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And he keeps going, and going, ....geesh, how much did this boy eat?! Does anybody who has done a clean out before know about how long until everything generally passes? He wants food now and I feel bad telling him to wait.

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what consistency are his stools? we were told to keep our kids on a full dose til their poop had a softer consistency then to back off to half a dose...we were never told to not give them anything to eat but they don't have the same problem as your child(dysmobility?) what about just giving him a small amount of something to eat?

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Oh, they have hit runny stage now! We haven't given anymore Miralax since the bowels started moving yesterday. This might be TMI, but at least I know that we have hit the food from 5 days ago. We had corn on the cob and apparently corn kernels don't digest all the way. ;)

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I'm so glad! I haven't contributed to this thread because I haven't had any answers, but I can tell you that this poor little boy has been on my mind so much that I actually dreamed about him last night. No matter how much WE suffer when we are sick, the thought of a sweet little child suffering is too much to bear. Give him a hug from me and give yourself one too. God bless you both!

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you might want to give him half a dose...in my experince once I stopped giving the miralax the constipation started. :( the runny stage sucks, but that's the new poop that's getting pushed around the old poop that is stuck in his colon..I think he has alot more to get out! it will be runny for awhile, then might come out in chuncks, then finally will have the softer formed poop.

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Bartfull, to put your mind at rest, here is our happy boy today! http://s1053.photobucket.com/albums/s464/lauriefrost/Fun%20in%20the%20sun/

And thank you so much for your kind words and your concern :)

Momof2boys, It is so hard to think of giving 'Mr. Runs' even a 1/2 dose, but yes you are right. We have done Miralax before and gone right back to constipation! The idea of the runs being pushed around the blockage makes sense. He went from pebbles to runs literally within less than an hour, so that would make sense.

Thanks again, everyone. His sister has now 'tentatively' joined him in the pool...ready to jump out should our boy have an urge to let loose! LOL

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He's ADORABLE!! My friend Wendy has a boy his age and they look so much alike they could be twins. I guess all four year olds with blond hair look sort of alike.

You know, it's funny, when I was young enough to have had kids I wanted no part of them. Couldn't stand to be around one! Now that I am past the "danger" of having one of my own, I LOVE kids. I had never even HELD a baby, but now whenever someone comes into my shop with a baby I have to hold it and talk to it and tell the mother if she ever needs a babysitter she can call on me.

I guess it's one of the compensations of getting old. :D

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For us, but remember my son isn't typical in the pooping dept....it can be 48-36hrs before we see a truly cleaned out child and have the MtDew colored liquid stool. For *us* though this is what we have to do since we have *a lot* of motility issues.

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Is the Mt. Dew colored stool going to be liquid, too? The boy's poor bum is hurting right now from the liquid poops. We have been putting A&D on it.

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Poor thing! And yep, liquid Mt Dew...our GI actually said it would be like looking in the toilet and seeing a 2L of Mt Dew poured into it. We were never able to get this at home (like I said a lot of intestinal dysmotility) and it took 3 days of inpt clean out to get it even remotly close to this. We were not 100% certain the colonoscopy could even be done, but thankfully they were able to see what they needed to.

If his stool is liquid and his tummy is soft, I would guess that he is much better off than he was before. I personally do not know if I would go the entire way like we have to without a GI involved. Many parents whom have a child like mine can give their GI a call and get a KUB (KidneysUrterBladder) x-ray ordered as it also shows the intestinal tract. I wish you were able to get into a GI like we have been able to! 2wks for the first and that was at Nationwide's in Columbus (one of the best in the country) and then our current one-2 days! Again, I am not certain how much more I would push things since you do not have a GI or a ped that can help you right now. Dehydration is a real thing to worry about when doing something like this. (((hugs)))

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Thank you. We did get an appointment with an allergist, but not until the 17th. I called my human resources department for my work to see if we need a referral to a GI, but she hasn't gotten back to me, yet.

I have been doing more research and the more I do, the more I think we need to get him in to a GI. I mentioned before that what started us on allergy testing was the fact that he started vomitting each morning for a month straight. When we found his allergies, I thought that was it. The weird thing was that his vomit actually smelled like poop. Now I read that that means SEVERE constipation. Even doing this 'clean out' it makes me worry that we might be dealing with a blockage of some sort. So, we see his 'doctor' on the 11th and the allergist on the 17th. Between the two, someone better get us an X-ray, or better yet, a GI! I am debating just taking my boy up to urgent care (even though there isn't anything so 'urgent') to see of we can get referred!

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I Just wanted to update everyone. The poops are thickening (no accidents today) and my son ate a great breakfast, asked for a snack between breakfast and lunch, and is currently devouring his lunch. His bum is also no longer sore. He says his tummy does not hurt and he is doing great.

Who would have thought he could make such a turn around after a day of the runs! :)

I just wanted to say thank you again for all of the support, concern, and advice. I cannot stress enough how great it is to have people out there who not only care, but listen and just get it!

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I have a quick question about poop if anyone is still following this thread. :)

So now that is has been 4 days since we fed Colton all of the Miralax, his poops are soft, but more solid (no longer liquid the last couple of days). My question is, his poop is still pencil thin. Is this because of the Miralax, or is this suggestive of continued blockage?

