2 2
jebby

Cow's Milk Protein Intolerance In Infants Of Mothers With Celiac?

Rate this topic

Recommended Posts

I am a pediatrician and I take care of predominantly newborn infants. I have been seeing more and more infants with cow's milk protein allergies/intolerances over the last 5 years than in the past. I am interested in this diagnosis because two of my four kids had issues with milk protein as infants (before I was diagnosed and gluten free). I have been unable to find any research linking cow's milk protein problems in babies with maternal celiac disease. I suspect that the 2 problems are linked and am considering doing a research study on this. In my case, my babies reacted to milk protein which passed into my breastmilk. Have any of you mothers on here had babies who do not tolerate cow's milk protein? Please message me if you can. If there are enough of us, then it will tip me toward trying to examine this scientifically.

Thank you!

Jess

Share this post


Link to post
Share on other sites
Ads by Google:
Ads by Google:


Investigate, please!!!

My son had bad colic and always had a bad reaction to formula. I did mixed feeding, breast and formula. He hated cows milk. He now eats yogurt and ice cream but no milk or cheese.

He now has asthma eczema hayfever and severe nut allergy, all classic atopic stuff.

When I was pregnant with my daughter, a colleague who specializes in nutrition suggested I avoid cows milk and products and had goat. She has no problems so far at 3.

Can't prove anything, not scientific. But I am glad I did the experiment.

I am going through celiac diagnosis.

This is a bit to the side of your question, but so many things are interrelated.

I wish there were more doctors like you who notice these things.

Good luck

Share this post


Link to post
Share on other sites

Definitely! I was un diagnosed at the time, but had celiac since childhood. With my first baby, she would scream after every nursing, I finally narrowed it down to my eating dairy. When I avoided it, she was fine. She is 13 now, also celiac, and reacts to casein with eczema, edema, fatigue and ADHD/OCD behaviors. My son also reacted to dairy as a baby, was dx with reflux, would scream in agony with every bowel movement even though he was breastfed. I was told he just had a small colon. He developed severe suicidal depression by the age of 6, as well as ADHD, sensory processing disorder and peripheral neuropathy. He was also anemic and pre-diabetic. Dx as celliac at age 7. gluten-free diet helped some. Removing all trace casein resulted in complete reversal of all symptoms. He is a happy healthy 9 yr old now. If he gets even small amounts of casein he reacts with violent mood swings and crying.

I definitely think there is a connection, and really wish someone would do serious research into it to spare others!

Share this post


Link to post
Share on other sites

FWIW, I'm gluten-intolerant (I went gluten free prior to testing, which was inconclusive, so I'm not really diagnosable :) ), and my daughter doesn't appear to have a problem with cow milk.

That said, I *do* have trouble with cow milk, and stayed completely dairy free during pregnancy and for many months afterwards, and then added small quantities of goat milk. So she didn't have any exposure to cow milk protein for the first many months of her life. She did get regular yogurt starting at 7 or 8 months, though, and loved it and didn't have any trouble. She still prefers to drink my almond or coconut milk, and doesn't really like fluid cow milk, despite liking other cow dairy products (cheese, yogurt, ice cream).

Share this post


Link to post
Share on other sites

My son is strongly casein-intolerant (and likely celiac, though undiagnosed) and I was undiagnosed celiac when pregnant. He was always fussy as a baby and never felt "well" as a child, but we didn't isolate his reaction to cow's milk protein until he was 15.

I'm glad you're interested in that type of research - very helpful. I'm trying to get my son (who wants to be an MD) to go into celiac or genetic research.

Share this post


Link to post
Share on other sites
Ads by Google:


My birth mother (deceased) had a "problem with wheat" according to my dad. Whether Celiac or NCGI we'll never know. I went gluten-free before testing and then could not take on a gluten challenge due to my reaction to gluten when ingested; that was all the test I needed. However I had the genetic testing done and came back double DQ7 (one from each parent), which is associated with cow's milk intolerance. Indeed, dairy is harder on me in the short term than gluten. Exploring the possible connection between a mother's Celiac and child's casein intolerance would be fascinating and valuable research!

Share this post


Link to post
Share on other sites

I was an undiagnosed celiac until I was 38 so I was eating gluten while pg with my children. My oldest son, we are just now starting to realize, seems to have a problem with milk. He told me he sometimes gets stomachaches after drinking milk, and often gets headaches.

