[annelb]

I believe that high on the list should be other food intolerances. IMHO this should be #2. #1 is continued exposure to gluten. I also think that some people have been so badly damaged by years of gluten exposure that repair will take a very long time and may never be complete. Another reason to get diagnosed "before the villi are gone".
Anne

Gastrointest Endosc Clin N Am. 2006 Apr;16(2):317-27.Click here to read Links
Monitoring nonresponsive patients who have celiac disease.

* Krauss N,
* Schuppan D.

Department of Medicine I (Gastroenterology, Hepatology, Pneumonology and Endocrinology), University Hospital, Ulmenweg 18, Erlangen 91054, Germany. Norbert.Krauss@med1.imed.uni-erlangen.de

Because of the wide variations in the clinical presentation of celiac disease and because treatment exists that is effective in most cases, screening of the general population for celiac disease has been considered. There is still no evidence that patients who have symptom-free celiac disease are at increased risk of small intestinal lymphoma or other complications. Prevention of osteoporosis seems to be the strongest indicator for widespread screening today [22].The major cause of failure to respond to a gluten-free diet is continuing ingestion of gluten, but other underlying diseases must be considered.Many different drugs (eg, anti-tumor necrosis factor [TNF]-alpha) have been used in patients who have RCD [23]. Steroid treatment has been reported to be effective even in patients who have underlying early EATL.Histologic recovery in patients who have celiac disease usually takes several months but can take up to 1 year, even if the patient remains on a strict gluten-free diet. Some patients report celiac-related symptoms for months after a single gluten intake.The definitions for RCD in literature vary. The authors consider the definition give by Daum and colleagues [24] suitable. They defined true RCD as villous atrophy with crypt hyperplasia and increased IELs persisting for more than 12 months in spite of a strict gluten-free diet.If a patient is not responding well to a gluten-free diet, three considerations are necessary: (1) the initial diagnosis of celiac disease must be reassessed;(2) the patient should be sent to a dietician to check for errors in diet or compliance problems, because problems with the gluten-free diet are the most important cause for persisting symptoms; (3) other reasons for persisting symptoms (eg, pancreatic insufficiency, irritable bowel syndrome, bacterial overgrowth, lymphocytic colitis, collagenous colitis, ulcerative jejunitis, protein-losing enteropathy,T-cell lymphoma, fructose intolerance, cavitating lymphadenopathy, and tropical sprue) should be considered.Other causes for villous atrophy are Crohn's disease, collagenous sprue, and autoimmune enteropathy.Abdulkarim and colleagues [25] examined 55 patients who had a diagnosis of nonresponsive celiac disease. He found that 6 did not have celiac disease, and25 still had some gluten ingestion.Tursi and colleagues [26] reported 15 patients who had celiac disease with persisting symptoms. Because histology improved in all patients after several months, RCD was excluded. Of the 15 patients, 10 had small intestinal bacterial overgrowth, 2 showed lactose malabsorption causing the described symptoms, 1 had mistakenly taken an antibiotic containing gluten, and 1 patient each had Giardia lamblia and Ascaris lumbricoides. Thus, other entities must be considered in patients who have celiac disease and ongoing symptoms.In a follow-up clinical trial, 158 patients who had celiac disease underwent follow-up small intestine biopsies within 2 years after starting a gluten-free diet.Eleven patients (7.0%) with persisting (partial) villous atrophy were considered to have RCD; 5 of them developed EATL [27].RCD type I is characterized by normal expression of T-cell antigens and polyclonal TCR gene rearrangement.RCD type II is characterized by an abnormal IEL phenotype with the expression of intracytoplasmic CD3e, surface CD103, and the lack of classic surface T-cell markers such as CD8, CD4, and TCR-alpha/beta. This clonal IEL population can be considered crypt IEL [24]. RCD II has a poor prognosis, which is a problem for therapy.Clonal TCR gene rearrangements and loss of T-cell antigens such as CD8 and TCR-beta in IELs may indicate the development of an EATL in patients who have RCD.The markers for an overt EATL are a positive stool blood test, increased lactate dehydrogenase, or beta2-microglobulin [24]. If an overt lymphoma is suspected, upper and lower endoscopy, an ear, nose, and throat work-up, CT scan, capsule endoscopy, and possibly double-balloon enteroscopy should be performed.Most reports of the difficulties in treating patients who have true RCE are casereports. Turner and colleagues [28] reported on an induction of remission by useof the anti-TNF-alpha antibody infliximab and maintenance with prednisoloneand azathioprine. Olaussen and colleagues [29] and Mandal and colleagues [30]tried a nonimmunogenic elemental diet.Gillet and colleagues [31] reported successful treatment of a patient who hadRCD using anti-TNF-alpha antibodies (infliximab) for induction and azathioprinefor maintenance.Maurino and colleagues [32] studied seven consecutive patients diagnosed ashaving refractory sprue and no response to oral or parenteral steroids. Aftertreatment with azathioprine (2 mg/kg/d) and oral prednisone (1 mg/kg/d), fivepatients had a complete clinical remission. Two patients who did not respond totreatment at any time died.Goerres and colleagues [33] described 18 patients who had RCD, 10 of whomhad type I RCD, and 8 of whom had type II RCD. Treatment consisted ofazathioprine combined with prednisone for 1 year. Consistent with reports byother investigators, the response rates in the two groups differed. Eight of the10 patients who had type I RCD had a histologic response. Seven of the eightpatients who had type II RCD died, and six of the eight developed a lymphoma.At present there is no effective treatment for type II RCD.Fig. 3 presents a proposed algorithm for monitoring patients who have ce-liac disease.

PMID: 16644460 [PubMed - indexed for MEDLINE]

[rachelb]

Yes, Anne, I totally agree with you. Often removing one item you're sensitive to will uncover other sensitivities that need to be addressed as well. #2 should definitely be look for other sensitivities (esp casein and soy!).

I wish this was more known. I wish more people were open to the idea that you are what you eat. And while I'm glad that gluten sensitivity is getting more attention, if docs and such don't pay attention to other food sensitivities, too, a lot of people will remove gluten and presume they're done and then wonder why they don't feel better.

Oh, and just a little vent for people who need to remove gluten but refuse to stick with it or who just limit it and then can't fathom why they keep getting more and more ill. Just makes you want to whack them upside the head a bit.

Rachel

[jccgf]

I recently added a page to TGF about this. I agree that other food intolerance needs to be considered up high on the list, especially the ones known to cause villi damage like milk and soy, but the other biggie seems to be bacterial overgrowth. I still wonder about this in my daughter, since she has so much gas~

http://jccglutenfree.googlepages.com/notceliac