Medscape (Medical Professionals' Continuing Ed site) Celiac Disease/Gluten Sensitivity articles

canadjineh

March 6/2015 in my email inbox (I get regular updates sent to me by Medscape): Italics & bolding - mine)

Re: Alimentary Pharmacology & Therapeutics

Metabolic Syndrome in Patients With Coeliac Disease on a Gluten-free Diet
R. Tortora, P. Capone, G. De Stefano, N. Imperatore, N. Gerbino, S. Donetto, V. Monaco, N. Caporaso, A. Rispo
Disclosures
Aliment Pharmacol Ther. 2015;41(4):352-359.

Discussion

"The clinical presentation of CD has changed over time and symptoms like diarrhoea and weight loss have become less frequent, especially in adult patients.[1,5] Several studies in adults and children affected by CD indicate that obesity/overweight at diagnosis is not unusual and that there is a trend towards the development of overweight/obesity in CD subjects who comply with a gluten-free diet. However, to date no study has focused on the prevalence of MS in patients with CD on free diet and after GFD. The present study was planned to generate new information on this underexplored issue.

Our study highlighted that patients with CD are at high risk of developing MS 1 year after starting GFD. In our sample, at this time point the prevalence of MS in patients with CD appeared to be about 30% (2% vs. 29.5%, P < 0.01). This data relate to the significantly higher proportion of patients with CD whose waist circumference exceeded the cut-off value at follow-up (mean values 85 cm ± 11 vs. 88 cm ± 12; P < 0.01; OR: 2.8), as this criterion is essential for the diagnosis of MS according to the IDF definition.[19]

Our results suggest that the majority of newly diagnosed patients with CD who are normal or overweight at baseline are likely to become overweight or obese after the introduction of GFD, with the potential development of MS and/or HS. The increase in weight could be a consequence of the improvement in intestinal absorption (caused by the exclusion of gluten from the diet) in subjects who are in a compensative hyperphagic status. However, it remains to be established whether the GFD itself contributes to the development of overweight/obesity in patients with CD. Several studies have confirmed that long-term GFD may not be nutritionally balanced. Indeed, there is clinical evidence indicating high intake of simple sugars, proteins and saturated fat and intake of complex carbohydrates and fibre in such diets.[28–30] In addition, increased total caloric intake, the macronutrient composition of the diet, may be involved in the pathogenesis of overweight and obesity in patients with CD. Many gluten-free foods are characterised by a glycemic index which is higher than that of equivalent gluten-containing foods,[31,32] although this is refuted by some authors.[33] The higher glycemic index of gluten-free foods could be partially explained by the fact that in 'normal' conditions gluten does not allow the amylase to easily access and hydrolyse starch granules in the lumen of the small intestine, thus reducing starch adsorption. Also, the unpalatability of some gluten-free foods may induce a preference towards hyperproteic and hyperlipidemic foods,[28,34] which, in turn, may lead to increased energy intake and subsequent weight gain.

Among the other MS criteria showing significant changes, blood pressure was the most important: our results highlight that patients with CD on GFD show a 4-fold increase in their risk of developing systemic hypertension.

Glucose profile also appeared significantly different in patients with CD at diagnosis and after 1 year of GFD, with the latter time point being characterised by an approximately 4.5-fold increase in risk for the onset of hyperglycaemia. An elevated fasting plasma glucose concentration is an indicator of insulin resistance, which, in turn, is a potential causing factor of MS with central obesity. These two elements have a mutual relationship: tumour necrosis factor-a (TNF-a), whose increased expression has been demonstrated in human obesity, is thought to participate importantly in insulin resistance by inhibiting tyrosine kinase activity at the insulin receptor. Therefore, BMI increase after GFD might explain the higher prevalence of insulin resistance in patients with CD at follow-up.[35–37] Another hypothesis about the pathogenesis of insulin resistance directly involves CD: a recent study[38] reports that tTG drives inflammation in CD through the down-regulation of peroxisome proliferator-activated receptor γ (PPARG). As PPARG up-regulation is implicated in type 2 diabetes susceptibility,[39] it is possible that by reducing inflammation the GFD might also influence this pathway. However, this theory needs to be corroborated by further research.

Our data about the lipid profile of patients with CD suggest that this shows no significant differences before and after the introduction of GFD. This finding, apparently in contrast with the other data,[40] is confirmed by several studies[41,42] which report increased serum levels of HDL cholesterol in patients with CD after starting a GFD in relation to an increment of body fat stores. However, the HDL increase is usually accompanied by an increase also in LDL, due to high fat consumption in patients with CD.[28,34,43] The difference between levels of triglycerides at diagnosis and follow-up is at the limit of significance (P = 0.05).

Our results on the prevalence of MS, although not comparable with similar studies at this time, are indirectly confirmed by results from the analysis of BMI status. In our study: many patients with CD had a high or normal BMI at diagnosis (mean value 22.9 kg/m2), and this value increased after the adoption of a GFD. This pattern is confirmed by other studies.[44] Dickey et al.[10] demonstrated further weight gain in patients already overweight at the time of CD diagnosis after the introduction of a GFD. A recent American study confirmed these findings,[44] and reported that BMI increase was predominant in the GFD adherent group (evaluated using a GFD adherence score). In contrast with our findings, however, Cheng et al.[45] showed a positive effect of GFD by demonstrating weight gain in previously underweight patients and weight loss in those previously overweight.

With regard to the prevalence of HS, in our study patients with MS had a higher risk of excessive fat accumulation in their liver than patients without MS (65% vs. 13%; P < 0.01). This finding confirms the experience of other authors who demonstrated that HS is strongly associated with MS.[46–48]

The present work shows some limitations that we briefly discuss. First of all, ours was not designed as an interventional study so that the 'sample size' of the population was not calculated. However, we think that a number of about 100 patients affected by CD and prospectively followed-up for 1 year could offer interesting news and information about the potential risk of MS in subjects with CD on GFD; this could represent a stimulating starting-point for further studies including a larger population. In addition, obesity and MS seems to increase in general population similar to CD[49] and the lack of control group of 'healthy' subjects in our study could represent a methodological shortcoming.

In view of our findings, we recommend that an in-depth nutritional assessment is carried out for all patients with CD at the time of diagnosis as well as at medium-term follow-up (3–6 months) in order to prevent excessive weight gain and the onset of MS. From this point of view, all Gastroenterological Units diagnosing CD should contemplate including in their staff of a nutritionist with experience in this particular clinical field.