He has a few other health problems which has prompted me to start him gluten-free even though he tested negative. My concerns and past problems:

Colicky breast fed baby (cried about 3-6 hours an evening)

Aspergers (did not complete diagnostic process since we homeschool and there would be no benefit to further testing - it is mild)

Allergies (tree nuts and environmetal)

Asthma (mild)

Minor GI issues (infrequent stomaches and C)

Headaches (infrequent)

I plan to remove milk products from his diet this fall. I'll do it slowly since he does not do well with change and has a fairly limit palet.

Share this post


Link to post
Share on other sites

Thanks for all of your replies! I will press forward with this project in some form and will hopefully eventually be able to report back on what I find in the future.

Share this post


Link to post
Share on other sites

I would love to know if there is any connection. My son is now 3 and I breastfed for 2.5 years. I could not have even the smallest amount of dairy or soy for the 1st year and a half of his lift. He has intestinal bleeding at 2 weeks and I found out after that about his intolerance. After i cut out the dairy from my diet is when i started have a lot of stomach issues and went through numerous test to be diagnosed celiacs. I was tested the first time 2 .5 years ago but my blood tests were inclusive because of an iga deficiency and my doctor said it wasn't a wheat issue but IBS. I the past 6 months I've had many health issues and finally a new doctor realized the iga deficiency caused the wrong blood test results and I was diagnosed a week ago. My son now has no issues with dairy or soy but I always knew dairy wasn't the best thing for me but still ate it. I am worried for him in the future and would love to know any correlation.

Share this post


Link to post
Share on other sites

I've been looking for research on the topic. My son has been suffering with GERD and Milk Soy Protein Intolerance (MSPI) since birth, now 12 months of age. I didn't realize I was suffering with celiac disease until after he was born and my symptoms went into over drive. I am interested if anyone has found any information on the topic?

Share this post


Link to post
Share on other sites


Ads by Google:


I realize this thread is months old, but I just found it and wanted to add something in case anyone reads it later. I'm a 37-year-old woman in the process of getting tested for celiac myself, after having symptoms consistent with celiac for my whole life. After three years of fertility treatments, I finally conceived my daughter through IVF when I was 32. I strongly suspect that I had very active, undiagnosed celiac during pregnancy and birth. My daughter was born just over 4 weeks early after a 30-hour labor with complications, and she almost died at birth. A wonderful team of nurses and doctors saved her life, and I am immensely grateful to them.

 

I had intense morning sickness for the first six months of the pregnancy, and consequently I ate almost nothing but soup and yogurt. In retrospect, this is probably the best thing that could have happened, since my gluten-consumption was very low due to the solid-food aversions. I exclusively breastfed my daughter, but the very day my milk came in she screamed uncontrollably for hours and hours. She was a good nurser and gained weight just fine, but she was constantly irritable, started projectile vomiting within her first month (but did not have pyloric stenosis), and had extreme sleep problems where she twitched and kicked constantly and never, ever slept more than 45 minutes at a time. It became clear within the first few months that she couldn't tolerate breastmilk when I ate any dairy at all, so I eliminated it completely. Her problems improved slightly but did not go away. By 5 1/2 months we'd seen an allergist, pediatric GI doctor, and neurologist because she also had muscle clenching, reflex abnormalities, and other signs of possible CP.

 

No one had any idea what was going on. Allergy tests were negative, though they're unreliable in babies so young (but they remained negative two years later, too). We eventually put her on Neocate formula and I stopped breastfeeding. She'd still had no solids at all. She could not tolerate Alimentum (hypo-allergenic but milk-based), but her response to Neocate was amazing. Within 36 hours, she was like a new baby! She thrived on Neocate, and within six months her neurological problems had improved enough that she tested out of early intervention and the neurologist concluded that she didn't have CP. We started solids late because she gagged and refused them until she was almost a year old, but when she finally started eating solids regularly things started going downhill again. For the last three years she's had daily stomach pains, increasing irritability and tantrums (that kept worsening even after the "terrible twos" were over), fatigue, and other celiac symtpoms. And she's never been able to handle dairy well, though we sometimes give her very small amounts. (She only drinks fortified rice milk and water.) We're seeing a new doctor next week because her old doctor wouldn't take our concerns seriously. I'm going to insist that they test her for celiac.

 

Regardless of how the tests turn out, my point is that it definitely IS possible for infants to develop food sensitivities through breastmilk alone. We had so many doctors insist that it wasn't possible, but no one could deny the evidence of my daughter's immediate improvement on Neocate. I don't know whether she was reacting to gluten in my diet, or reacting to remaining traces of dairy even after I'd stopped eating it, or whether she was simply reacting to antibodies that I was producing because of my own undiagnosed digestive problems. But please do research this issue! As a parent, it's very frustrating to be constantly told that babies can't develop allergies or food intolerances through breastmilk alone. It's a misconception that needs to be disproven once and for all!