His doctor did feel his stomach and said it was soft and he could feel a 'normal amount of stool' in there (which was interesting because Colton's poop was all liquid up until that point), but if you have followed my posts then you know how highly I think of our doctor (sarcasm intended).

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I have never heard of Miralax causing pencil thin stools to pass unless there was still a blockage somewhere. Can you get someone to oder a KUB (KidneyUrtersBladder) x-ray? This will also show the intestinal tract and see what and/or how much "stuff" is in their.

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Can you get someone to oder a KUB (KidneyUrtersBladder) x-ray? This will also show the intestinal tract and see what and/or how much "stuff" is in their.

That is one of the things that I am hoping to get through our GI referral. I hope the process does not take too long. Our doctor 'handles it from their end', so I don't have a number for a GI. We are supposed to wait for a call from the GI doctor. How long do you think we should wait before I start hounding the doctor?

Thank you for answering all of my questions! I didn't think pencil thin stools were a result of the Miralax, but I have never given him that much before. I do know that he still has a hard time even passing the 'pencil stools'. I have had to make a game of it with him of getting him to try to 'toot' on the pot (which causes him to pass the stool, too) and we make a big deal of belly laughing when he can make a noise. It is quite strange the things we find ourselves doing to make our kids feel better, you know?! LOL

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That is one of the things that I am hoping to get through our GI referral. I hope the process does not take too long. Our doctor 'handles it from their end', so I don't have a number for a GI. We are supposed to wait for a call from the GI doctor. How long do you think we should wait before I start hounding the doctor?

Thank you for answering all of my questions! I didn't think pencil thin stools were a result of the Miralax, but I have never given him that much before. I do know that he still has a hard time even passing the 'pencil stools'. I have had to make a game of it with him of getting him to try to 'toot' on the pot (which causes him to pass the stool, too) and we make a big deal of belly laughing when he can make a noise. It is quite strange the things we find ourselves doing to make our kids feel better, you know?! LOL

We had to wait for a while for our referral to go through. My ped's office told me the process should take a week, so if I didn't hear anything, call. So I did and somehow my referral had been "lost". After yet another week of waiting, I had to call again to find my referral had been "lost" for a 2nd time. I guess I should have taken it as a sign not to go to this GI's office. But they called me the next day with an appointment finally. I hope your offices are more organized than mine.

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We had to wait for a while for our referral to go through. My ped's office told me the process should take a week, so if I didn't hear anything, call. So I did and somehow my referral had been "lost". After yet another week of waiting, I had to call again to find my referral had been "lost" for a 2nd time. I guess I should have taken it as a sign not to go to this GI's office. But they called me the next day with an appointment finally. I hope your offices are more organized than mine.

Oh my gosh! How frustrating!

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We have always been told a week but I never wait that week and give them 5 instead. I don't want them thinking that this can wait, I don't think they like me much ;)

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    Jefferson Adams
    Celiac.com 06/18/2018 - Celiac disease has been mainly associated with Caucasian populations in Northern Europe, and their descendants in other countries, but new scientific evidence is beginning to challenge that view. Still, the exact global prevalence of celiac disease remains unknown.  To get better data on that issue, a team of researchers recently conducted a comprehensive review and meta-analysis to get a reasonably accurate estimate the global prevalence of celiac disease. 
    The research team included P Singh, A Arora, TA Strand, DA Leffler, C Catassi, PH Green, CP Kelly, V Ahuja, and GK Makharia. They are variously affiliated with the Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Lady Hardinge Medical College, New Delhi, India; Innlandet Hospital Trust, Lillehammer, Norway; Centre for International Health, University of Bergen, Bergen, Norway; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Gastroenterology Research and Development, Takeda Pharmaceuticals Inc, Cambridge, MA; Department of Pediatrics, Università Politecnica delle Marche, Ancona, Italy; Department of Medicine, Columbia University Medical Center, New York, New York; USA Celiac Disease Center, Columbia University Medical Center, New York, New York; and the Department of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
    For their review, the team searched Medline, PubMed, and EMBASE for the keywords ‘celiac disease,’ ‘celiac,’ ‘tissue transglutaminase antibody,’ ‘anti-endomysium antibody,’ ‘endomysial antibody,’ and ‘prevalence’ for studies published from January 1991 through March 2016. 
    The team cross-referenced each article with the words ‘Asia,’ ‘Europe,’ ‘Africa,’ ‘South America,’ ‘North America,’ and ‘Australia.’ They defined celiac diagnosis based on European Society of Pediatric Gastroenterology, Hepatology, and Nutrition guidelines. The team used 96 articles of 3,843 articles in their final analysis.
    Overall global prevalence of celiac disease was 1.4% in 275,818 individuals, based on positive blood tests for anti-tissue transglutaminase and/or anti-endomysial antibodies. The pooled global prevalence of biopsy-confirmed celiac disease was 0.7% in 138,792 individuals. That means that numerous people with celiac disease potentially remain undiagnosed.
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    Source:
    Clin Gastroenterol Hepatol. 2018 Jun;16(6):823-836.e2. doi: 10.1016/j.cgh.2017.06.037.

    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.
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    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.
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    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.
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    Source:
    Alimentary Pharmacology & Therapeutics