Gastroenterol 1998;93:1300-1305.
    Gruy-Kapral C, Emmett M, Santa Ana CA, Porter JL, Fordtran JS, Fine KD. Evaluation of cathartic-resin therapy for management of hyperkalemia. J Am Soc Nephrol 1998;9:1924-1930.
    Fine KD, Meyer R, Lee EL. Colonic histopathology in untreated celiac sprue and refractory sprue: Is it lymphocytic colitis or colonic lymphocytosis? Human Pathology 1998;29:1433-1440.
    Fine KD, Ogunji F, Florio R, Porter J, Santa Ana C. Investigation and diagnosis of diarrhea caused by sodium phosphate. Dig Dis Sci 1998;43:2708-2714.
    Fine KD, Schiller LR. AGA technical review on the evaluation and management of chronic diarrhea. Gastroenterology 1999;116:1464-1486.
    Fine KD, Stone MJ. Alpha-heavy chain disease, mediterranean lymphoma, and immunoproliferative small intestinal disease:a review of clinicopathologic features, pathogenesis, and differential diagnosis. Am J Gastroenterol 1999;94:1139-1152.
    Fine KD, Nelson AC, Mossburg A, Ellington RT. Comparison of the color of fecal blood with the anatomical location of gastrointestinal bleeding lesions: potential misdiagnosis using only flexible sigmoidoscopy for bright red blood per rectum. Am J Gastroenterol. 1999;94:3202-3210.
    Fine KD, Seidel RH, Do K. The prevalence, anatomic distribution, and diagnosis of colonic causes of chronic diarrhea. Gastrointest Endosc. 2000;51:318-326.
    Fine KD, Ogunji F. A New Method of Quantitative Fecal Fat Microscopy and its Correlation with Chemically Measured Fecal Fat Output. Am J Clin Pathol. 2000;113:528-534.
    Fine K, Lafon G, Ogunji F, Do K, Schulte K, Osowski L, McCormack J, Guerra R. High Prevalence of Celiac Sprue-Like HLA-DQ Genes and Enteropathy in Patients with the Microscopic Colitis Syndrome. Am J Gastroenterol 2000;95:1974-1982.
    Fine KD, Ogunji F, Saloum YA, Beharry S, Crippin JS, Weinstein JS. Celiac Sprue: Another Autoimmune Syndrome Associated with Hepatitis C. Am J Gastroenterol 2001;96:138-145.


    Fine KD, Krejs GJ, Fordtran JS. Diarrhea, Chapter 20 in Sleisenger MH, Fordtran JS. Gastrointestinal Disease. Pathophysiology, Diagnosis, Management, 4th Edition. Philadelphia, W. B. Saunders Co., 1989.
    Fine KD, Krejs GJ, Fordtran JS. Diarrhea, Chapter 49 in Sleisenger MH, Fordtran JS. Gastrointestinal Disease. Pathophysiology, Diagnosis, Management, 5th Edition. Philadelphia, W.B. Saunders Co., 1993.
    Fine KD, Schiller LR. Diarrhea. In: Consultations in Gastroenterology. Snape W Jr, ed. Philadelphia, W.B. Saunders Co. 1996.
    Fine KD. Diarrhea, Chapter 10 in Feldman M, Scharschmidt BF, Sleisenger MH. Gastrointestinal Disease. 6th Edition. Philadelphia, W.B. Saunders Co., 1998.


    Fine KD, Santa Ana CA, Porter JL, Schiller LR, Fordtran JS. Evaluation of passive glucose absorption in the human jejunum in vivo. Gastroenterology 1991;100:A685(Abstr).
    Brandabur JJ, Fine KD, Loeb PM, Miranda S, McCarthy JH. Pancreaticoduodenectomy - better results than expected. Gastroenterology 1991; 100:A352(Abstr).
    Fine KD and Lee EL. An Open Label Trial of Bismuth Subsalicylate for the Treatment of Microscopic Colitis. Gastroentrology 1997; 112: A362 (Abstr).
    Fine K, Ogunji F, Lee E, Lafon G, Tanzi M. Randomized, Double-Blind, Placebo-Controlled Trial of Bismuth Subsalicylate for Microscopic Colitis. 1999; 116: A880 (Abstr).
    Fine K, Lafon G, Ogunji F, Do K, Schulte K, Osowski L, McCormack J, Guerra R. The Genetic and Histopathologic Relationship of Microscopic Colitis and Celiac Sprue or Refractory Sprue. 1999; 116: A879 (Abstr).
    Fine KD, Ogunji FO, Saloum YA, Beharry SL, Crippin JS, Weinstein JW. Celiac Sprue: Another Autoimmune Syndrome Associated with Hepatitis C. Gastroenterology 2000;118:A697 (Abstr).


    Fordtran JS, Fine KD. Sodium-glucose cotransport and epithelial permeability. Gastroenterology 1994;107:319-324.
    Fine KD. Occult gastrointestinal bleeding in celiac sprue. N Engl J Med 1996;335:752-753.
    Fine KD. Chronic diarrhea in treated celiacs: Are they really celiacs? Gastroenterology 1998;114:420-421.
    Fine KD. Microscopic and collagenous colitis in treated celiac disease due to food allergy? Gastroenterology 1999;116:778.
    Fine KD. Colonoscopy and Chronic Diarrhea. Gastrointestinal Endoscopy 2000;52:589-590.