Share this post


Link to post
Share on other sites

I realise those thread is many years old but would like to know if you did research this further?

i am a coeliac mother of two boys, my eldest is 3 and has a cows milk protein allergy that manifested itself as silent reflux and constipation and took 2years to diagnose and my 3month old son has chronic nasal congestion that I believe may be due to a cows milk allergy but am in the process of getting him diagnosed.

while pregnant with both I had a couple of inadvertent episodes when I ate some gluten when out for a meal and have always wondered if that autoimmune reaction could trigger the unborn child to develop an allergy.

i would love to find more research into this topic so if there have been any developments since this thread was posted I would be very interested in hearing about it.

thanks,

claire

 

Share this post


Link to post
Share on other sites
3 hours ago, Coups said:

I realise those thread is many years old but would like to know if you did research this further?

i am a coeliac mother of two boys, my eldest is 3 and has a cows milk protein allergy that manifested itself as silent reflux and constipation and took 2years to diagnose and my 3month old son has chronic nasal congestion that I believe may be due to a cows milk allergy but am in the process of getting him diagnosed.

while pregnant with both I had a couple of inadvertent episodes when I ate some gluten when out for a meal and have always wondered if that autoimmune reaction could trigger the unborn child to develop an allergy.

i would love to find more research into this topic so if there have been any developments since this thread was posted I would be very interested in hearing about it.

thanks,

claire

 

Some of these members have not been around for a while.  You can check out Jebby’s blog site.  She is a Neonatologist and also has celiac disease.  Her website might have some current information on this topic.  

http://www.jessicamaddenmd.com/

 

Share this post


Link to post
Share on other sites

Hi Claire,

I haven't been on these boards much lately, but I just happened to see your message and wanted to follow up on my original post above (from 2013). 

My daughter was indeed diagnosed with celiac a couple weeks after that post, right around her fourth birthday. She had high positives for every test on the panel, and the diagnosis was confirmed by biopsy. It took quite a while for her tTG to completely normalize, but she's been doing great for the past few years. I have no doubt whatsoever that she would have diagnosed much sooner if anyone had tested her. (I also ended up with an official celiac diagnosis from a GI myself, although my case was less clear-cut and involved a miserable gluten challenge.)

The interesting development now is that my daughter's tTG started to rise again last year. It had been a very low negative for two years, then rose steadily until it was just below the positive level again. She also started getting mouth sores and tiny bumps on the back of her arms again, which had gone away shortly after her diagnosis. We never eat out, have little processed food, make sure that all grain products are from a dedicated gluten-free facility, and check all toiletries too. I was baffled once again. And I felt fine myself, so I didn't think that we'd had any contaminated food.

The only major change had been that my daughter had started putting milk in her cereal! She'd always preferred it dry before, and was eating the same cereal that she'd been tolerating fine for years. She is not lactose intolerant and doesn't really have digestive symptoms from milk, but it has always made her incredibly irritable so she never got in the habit of drinking milk or eating much dairy. We do have cheese a couple times a week, and I never worried about small amounts of dairy in baked goods and whatnot, but she didn't typically have dairy on a daily basis until last year. 

Then I found this recent article on PubMed, about cow's milk raising tTG in some celiacs:

https://www.ncbi.nlm.nih.gov/pubmed/29555204

I know this isn't quite what you were asking about, but I found it fascinating. My daughter stopped having milk in cereal a few weeks ago, and her mouth sores and arm bumps went away again. She has a tTG test schedule for next month. If milk is the culprit, I'd expect it be headed downward again by then. Anyhow, I was thrilled to see research on this, and I hope there will be more info coming along about non-lactose-intolerance milk-related problems in celiacs soon!

  • Upvote 1

Share this post


Link to post
Share on other sites

Create an account or sign in to comment

You need to be a member in order to leave a comment

Create an account

Sign up for a new account in our community. It's easy!

Register a new account

Sign in

Already have an account? Sign in here.

Sign In Now
2 2

  • Who's Online   19 Members, 1 Anonymous, 967 Guests (See full list)

  • Top Posters +

  • Recent Articles

    Jefferson Adams
    Celiac.com 06/16/2018 - Summer is the time for chips and salsa. This fresh salsa recipe relies on cabbage, yes, cabbage, as a secret ingredient. The cabbage brings a delicious flavor and helps the salsa hold together nicely for scooping with your favorite chips. The result is a fresh, tasty salsa that goes great with guacamole.
    Ingredients:
    3 cups ripe fresh tomatoes, diced 1 cup shredded green cabbage ½ cup diced yellow onion ¼ cup chopped fresh cilantro 1 jalapeno, seeded 1 Serrano pepper, seeded 2 tablespoons lemon juice 2 tablespoons red wine vinegar 2 garlic cloves, minced salt to taste black pepper, to taste Directions:
    Purée all ingredients together in a blender.
    Cover and refrigerate for at least 1 hour. 
    Adjust seasoning with salt and pepper, as desired. 
    Serve is a bowl with tortilla chips and guacamole.