In the last few years, GFD has been proposed as a treatment for conditions other than CD. In particular, it has been proposed as an affective dietary approach to noncoeliac gluten sensitivity,[50] irritable bowel syndrome,[51] inflammatory bowel diseases[52] and several other conditions.[53] The findings from our study have relevance for these different pathological settings and suggest that GFD should be prescribed with caution and only for the right indication.

In conclusion, patients with CD on a gluten-free diet are at risk of metabolic syndrome and hepatic steatosis and an in-depth nutritional assessment is required at diagnosis and during follow-up. "
This shows the importance of keeping your BMI down by eating foods that are naturally gluten free and quality sources of nutrition (like fresh vegetables & fruits, lean meats, fish, eggs, & legumes) as opposed to eating commercially prepared 'substitute foods' like GF pizzas, cookies, cakes, breads, etc.

canadjineh

March 23/2015 article and references on Medscape (Italics and bolding mine)

Gluten-free Diet in the Management of Patients With Irritable Bowel Syndrome, Fibromyalgia and Lymphocytic Enteritis
Umberto Volta
Disclosures
Arthritis Res Ther. 2014;16(505)

Authors and Disclosures
Umberto Volta

Department of Medical and Surgical Sciences, University of Bologna, via Massarenti 9, Bologna 40138, Italy

Correspondence
umberto.volta@aosp.bo.it
Competing interests
The author declares that he has no competing interests.

"An evaluation of the effect of 1 year of a gluten-free diet was performed in patients with irritable bowel syndrome and fibromyalgia syndrome displaying lymphocytic enteritis. Gluten withdrawal produced a slight but significant improvement of the functional symptoms, suggesting that gluten might be partly responsible for this clinical picture. This hypothesis should be confirmed by a double-blind placebo-controlled trial since it cannot be ruled out that the studied patients displayed a subjective sensation of improvement due to the placebo effect of gluten withdrawal. Further investigations are needed before recommending gluten withdrawal in patients with fibromyalgia and lymphocytic enteritis.

In their paper published in a recent issue of Arthritis Research and Therapy, Rodrigo and colleagues evaluated the effect of 1 year of a gluten-free diet on the clinical evolution of irritable bowel syndrome (IBS) plus fibromyalgia syndrome (FMS) in patients with lymphocytic enteritis (LE).[1] The study sample included 97 adult females with IBS and FMS, of whom 58 had LE and the remaining 39 had a normal intraepithelial lymphocytic (IEL) count. All subjects fulfilled the Rome III criteria for IBS and the American College of Rheumatology 1990 criteria for FMS and none of them satisfied the diagnostic criteria for celiac disease diagnosis (absence of villous atrophy and negativity for tissue transglutaminase antibodies).

IBS and FMS are two chronic functional disorders that are found in a high number of people in the general population and are frequently detected in the same subject.[2] A subset of patients complaining of IBS and FMS displays LE, a morphological finding that by itself is not specific for celiac disease, also being found in many other pathological conditions such as food allergy, autoimmune disorders, Helicobacter pylori infection, nonsteroidal anti-inflammatory drug treatment and common variable immunodeficiency.[3]

The spectrum of gluten-related disorders has recently acquired a new syndrome, defined as nonceliac gluten sensitivity according to the criteria established in the two Consensus Conferences held in London and Munich.[4] This new clinical entity is characterized by IBS-like symptoms and several extraintestinal manifestations occurring after gluten ingestion in patients without celiac disease and wheat allergy. In a recent prospective multicenter survey of 486 patients with nonceliac gluten sensitivity, IBS and FMS were respectively detected in 47% and 31% of cases and about one-third of these patients had LE.[5]

Along with IBS-related and FMS-related symptoms, the patients studied by Rodrigo and colleagues also showed other manifestations resembling the clinical picture of nonceliac gluten sensitivity such as skin rash, cognitive dysfunction, headache, numbness, anxiety and depression.[1]

In Rodrigo and colleagues' paper, the gluten-free diet produced a slight but significant improvement of both IBS-related (chronic abdominal pain, changes in intestinal habit, bloating) and FMS-related symptoms (chronic widespread pain, generalized tender points, fatigue and restless sleep) in the LE subgroup versus the non-LE subgroup. These results stress the potential role of gluten as a trigger of the clinical manifestations of IBS and FMS and indicate that LE might be useful to identify those patients who potentially benefit from gluten withdrawal. One relevant limitation of this study is the lack of a double-blind placebo-controlled challenge, which is the only procedure to confirm the role of gluten proteins in the development of these clinical manifestations. Indeed, it cannot be ruled out that some patients displayed a subjective sensation of improvement due to the placebo effect of a gluten-free diet.[6] The search for antigliadin antibodies could be of help to elucidate whether gluten can be partly responsible for the clinical picture observed in Rodrigo and colleagues' patients. Indeed, antigliadin antibodies (particularly those belonging to the IgG class) are the only marker observed in patients with symptoms elicited by gluten ingestion, being positive in more than 50% of cases.[7] These antibodies are not specific for gluten-related symptoms, but their finding in patients with symptoms potentially evoked by gluten ingestion should be regarded as an indication for a gluten-free diet trial in patients with LE.[8] Antigliadin antibodies of the IgG class are closely related to the gluten-induced symptoms and tend to disappear very quickly (within a few weeks) together with the remission of symptoms after a gluten-free diet.[9]

An interesting finding emerging from the Spanish study is that about 20% of IBS/FMS patients with LE had relatives with celiac disease, whereas no familial case of celiac disease was observed among patients without LE.[1] In the same guise, familial cases of FMS were found, although to a lesser extent, only in the group with LE (7%). These data suggest that first-degree relatives of IBS/FMS patients with LE should be carefully investigated for the possible presence of undetected cases of celiac disease and FMS. For LE, the mean IEL number reported in Rodrigo and colleagues' paper was 35/100. This result confirms that LE found in gluten-sensitive patients is mild, with a lower mean IEL number than that usually observed in celiac disease patients (usually >40/100).[10]

The caution in the conclusions of Rodrigo and colleagues' study is appreciable and shareable. A gluten-free diet is not appropriate in patients with IBS/FMS with normal intestinal mucosa (normal IEL count). Moreover, although the reported results suggest a significant improvement of symptomatology after a gluten-free diet in the LE subgroup, further studies including double-blind placebo-controlled trials are needed before proposing gluten withdrawal in IBS/FMS patients with LE.