    Small Bowel Enteropathy in Patients with Microscopic Colitis: Is It Gluten-Sensitive? J Clin Gastroenterol 2001;32:193-195.

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    The team divided the TCR-GR patterns into clonal, polyclonal and prominent clonal peaks (PCPs), and correlated these patterns with clinical and pathological features. In all, they detected clonal TCR-GR products in biopsies from 67% of patients with RCDII, 17% of patients with RCDI and 6% of patients with gluten-free diet. They found PCPs in all disease phases, but saw no significant difference in the TCR-GR patterns between the non-RCDII disease categories (p=0.39). 
    They also noted a higher frequency of surface CD3(−) IELs in cases with clonal TCR-GR, but the PCP pattern showed no associations with any clinical or pathological feature. 
    Repeat biopsy showed that the clonal or PCP pattern persisted for up to 2 years with no evidence of RCDII. The study indicates that better understanding of clonal T cell receptor gene rearrangements may help researchers improve refractory celiac diagnosis. 
    Journal of Clinical Pathologyhttp://dx.doi.org/10.1136/jclinpath-2018-205023

    Jefferson Adams
    Celiac.com 06/13/2018 - There have been numerous reports that olmesartan, aka Benicar, seems to trigger sprue‐like enteropathy in many patients, but so far, studies have produced mixed results, and there really hasn’t been a rigorous study of the issue. A team of researchers recently set out to assess whether olmesartan is associated with a higher rate of enteropathy compared with other angiotensin II receptor blockers (ARBs).
    The research team included Y.‐H. Dong; Y. Jin; TN Tsacogianis; M He; PH Hsieh; and JJ Gagne. They are variously affiliated with the Division of Pharmacoepidemiology and Pharmacoeconomics, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School in Boston, MA, USA; the Faculty of Pharmacy, School of Pharmaceutical Science at National Yang‐Ming University in Taipei, Taiwan; and the Department of Hepato‐Gastroenterology, Chi Mei Medical Center in Tainan, Taiwan.
    To get solid data on the issue, the team conducted a cohort study among ARB initiators in 5 US claims databases covering numerous health insurers. They used Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for enteropathy‐related outcomes, including celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy. In all, they found nearly two million eligible patients. 
    They then assessed those patients and compared the results for olmesartan initiators to initiators of other ARBs after propensity score (PS) matching. They found unadjusted incidence rates of 0.82, 1.41, 1.66 and 29.20 per 1,000 person‐years for celiac disease, malabsorption, concomitant diagnoses of diarrhea and weight loss, and non‐infectious enteropathy respectively. 
    After PS matching comparing olmesartan to other ARBs, hazard ratios were 1.21 (95% CI, 1.05‐1.40), 1.00 (95% CI, 0.88‐1.13), 1.22 (95% CI, 1.10‐1.36) and 1.04 (95% CI, 1.01‐1.07) for each outcome. Patients aged 65 years and older showed greater hazard ratios for celiac disease, as did patients receiving treatment for more than 1 year, and patients receiving higher cumulative olmesartan doses.
    This is the first comprehensive multi‐database study to document a higher rate of enteropathy in olmesartan initiators as compared to initiators of other ARBs, though absolute rates were low for both groups.
    Alimentary Pharmacology & Therapeutics

    Jefferson Adams
    Celiac.com 06/12/2018 - A life-long gluten-free diet is the only proven treatment for celiac disease. However, current methods for assessing gluten-free diet compliance are lack the sensitivity to detect occasional dietary transgressions that may cause gut mucosal damage. So, basically, there’s currently no good way to tell if celiac patients are suffering gut damage from low-level gluten contamination.
    A team of researchers recently set out to develop a method to determine gluten intake and monitor gluten-free dietary compliance in patients with celiac disease, and to determine its correlation with mucosal damage. The research team included ML Moreno, Á Cebolla, A Muñoz-Suano, C Carrillo-Carrion, I Comino, Á Pizarro, F León, A Rodríguez-Herrera, and C Sousa. They are variously affiliated with Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Sevilla, Spain; Biomedal S.L., Sevilla, Spain; Unidad Clínica de Aparato Digestivo, Hospital Universitario Virgen del Rocío, Sevilla, Spain; Celimmune, Bethesda, Maryland, USA; and the Unidad de Gastroenterología y Nutrición, Instituto Hispalense de Pediatría, Sevilla, Spain.
    For their study, the team collected urine samples from 76 healthy subjects and 58 patients with celiac disease subjected to different gluten dietary conditions. To quantify gluten immunogenic peptides in solid-phase extracted urines, the team used a lateral flow test (LFT) with the highly sensitive and specific G12 monoclonal antibody for the most dominant GIPs and an LFT reader. 
    They detected GIPs in concentrated urines from healthy individuals previously subjected to gluten-free diet as early as 4-6 h after single gluten intake, and for 1-2 days afterward. The urine test showed gluten ingestion in about 50% of patients. Biopsy analysis showed that nearly 9 out of 10 celiac patients with no villous atrophy had no detectable GIP in urine, while all patients with quantifiable GIP in urine showed signs of gut damage.
    The ability to use GIP in urine to reveal gluten consumption will likely help lead to new and non-invasive methods for monitoring gluten-free diet compliance. The test is sensitive, specific and simple enough for clinical monitoring of celiac patients, as well as for basic and clinical research applications including drug development.
    Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.