    Dr. Ron Hoggan, Ed.D.
    Celiac.com 06/15/2018 - There seems to be widespread agreement in the published medical research reports that stuttering is driven by abnormalities in the brain. Sometimes these are the result of brain injuries resulting from a stroke. Other types of brain injuries can also result in stuttering. Patients with Parkinson’s disease who were treated with stimulation of the subthalamic nucleus, an area of the brain that regulates some motor functions, experienced a return or worsening of stuttering that improved when the stimulation was turned off (1). Similarly, stroke has also been reported in association with acquired stuttering (2). While there are some reports of psychological mechanisms underlying stuttering, a majority of reports seem to favor altered brain morphology and/or function as the root of stuttering (3). Reports of structural differences between the brain hemispheres that are absent in those who do not stutter are also common (4). About 5% of children stutter, beginning sometime around age 3, during the phase of speech acquisition. However, about 75% of these cases resolve without intervention, before reaching their teens (5). Some cases of aphasia, a loss of speech production or understanding, have been reported in association with damage or changes to one or more of the language centers of the brain (6). Stuttering may sometimes arise from changes or damage to these same language centers (7). Thus, many stutterers have abnormalities in the same regions of the brain similar to those seen in aphasia.
    So how, you may ask, is all this related to gluten? As a starting point, one report from the medical literature identifies a patient who developed aphasia after admission for severe diarrhea. By the time celiac disease was diagnosed, he had completely lost his faculty of speech. However, his speech and normal bowel function gradually returned after beginning a gluten free diet (8). This finding was so controversial at the time of publication (1988) that the authors chose to remain anonymous. Nonetheless, it is a valuable clue that suggests gluten as a factor in compromised speech production. At about the same time (late 1980’s) reports of connections between untreated celiac disease and seizures/epilepsy were emerging in the medical literature (9).
    With the advent of the Internet a whole new field of anecdotal information was emerging, connecting a variety of neurological symptoms to celiac disease. While many medical practitioners and researchers were casting aspersions on these assertions, a select few chose to explore such claims using scientific research designs and methods. While connections between stuttering and gluten consumption seem to have been overlooked by the medical research community, there is a rich literature on the Internet that cries out for more structured investigation of this connection. Conversely, perhaps a publication bias of the peer review process excludes work that explores this connection.
    Whatever the reason that stuttering has not been reported in the medical literature in association with gluten ingestion, a number of personal disclosures and comments suggesting a connection between gluten and stuttering can be found on the Internet. Abid Hussain, in an article about food allergy and stuttering said: “The most common food allergy prevalent in stutterers is that of gluten which has been found to aggravate the stutter” (10). Similarly, Craig Forsythe posted an article that includes five cases of self-reporting individuals who believe that their stuttering is or was connected to gluten, one of whom also experiences stuttering from foods containing yeast (11). The same site contains one report of a stutterer who has had no relief despite following a gluten free diet for 20 years (11). Another stutterer, Jay88, reports the complete disappearance of her/his stammer on a gluten free diet (12). Doubtless there are many more such anecdotes to be found on the Internet* but we have to question them, exercising more skepticism than we might when reading similar claims in a peer reviewed scientific or medical journal.
    There are many reports in such journals connecting brain and neurological ailments with gluten, so it is not much of a stretch, on that basis alone, to suspect that stuttering may be a symptom of the gluten syndrome. Rodney Ford has even characterized celiac disease as an ailment that may begin through gluten-induced neurological damage (13) and Marios Hadjivassiliou and his group of neurologists and neurological investigators have devoted considerable time and effort to research that reveals gluten as an important factor in a majority of neurological diseases of unknown origin (14) which, as I have pointed out previously, includes most neurological ailments.
    My own experience with stuttering is limited. I stuttered as a child when I became nervous, upset, or self-conscious. Although I have been gluten free for many years, I haven’t noticed any impact on my inclination to stutter when upset. I don’t know if they are related, but I have also had challenges with speaking when distressed and I have noticed a substantial improvement in this area since removing gluten from my diet. Nonetheless, I have long wondered if there is a connection between gluten consumption and stuttering. Having done the research for this article, I would now encourage stutterers to try a gluten free diet for six months to see if it will reduce or eliminate their stutter. Meanwhile, I hope that some investigator out there will research this matter, publish her findings, and start the ball rolling toward getting some definitive answers to this question.
    Sources:
    1. Toft M, Dietrichs E. Aggravated stuttering following subthalamic deep brain stimulation in Parkinson’s disease--two cases. BMC Neurol. 2011 Apr 8;11:44.
    2. Tani T, Sakai Y. Stuttering after right cerebellar infarction: a case study. J Fluency Disord. 2010 Jun;35(2):141-5. Epub 2010 Mar 15.
    3. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    4. Jäncke L, Hänggi J, Steinmetz H. Morphological brain differences between adult stutterers and non-stutterers. BMC Neurol. 2004 Dec 10;4(1):23.
    5. Kell CA, Neumann K, von Kriegstein K, Posenenske C, von Gudenberg AW, Euler H, Giraud AL. How the brain repairs stuttering. Brain. 2009 Oct;132(Pt 10):2747-60. Epub 2009 Aug 26.
    6. Galantucci S, Tartaglia MC, Wilson SM, Henry ML, Filippi M, Agosta F, Dronkers NF, Henry RG, Ogar JM, Miller BL, Gorno-Tempini ML. White matter damage in primary progressive aphasias: a diffusion tensor tractography study. Brain. 2011 Jun 11.
    7. Lundgren K, Helm-Estabrooks N, Klein R. Stuttering Following Acquired Brain Damage: A Review of the Literature. J Neurolinguistics. 2010 Sep 1;23(5):447-454.
    8. [No authors listed] Case records of the Massachusetts General Hospital. Weekly clinicopathological exercises. Case 43-1988. A 52-year-old man with persistent watery diarrhea and aphasia. N Engl J Med. 1988 Oct 27;319(17):1139-48
    9. Molteni N, Bardella MT, Baldassarri AR, Bianchi PA. Celiac disease associated with epilepsy and intracranial calcifications: report of two patients. Am J Gastroenterol. 1988 Sep;83(9):992-4.
    10. http://ezinearticles.com/?Food-Allergy-and-Stuttering-Link&id=1235725 
    11. http://www.craig.copperleife.com/health/stuttering_allergies.htm 
    12. https://www.celiac.com/forums/topic/73362-any-help-is-appreciated/
    13. Ford RP. The gluten syndrome: a neurological disease. Med Hypotheses. 2009 Sep;73(3):438-40. Epub 2009 Apr 29.
    14. Hadjivassiliou M, Gibson A, Davies-Jones GA, Lobo AJ, Stephenson TJ, Milford-Ward A. Does cryptic gluten sensitivity play a part in neurological illness? Lancet. 1996 Feb 10;347(8998):369-71.