References

1.Rodrigo L, Blanco I, Bobes J, de Serres F: Effect of one year of a gluten-free diet on the clinical evolution of irritable bowel syndrome plus fibromyalgia in patients with associated lymphocytic enteritis: a case–control study. Arthritis Res Ther 2014, 16:421.

2.Whitehead WE, Palsson O, Jones KR: Systematic review of the comorbidity of irritable bowel syndrome with other disorders: what are the causes and implications? Gastroenterology 2002, 122:1140–1156.

3.Brown I, Mino-Kenudson M, Deshpande V, Lauwers GY: Intraepithelial lymphocytosis in architecturally preserved proximal small intestinal mucosa: an increasing diagnostic problem with a wide differential diagnosis. Arch Pathol Lab Med 2006, 130:1020–1025.

4.Catassi C, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A: Non-celiac gluten sensitivity: the new frontier of gluten related disorders. Nutrients 2013, 5:3839–3853.

5.Volta U, Bardella MT, Calabrò A, Troncone R, Corazza GR: Study Group for Non-Celiac Gluten Sensitivity: An Italian prospective multicenter survey on patients suspected of having non-celiac gluten sensitivity. BMC Med 2014, 12:85.

6.Godlee F: Gluten sensitivity: real or not? BMJ 2012, 345:e7982.

7.Volta U, Tovoli F, Cicola R, Parisi C, Fabbri A, Piscaglia M, Fiorini E, Caio G: Serological tests in gluten sensitivity (nonceliac gluten intolerance). J Clin Gastroenterol 2012, 46:680–685.

8.Verdu EF: Can gluten contribute to irritable bowel syndrome? Am J Gastroenterol 2011, 106:516–518.

9.Caio G, Volta U, Tovoli F, De Giorgio R: Effect of gluten-free diet on immune response to gliadin in patients with non-coeliac gluten sensitivity. BMC Gastroenterol 2014, 12:85.

10.Volta U, Caio G, Tovoli F, De Giorgio R: Non-celiac gluten sensitivity: questions still to be answered despite an increasing awareness. Cell Mol Immunol 2013, 10:383–392.

canadjineh

April 19/2015 article Medscape:

Celiac Disease Linked to Miscarriages and Preterm Deliveries

Reuters Health) - Women with doctor-diagnosed celiac disease are more likely to miscarry or deliver preterm than women with no history of the condition, according to a small U.S. study.

Researchers say that women experiencing miscarriages or preterm deliveries should be checked for undiagnosed celiac.

While there are many more common causes of pregnancy complications, women who don't know why they can't conceive or carry a baby to term should find out if they have celiac disease, said lead study author Dr. Stephanie Moleski, a researcher at Thomas Jefferson University Hospital in Philadelphia.

"Miscarriage in celiac disease patients has been linked to vitamin deficiencies of zinc, selenium, iron and folate," Moleski said by email. "When I see patients who have had fertility or pregnancy complications I feel it is appropriate to consider testing for celiac disease."

Moleski and colleagues surveyed 329 women with biopsies confirming celiac disease as well as 641 women without the condition. Using online questionnaires, the researchers asked reproductive health questions ranging from the age the women started menstruating to the number of pregnancies they experienced and the birth circumstances for any babies delivered.

There wasn't any difference in the number of women with or without celiac disease who got pregnant at least once, but the women with celiac disease were less likely to give birth, the study found.

Women with celiac disease had miscarriages about half the time, compared with 40% of the time among the other women in the study. About one in four women with celiac disease had premature deliveries, compared with about 16% of the other women.

Limitations of the study, according to the April 15 Annals of Gastroenterology online report, include its reliance on the online questionnaires, which depend on patients having accurate recollections, and which didn't verify whether participants had other health conditions that might lead to miscarriages or preterm deliveries.

Restricting the celiac group to women diagnosed with a biopsy also means that some women in the non-celiac group might have had undiagnosed celiac, which would skew the results.

While previous research has linked celiac diseases to fertility and pregnancy problems, the exact reason the condition leads to miscarriages and premature babies is unknown, Dr. Govind Makharia, a professor of gastroenterology and nutrition at All India Institute of Medical Sciences in New Delhi, said by email.

"At present, the association between infertility, miscarriage, preterm babies and celiac disease is conjectural and not definitive," said Makharia, who wasn't involved in the study. Celiac might be a cause, but other causes are more likely.

"However, there may not be any harm in screening for celiac disease," Makharia said.

SOURCE: http://bit.ly/1zl3ahj

Ann Gastroenterol 2015.

canadjineh

Updated Nov 18/2014 Medscape:

Pediatric Celiac Disease Author: Stefano Guandalini, MD; Chief Editor: Carmen Cuffari, MD more...

Epidemiology

Frequency

United States

The availability of sensitive and specific serological tests has made it possible to assess the true prevalence of celiac disease by detecting minimally symptomatic or even asymptomatic cases with typical mucosal changes.[7] Screening studies have shown that celiac disease has a very high prevalence, occurring in almost 1% of the general population throughout North America.[8, 9]

International

Celiac disease is as common in Europe as it is in North America, but it has now been detected in populations from many other parts of the world, including African and Middle Eastern countries, and in Asia, with the highest prevalence worldwide in Saharawi children.[10]

Furthermore, the prevalence of celiac disease appears to be increasing quite dramatically during the past few decades.[8, 11, 12, 9] In Northern Sweden, an epidemiological investigation using a combined serological/endoscopic approach in an unselected population of 1000 adults found a prevalence of almost 2%.[13]

Epidemiological data do document worldwide a true increase in prevalence, with rates doubling approximately every 20 years. A concomitance of environmental factors are likely responsible for this, but most of them are still unclear. Among the hypotheses to explain such increase are: the hygiene hypothesis,[14] increased rates of births through elective cesarean delivery,[15] changes in infant feeding practices as dramatically documented by the so-called Swedish epidemic,[16] and repeated infections—by rotavirus but also generic, nongastrointestinal infections in early infancy.[17]

A recent investigation in Sweden proved that early vaccinations are not risk factors for the development of celiac disease.[18]

Mortality/Morbidity

The morbidity rate of celiac disease can be high. Its complications range from osteopenia, osteoporosis, or both to infertility in women, short stature, delayed puberty, anemia, and even malignancies (mostly related to the GI tract [eg, intestinal T-cell lymphoma]). As a result, the overall mortality in patients with untreated celiac disease is increased.