    Jefferson Adams
    Celiac.com 06/14/2018 - Refractory celiac disease type II (RCDII) is a rare complication of celiac disease that has high death rates. To diagnose RCDII, doctors identify a clonal population of phenotypically aberrant intraepithelial lymphocytes (IELs). 
    However, researchers really don’t have much data regarding the frequency and significance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. Such data could provide useful comparison information for patients with RCDII, among other things.
    To that end, a research team recently set out to try to get some information about the frequency and importance of clonal T cell receptor (TCR) gene rearrangements (TCR-GRs) in small bowel (SB) biopsies of patients without RCDII. The research team included Shafinaz Hussein, Tatyana Gindin, Stephen M Lagana, Carolina Arguelles-Grande, Suneeta Krishnareddy, Bachir Alobeid, Suzanne K Lewis, Mahesh M Mansukhani, Peter H R Green, and Govind Bhagat.
    They are variously affiliated with the Department of Pathology and Cell Biology, and the Department of Medicine at the Celiac Disease Center, New York Presbyterian Hospital/Columbia University Medical Center, New York, USA. Their team analyzed results of TCR-GR analyses performed on SB biopsies at our institution over a 3-year period, which were obtained from eight active celiac disease, 172 celiac disease on gluten-free diet, 33 RCDI, and three RCDII patients and 14 patients without celiac disease. 
    Clonal TCR-GRs are not infrequent in cases lacking features of RCDII, while PCPs are frequent in all disease phases. TCR-GR results should be assessed in conjunction with immunophenotypic, histological and clinical findings for appropriate diagnosis and classification of RCD.
    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. 
    Source:
    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.
    Source:
    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.
    Source:
    Gut. 2017 Feb;66(2):250-257.  doi: 10.1136/gutjnl-2015-310148.