Evidence also suggests that the risk of mortality is increased in proportion to the diagnostic delay and clearly depends on the diet; subjects who do not follow a gluten-free diet have an increased risk of mortality, as high as 6 times that of the general population. The increased death rates are most commonly due to intestinal malignancies that occur within 3 years of diagnosis.[19, 20] Some indirect epidemiological evidence suggests that intestinal malignancies can be a cause of death in patients with undiagnosed celiac disease.[21]

Race

In some ethnicities, such as in the Saharawi population, celiac disease has been found in as many as 5% of the population. As mentioned, celiac disease is considered extremely rare or nonexistent in people of African, Chinese, or Japanese descent.

Sex

Most studies indicate a prevalence for the female sex, ranging from 1.5:1 to 3:1.

Age

Celiac disease can occur at any stage in life; a diagnosis is not unusual in people older than 60 years. Classic GI pediatric cases usually appear in children aged 9-18 months. Celiac disease may also occur in adults and is usually precipitated by an infectious diarrheal episode or other intestinal disease.

The Academy of Nutrition and Dietetics (AND) (once American Dietetic Association (ADA)) publishes guidelines for the dietary treatment of celiac disease. They are a reliable source of information for a gluten-free. However, because of the dynamics of this field, the diet requires ongoing collaboration between patients, health care providers, and dietitians.
http://www.eatright.org/resources/health/diseases-and-conditions

canadjineh

Bone Microarchitecture Impaired in Active Celiac Disease
By Will Boggs MD

April 23, 2015

NEW YORK (Reuters Health) - Bone microarchitecture is impaired in premenopausal women with active celiac disease, a new study from Argentina shows.

"This report helps us to understand how bone is affected in celiac disease: increasing bone resorption and thinning trabeculae, even losing some number of them," Dr. María Belén Zanchetta from Instituto de Diagnóstico e Investigaciones Metabólicas in Buenos Aires told Reuters Health by email. "We do not know yet if this damage can be completely reversed with gluten-free diet."

Osteopenia and osteoporosis are recognized complications of celiac disease, but no studies have assessed the microarchitectural quality of bones in celiac disease patients.

Dr. Zanchetta's team used high-resolution peripheral quantitative computed tomography (HR-pQCT) to compare microarchitectural characteristics of peripheral bone in 31 adult premenopausal women with active celiac disease and 22 healthy premenopausal women of similar age and body mass index (BMI).

Compared with controls, women with celiac disease had 26.4% lower trabecular density, 18% lower trabecular thickness, and 10.5% lower trabecular number in the distal radius, along with 15% higher trabecular spacing and 23% higher heterogeneity of the trabecular network (all statistically significant).

Results were similar at the distal tibia, the researchers report in Bone, online March 14.

Microarchitectural deficits were more substantial among women with symptomatic celiac disease than among those with subclinical celiac disease.

Bone mineral density (BMD) z-scores were significantly lower at lumbar spine, femoral neck, and distal radius among women with celiac disease than among healthy controls, although the mean scores were within the normal range.

Seven patients had serum calcium concentrations below the lower end of the reference range, nine patients had elevated C-telopeptide concentrations, and only three patients had serum vitamin D levels above 30 ng/mL.

HR-pQCT results correlated significantly with age, BMI, C-telopeptide concentrations and vitamin D levels.

"In the prospective follow-up of this group we hope to be able to assess if bone microarchitecture can be restored to normal after gluten free diet," Dr. Zanchetta said. "In the meantime, we would recommend to assess and prescribe adequate calcium (diet or pills) and vitamin D supplementation in celiac disease patients, apart from exercise and smoking avoidance."


Dr. William Dickey from Altnagelvin Hospital in Londonderry, Northern Ireland, who has published extensively on celiac disease, said the new work "reinforces that bone health is significantly impaired in premenopausal women with celiac, and the importance of assessing wrist as well as spine and femur density."

"It remains to be shown whether HR-pQCT is superior to DXA as a clinical tool for the prediction of increased fracture risk," he told Reuters Health by email. "This is important, as DXA is much more widely available and probably cheaper with lower radiation exposure."

SOURCE: http://bit.ly/1Gi8ruU

Bone 2015.

duckykissy

These are all really interesting thanks for posting them.

canadjineh

Medscape Medical News > Neurology

Increased Neuropathy Risk in Celiac Disease
Pauline Anderson

May 14, 2015

"Having celiac disease (CD), an autoimmune disorder characterized by a sensitivity to gluten, more than doubles the risk for neuropathy, a new study shows.

"In patients with neuropathy and no obvious cause, celiac disease should be considered," said Jonas Ludvigsson, MD, PhD, professor of clinical epidemiology, Karolinska Institutet, a pediatrician at Örebro University Hospital, Stockholm, and president, Swedish Pediatric Society.

As well, said Dr Ludvigsson, physicians managing patients with CD should be aware of their increased risk for neuropathy. The study was published online May 11 in JAMA Neurology."

"There were no differences in increased neuropathy risk between male and female patients with CD. Age at diagnosis also didn't influence risk estimates for neuropathy.

When the outcome was restricted to neuropathy in those with a record of neuropathy-associated medications, the association between CD and neuropathy remained.

The risk varied according to type of neuropathy. Celiac disease was most strongly associated with mono-neuritis multiplex (with an HR of 7.6). The next strongest link was to autonomic neuropathy (HR, 4.2). There was no association between CD and acute inflammatory demyelinating polyneuropathy (HR, 0.8).

The study did not have enough statistical power to examine the association between CD and multifocal motor neuropathy, which has been reported by other researchers.

Bidirectional Association

There also seemed to be a bidirectional association between CD and neuropathy in that the association existed before the CD diagnosis.

"That is probably because some patients have undiagnosed celiac disease and are then at increased risk of neuropathy — and only after the neuropathy diagnosis is the celiac disease detected," commented Dr Ludvigsson. "But it could also mean that celiac disease and polyneuropathy share a common cause or risk factor."

Other possible mechanisms linking celiac disease with neuropathy include chronic inflammation and malnutrition. A deficiency of vitamin B12 has been found to be associated with CD and with neuropathy, suggesting that this deficiency may help explain the connection between the two conditions, said Dr Ludvigsson.

However, the authors noted that the influence of vitamin deficiencies did not significantly affect the risk estimate in the study.

The researchers didn't investigate whether a strict gluten-free diet would prevent neuropathy in patients with CD, but according to Dr Ludvigsson "that would make an interesting study."

Given the autoimmune nature of CD, the data reinforce the potential role of immunologic mechanisms for the development of neuropathy, said the authors.

While other studies have found a similar association between celiac disease and neuropathy, this new analysis used a nationwide sample of patients, so it included "average patients" with CD, commented Dr Ludvigsson. "Some earlier studies primarily studied patients with celiac disease in specialist centers, which makes it is difficult to calculate a correct risk for neuropathy."


The size of the study sample also enabled researchers to calculate a more precise risk estimate than was the case in the past, according to Dr Ludvigsson. The large number of patients also allowed investigators to study subtypes of neuropathy. "That has not been done on a large scale before," he said.

Future related research should include electrophysiologic studies, thorough serum evaluations, prior drug histories, and skin biopsies to evaluate for small-fiber neuropathy, said the authors. The study results suggest that screening could be beneficial in patients with neuropathy, they concluded.

"In patients with neuropathy where there is a plausible cause, such as high alcohol consumption or type 1 diabetes, looking for celiac disease may not be necessary," said Dr Ludvigsson. "But in cases where there is no obvious cause for the neuropathy, I think screening for celiac disease is appropriate."


The estimated prevalence of CD is 1%. Research indicates that about 60% of patients with CD are women.

The association between CD and neuropathy was first reported in 1966. Other autoimmune disorders also increase the risk for neuropathy.

Asked to comment, Shamik Bhattacharyya, MD, Department of Neurology, clinical fellow in neurology, Massachusetts General Hospital, Brigham & Women's Hospital, and Harvard Medical School, Boston, noted the study's strengths, particularly the very large number of participants in both study groups, and the duration of follow-up.
Any person with neuropathy is also at relatively increased risk for CD — again a small absolute risk — but who those patients are remains unknown, added Dr Bhattacharyya.
But what he found "particularly provocative" about the study was that the risk for neuropathy remained increased for years after the diagnosis of celiac disease.

"The patients in this study probably were treated for celiac disease with a gluten-free diet. Since their risk remained elevated even with this diet, we really don't know whether this treatment even has any effect on the risk of neuropathy. This is particularly relevant for patients with neuropathy without diarrhea who test positive for antibodies associated with celiac disease."

Dr Ludvigsson and Dr Bhattacharyya have disclosed no relevant financial relationships.

JAMA Neurol. Published online May 11, 2015. Abstract

canadjineh

New Quickie notes from Digestive Diseases Week (Washington DC):
Keeping 'Tract': GI Updates From DDW 2015 Dr David Johnson, professor of medicine and chief of gastroenterology at Eastern Virginia Medical School in Norfolk, Virginia.
Celiac Disease

This one got a lot of press. If you haven't seen this, you probably will, or you'll hear about it.

A group from Columbia University[2] looked at the widespread contamination of probiotics with gluten. How many of your patients take probiotics? Mine come in all the time and tell me that they do. How many of you recommend probiotics? Be careful what you recommend, because this was a very interesting study.

Dr Green and his colleagues at Columbia looked at the gluten component using liquid chromatography. They looked at a composite of 22 probiotics, and a little more than two thirds of these were listed as gluten-free. When they actually studied them, however, they found that 55% contained gluten and two of them contained an incredibly high amount of gluten—amounts that they would view as a very alarming amount.

Of the 15 probiotics that were labeled gluten-free, eight (53%) tested positive for gluten, including two that contained gluten levels more than 20 parts per million—suggesting that gluten is in a lot of these probiotics, even when they say it isn't. A variety of gluten-containing products were in some of these probiotics. Two of them actually tested positive for barley and rye.

This may be something to question your patients about when they may not be responding to treatment. Certainly, be cautious when you recommend probiotics across the board, especially within the population with celiac disease.

dalansteiner

Wow. Canadjineh you rock! Very helpful articles! Thanks

canadjineh

dalansteiner wrote: »

Wow. Canadjineh you rock! Very helpful articles! Thanks

Thanks @dalansteiner , I know we don't always have the most informed general practitioners as they have to cover so many disease possibilities in their wide range of patients. It's good to take a look for ourselves and approach our docs with the studies/info so that we can get better care (and update them too )

canadjineh

'Silent' Celiac Disease Found in Kids at Rheumatology Clinic

Janis C. Kelly
June 15, 2015

"Silent" celiac disease (CD), or CD without gastrointestinal symptoms, was present in 2.0% of children presenting for initial pediatric rheumatology evaluation, researchers from the Hospital for Special Surgery, New York City, report in an article published online June 15 in Pediatrics. The authors say celiac testing should be included in the standard initial laboratory workup for pediatric rheumatology patients, as they found that initiation of a gluten-free diet led to resolution of musculoskeletal symptoms in many of the affected patients.

Yekaterina Sherman, BA, and a research team led by Thomas J. A. Lehman, MD, retrospectively reviewed medical charts and data from standardized serologic screening for 2125 patients (age, 2 - 16 years) who presented for care at the Hospital for Special Surgery, Division of Pediatric Rheumatology, between June 2006 and December 2013. The researchers found that 36 patients had previously unsuspected CD. Together with the eight patients known to have CD at study entry, the prevalence of CD during the 6.5-year study period was 2.0%, or about 1 in 48 patients. Prevalence in the general population was 0.7%.

Thirty of the 36 "silent CD" cases were confirmed by endoscopy. Six refused endoscopy but had significant reduction of symptoms with a gluten-free diet.

"The majority of the newly diagnosed CD cases, 22 out of 36 (61.1%), presented with musculoskeletal complaints alone and none of the classic symptoms of CD, such as abdominal pain, short stature, weight loss, and failure to thrive,” the authors write. “In fact, only 12 patients reported a history of [gastrointestinal]-related complaints." They note that these data provide further evidence that symptom-based case finding will miss the majority of CD cases in children.

Pediatric CD Guidelines Need a Rewrite

The researchers suggest that current clinical guidelines for CD screening published by the American College of Gastroenterology and the North American Society for Pediatric Gastroenterology, Hepatology and Nutrition be revised to include children with musculoskeletal complaints.

Current guidelines do not consider such patients to be a high-risk group and do not specifically recommend screening of this population. The guidelines recommend CD screening for children with failure to thrive, persistent diarrhea, recurrent abdominal pain, constipation and vomiting, dermatitis herpetiformis, dental enamel hypoplasia, osteoporosis, short stature, delayed puberty, iron-deficient anemia, asymptomatic diabetes mellitus, autoimmune thyroiditis, Down syndrome, Turner syndrome, Williams syndrome, selective immunoglobulin A deficiency, and a history of a first-degree relative with CD.

Clinicians using the current guidelines rather than screening all children with musculoskeletal complaints would have missed all but six of the asymptomatic CD cases in the study population. The authors note that prompt detection of CD would not only enable the patient to achieve the benefits of early initiation of a gluten-free diet but also avoid the dangers of unnecessary immunosuppressive therapy.

If CD Is Present, Is This Really Idiopathic Arthritis?

The association between CD and musculoskeletal complaints raised a further interesting question: Is this really "idiopathic arthritis" if it resolves with treatment of CD?

"Our data suggest that there may be a subset of patients with 'silent' CD who present with isolated musculoskeletal symptoms and that perhaps [juvenile idiopathic arthritis] is not an appropriate diagnosis in these cases. Clinicians must be vigilant in cases such as these to evaluate appropriately for CD," the authors note.

The authors have disclosed no relevant financial relationships.

Pediatrics. Published online June 15, 2015.

canadjineh

Comments in italics are mine - otherwise pasted verbatim from Medscape.

Celiac Disease Tied to Autoimmunity Risk in Spouses, Relatives

Ricki Lewis, PhD
July 08, 2015

First-degree relatives and spouses of patients with celiac disease are at increased risk for autoimmune diseases, according to results of a study published online January 30 and in the July issue of Clinical Gastroenterology and Hepatology.

The risk of developing celiac disease is elevated among people who have first-degree relatives with the condition, but little is known about their risk for other autoimmune disorders. Genetics, environmental factors, and ascertainment bias may be at play.

Louise Emilsson, MD, PhD, from the Primary Care Research Unit, Vårdcentralen Värmlands Nysäter, Värmland County, Sweden, and the Department of Health Management and Health Economy, Institute of Health and Society, University of Oslo in Norway, and colleagues conducted a population-based longitudinal cohort study to analyze the risk of developing Crohn's disease, type 1 diabetes mellitus, hypothyroidism, hyperthyroidism, psoriasis, rheumatoid arthritis, sarcoidosis, systemic lupus erythematosus, or ulcerative colitis among the relatives and spouses of 29,096 individuals with celiac disease. The researchers used information on duodenal and jejunal biopsies (villus atrophy) collected from 1969 through 2008 in Sweden.

Each individual with celiac disease was matched with up to five control patients for sex, age, county, and year. Healthcare registries were used to identify all first-degree relatives and spouses of individuals with celiac disease and control patients. The study included 84,648 first-degree relatives and spouses of patients with celiac disease and 430,942 people associated with the control patients.

For all diseases considered, the incidence was higher among relatives and spouses of patients with celiac disease than among controls. During the period assessed (median, 10.8 years), 3333 first-degree relatives of patients with celiac disease (3.9%) and 12,860 first-degree relatives of controls (3.0%) developed a nonceliac autoimmune disease.

Genetic relatives and spouses of people with celiac disease had a similar risk of developing nonceliac autoimmune disorders. The HR for any nonceliac autoimmune disease in relatives of patients with celiac disease was 1.28 (95% CI, 1.23 - 1.33), and the HR in spouses of celiac patients was 1.20 (95% CI, 1.06 - 1.35). The risk of developing nonceliac autoimmune diseases was highest in the first 2 years after diagnosis of the index patients.

The fact that 4.3% of celiac relatives developed nonceliac autoimmune disease compared with 3.3% among relatives of the control group suggests a genetic component to autoimmune susceptibility, but the higher risk among spouses suggests an environmental component. The investigators suggest that the environmental finding might reflect a shared microbiome profile between spouses who eat the same foods.

Ascertainment bias might have arisen from the greater awareness of autoimmune diseases among relatives and spouses of patients with celiac disease, and perhaps by healthcare providers.

A limitation of the study is that the patient register consulted may not have included autoimmune diagnoses handled only in primary care, such as hypothyroidism and hyperthyroidism.

This study was funded by the Swedish Research Council. The authors have disclosed no relevant financial relationships.

Clin Gastroenterol Hepatol. 2015;13:1271-1277. Abstract


(Interesting to note that even spouses can be at risk for increased incidence of Auto-immune Diseases of all sorts, pointing to possible environmental causes)

mmebouchon

Really interesting articles. Thanks for posting them canadjineh.

canadjineh

Italics are my added comments
The American Journal of Gastroenterology

Predictors and Significance of Incomplete Mucosal Recovery in Celiac Disease After 1 Year on a Gluten-free Diet

Henna Pekki, BM; Kalle Kurppa, MD, PhD; Markku Mäki, MD, PhD; Heini Huhtala, MSc; Harri Sievänen, PhD; Kaija Laurila, MSc; Pekka Collin, MD, PhD; Katri Kaukinen, MD, PhD
Disclosures
Am J Gastroenterol. 2015;110(7):1078-1085.


Abstract

Objectives: In celiac disease, a follow-up biopsy taken 1 year after diagnosis is considered important in monitoring histological recovery. In many cases, recovery is incomplete, and the clinical significance of this is poorly understood. We now investigated associated factors and the significance of imperfect histological recovery in patients in whom the follow-up had been completed.

*I have left out some major explanations (4 pages long) about exactly how the tests were administered and all the levels of markers taken*


Discussion

In this large cohort of celiac disease patients who had undergone a follow-up biopsy after 1 year on diet, the most prominent factor predicting incomplete small-bowel recovery was the presence at diagnosis of more severe disease in terms of histology and serology and signs of malabsorption. Further, while mucosal recovery was still ongoing, most of the clinical parameters measured had improved and were already at the same level in the Atrophy and Recovery groups, and the groups also showed no difference in long-term outcomes. Although the patients with incomplete recovery represented one-third of the subjects here, we have shown that in a highly adherent population at least 96% of patients achieve complete recovery on long-term treatment and only 0.3% develop refractory celiac disease.[12,34] In accord with this, only 2.3% of all patients here still showed no signs of histological improvement after 1 year, and only one presented with complications and type I refractory disease. These findings indicate that follow-up biopsy after 1 year correlates poorly with clinical outcome and long-term prognosis, and represents only a 'snapshot' rather than the end point of ongoing mucosal healing.

Altogether, 68% of the subjects evinced morphological mucosal recovery after 1 year on diet, which is in fact a relatively high percentage compared with previous reports.[5,6,9] Nevertheless, it is in line with our previous studies and very likely reflects the generally high dietary adherence in Finland.[4,35] The good availability and strict labeling of gluten-free products and financial subsidization by the government are all likely to reduce inadvertent gluten intake.[36] This was seen in the present study, as both the histologically recovered and non-recovered patients showed, in global perspective, excellent dietary adherence. It is thus evident that, in contrast to many previous reports,[6,10] dietary lapses explained only a small minority of non-responsive cases in this study.

The most conspicuous difference here was in the presence of more severe mucosal damage in the Atrophy group at diagnosis. In accord, Rubio-Tapia et al.[6] discovered an association between the severity of the baseline damage and slow histological recovery. Another recent study[37] showed that patients with less severe atrophy were also more likely to respond to the diet. However, this was the first time a quantitative approach has been used to assess the actual speed (ΔVh/CrD) of villous recovery and it was observed to be lower in the Atrophy group. This slower recovery combined with severe atrophy at diagnosis explains why these patients had not regained normal mucosa during 1 year despite a strict diet. Some studies have indirectly investigated whether the speed of histological recovery is associated with the severity of the baseline damage, but results have been controversial.[5,6,9,15,37,38] This might be explained by differences in dietary adherence and by the use of inexact grouped classifications (e.g., Marsh) in histology.[16]

Another indicator of the presence of more severe disease in the Atrophy group at diagnosis was their higher levels of TG2ab, even if these antibodies are poor predictors of the severity of histological and clinical findings in individual patients.[9,15,22] TG2ab also remained at a higher level in the incompletely recovered patients after 1 year, with the difference, however, being small and the median values in both groups falling within normal limits. Further, most of the patients in the Atrophy group also became seronegative, indicating that the disappearance of the antibodies occurs faster than the healing of the mucosa.

Of clinical presentations, the presence of malabsorption was associated with histological non-recovery. This was most evident in the lower levels of iron as well as hemoglobin in the Atrophy group. These results, together with the lower BMD T-scores also observed, probably reflect insufficient absorption of nutrients in patients with severe villous atrophy. Previous studies have likewise found a correlation between the presence of anemia at diagnosis and more severe histological and clinical presentation.[18,39,40] Despite the differences in mucosal healing, after 1 year all laboratory values, excluding a minor difference in hemoglobin, were comparable in both groups. This demonstrates that, as with serology, on treatment laboratory values improve faster than the mucosa. In contrast, BMD, although improved, still remained lower in the Atrophy group after 1 year on diet. Obviously, normalization of BMD takes more than 1 year to complete.

Similar to most of the other clinical parameters, we found no association between self-perceived symptoms and quality of life and mucosal recovery at follow-up. In fact, there was no significant difference between the groups even at diagnosis, this probably reflecting the high individual variation in these respects. On the contrary, there was a trend toward poorer GSRS and PGWB values at baseline in the Atrophy group, whereas after 1 year the results were practically identical. These findings further indicate that histological healing lags behind clinical recovery.

The poor correlation between histological recovery and other outcomes indicates that a follow-up biopsy taken after 1 year is not an optimal approach in monitoring celiac disease. Our long-term follow-up results support this view, as there were no differences between the groups in mortality and other complications or in gastrointestinal symptoms and quality of life. Then again, although their prevalence remains unclear, the risk of severe complications in the long run has been associated with incomplete mucosal recovery and warrants careful follow-up.[4,10,41] Unfortunately, there are currently no sensitive surrogate markers for ongoing mucosal damage, and endoscopic investigations are still needed.[15] Nevertheless, here only 1 out of 87 subjects evincing incomplete recovery after 1 year presented with complications, suggesting that in almost all cases it is merely a question of slow mucosal healing. Our results support the need to individualize the current procedures, taking into account both the baseline severity of the disease and the dietary response. Whether a routine follow-up biopsy is mandatory for all patients who have uncomplicated celiac disease with good clinical response is a subject for future studies.

Major strengths of this study are the large number of patients and the diversity of outcomes measured, and the use of validated questionnaires. Further, the fact that follow-up biopsies were taken systematically after 1 year and were analyzed by quantitative Vh/CrD reduces the risk of misclassification bias.[16] We were also able to collect a substantial body of long-term follow-up data regarding mortality and other complications.[6] The high dietary adherence in our cohort enabled us to evaluate other causes behind non-recovery than the usually dominating poor compliance; however, the results may not be directly applicable to countries where dietary lapses are common.[42] A limitation is that we were not able to compare subjects consenting to follow-up biopsy and those who refused (~15% of subjects in our center). This may cause bias as non-compliant patients may be more prone to refuse, and lack of follow-up biopsy has also been associated with increased mortality.[43] Also, no systematic follow-up was undertaken for those with incomplete recovery, as in our settings patients with uncomplicated disease are assigned to primary health care for further follow-up. Nevertheless, according to our clinical practice patients with persistent atrophy would have been referred to us for further investigations. Finally, as the study was initiated before routine biopsies from the duodenal bulb were recommended,[3] they were not systemically taken, and thus some cases with lesion only in the bulb might have been missed.[44]

In conclusion, we showed that only the presence of more severe disease in terms of histology and serology were associated with incomplete histological recovery at the follow-up biopsy. Moreover, differences in the speed of mucosal healing were not reflected in the short- or long-term clinical outcomes. Based on these findings a more personalized approach should be adopted when deciding the optimal timing of the histological follow-up. One year is often too short a time for the mucosa to recover, and postponing the biopsy, e.g., for another year,[45] would presumably result in lower number of cases with ongoing atrophy.


***Soooo, it just goes to show you that it takes a LONG time of complete adherence to actually have mucosal recovery, although you will feel clinically better before then.***

lithezebra

Among other things, it's important to eat vegetables, and fruit if you can afford the carbs, to get your fiber, not just start eating a lot of starchy gluten free grains as a substitute for more nutritious foods.

canadjineh

lithezebra wrote: »

Among other things, it's important to eat vegetables, and fruit if you can afford the carbs, to get your fiber, not just start eating a lot of starchy gluten free grains as a substitute for more nutritious foods.

Very true! Best to get increased proteins, veggies and fruits than to sub in a bunch of grains.

canadjineh

New Article from Medscape (good to provide link for your gastroenterologist or GP for the complete site). This could help those who need to be tested for CD but who have already been on a GF diet.
link: http://www.medscape.com/viewarticle/849368

Clinical Gastroenterology and Hepatology
Celiac Disease: Ten Things That Every Gastroenterologist Should Know
Amy S. Oxentenko; Joseph A. Murray
Disclosures
Clin Gastroenterol Hepatol. 2015;13(8):1396-1404.

5. How Does One Evaluate for Celiac Disease in a Patient on a Gluten-free Diet?

With increasing frequency, patients start a GFD before testing for CD.[39] With data showing that patients with diarrhea-predominant irritable bowel syndrome may benefit from a GFD[40,41] and because of the media focus on a GFD, the trend will continue. Although there is little harm beyond cost to a patient on a balanced GFD, CD may be overlooked and complications ignored.

Ideally, patients who self-initiated a GFD should be evaluated for CD. First, determine the patient's willingness to resume gluten intake for testing. In the patient who refuses to resume eating gluten, this poses a challenge. The sensitivity of serology and histology diminishes with longer duration on a GFD.[2] Although serology could be checked first,[42] a positive result is the only helpful result and indicates duodenal biopsies are needed. However, if the patient has been on a GFD for less than 1 month, begin with serology because the yield may be reasonable in this period.[3] In the patient on a prolonged GFD, HLA haplotyping can be done first. Although 30%–40% of the normal population will be positive for HLA DQ2 or DQ8,[43] the absence of permissive genes will allow 60%–70% of patients to be reassured that CD is ruled out. A gluten challenge should be discussed for those carrying HLA DQ2 or DQ8 before further testing.

In the past, a gluten challenge entailed consumption of 8–10 g gluten daily for 4 weeks.[30] However, as little as 3 g gluten daily for 2 weeks will allow 75% of patients to meet diagnostic criteria for CD.[42] For those intolerant to the gluten challenge after 2 weeks, serology and duodenal biopsies should be performed. In patients tolerating gluten ingestion after the 2-week period, the challenge should continue 6 additional weeks, with serology performed after the 8-week challenge. If serology is positive, then duodenal biopsies are done. If seronegative, repeat serology after 2–6 additional weeks because a delayed rise in serologic titers may occur.[42]

Practical Suggestion

In patients requiring an evaluation for CD while on a GFD, testing for the presence of HLA DQ2 or DQ8 identifies those requiring further testing. In patients positive for HLA DQ2 or DQ8 and not highly sensitive to gluten ingestion, testing after a low-dose (3 g daily) gluten challenge for 6 weeks may suffice to diagnose CD.

Azuriaz

The first one is my favorite, having sampled many gluten free foods while at the home of a celiac family member. Many of the chips and chocolates are far tastier than the run of the mill gluten containing varieties. I'd be so fat on a gluten free processed food diet!

So this:

"This shows the importance of keeping your BMI down by eating foods that are naturally gluten free and quality sources of nutrition (like fresh vegetables & fruits, lean meats, fish, eggs, & legumes) as opposed to eating commercially prepared 'substitute foods' like GF pizzas, cookies, cakes, breads, etc."

canadjineh

New article in my Medscape:
Alimentary Pharmacology & Therapeutics

Factors Governing Long-term Adherence to a Gluten-free Diet in Adult Patients With Coeliac Disease

J. Villafuerte-Galvez; R. R. Vanga; M. Dennis; J. Hansen; D. A. Leffler; C. P. Kelly; R. Mukherjee

Authors and Disclosures

J. Villafuerte-Galvez, R. R. Vanga, M. Dennis, J. Hansen, D. A. Leffler, C. P. Kelly & R. Mukherjee

Celiac Center, Division of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA.

Correspondence to
Dr R. Mukherjee, Celiac Center, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA 02215, USA. E-mail: rmukherj@bidmc.harvard.edu

Aliment Pharmacol Ther. 2015;42(6):753-760.

Abstract

Background A strict gluten-free diet is the cornerstone of treatment for coeliac disease. Studies of gluten-free diet adherence have rarely used validated instruments. There is a paucity of data on long-term adherence to the gluten-free diet in the adult population.

Aims To determine the long-term adherence to the gluten-free diet and potential associated factors in a large coeliac disease referral centre population.

Methods We performed a mailed survey of adults with clinically, serologically and histologically confirmed coeliac disease diagnosed ≥5 years prior to survey. The previously validated Celiac Disease Adherence Test was used to determine adherence. Demographic, socio-economic and potentially associated factors were analysed with adherence as the outcome.

Results The response rate was 50.1% of 709 surveyed, the mean time on a gluten-free diet 9.9 ± 6.4 years. Adequate adherence (celiac disease adherence test score <13) was found in 75.5% of respondents. A higher level of education was associated with adequate adherence (P = 0.002) even after controlling for household income (P = 0.0220). Perceptions of cost, effectiveness of the gluten-free diet, knowledge of the gluten-free diet and self-effectiveness at following the gluten-free diet correlated with adherence scores (P < 0.001).

Conclusions Long-term adherence to a gluten-free diet was adequate in >75% of respondents. Perceived cost remains a barrier to adherence. Perceptions of effectiveness of gluten-free diet as well as its knowledge, are potential areas for intervention.

The cornerstone of recommended treatment for CeD is the strict, complete and lifelong elimination of gluten from the diet and nondietary sources.[6] Clinical and histological remission through strict adherence to the gluten-free diet (GFD) has been associated with improvements in nutritional deficiencies, depression[7] and infertility[8] as well as a decrease in the risk of osteoporosis[9,10] and gastrointestinal malignancies.[11] Although the GFD is proven to be a safe and effective therapy, it is not ideal. The GFD is typically more expensive than a non-GFD, not readily available in many settings and often of suboptimal nutritional value.
** (my personal comments) I don't quite agree with this - it is a healthier diet higher in fresh fruits & veggies and quality proteins... IT IS THE SUBSTITUTION OF PROCESSED GF FOODS FOR 'REGULAR PROCESSED FOODS' THAT IS EXPENSIVE... but that is totally unnecessary.**
In addition, patients often report that the GFD is restrictive and difficult to follow especially when eating away from home. All of these factors can significantly impact adherence.[12,13] In fact, in one recent study, patients with CeD reported that the burden of treatment with the GFD was similar or higher to that of type I diabetes mellitus.[14]

Study Population

Patients aged 18 years or older with a definite diagnosis of CeD based on a combination of their clinical presentation, positive antibodies (tTG-IgA, AGA and EMA) and a duodenal biopsy with findings consistent with Marsh I to Marsh III categories were selected from the Institutional Review Board (IRB)-approved Celiac Center Patient and Serum Databases (PSDB) at Beth Israel Deaconess Medical Center (BIDMC), Boston, MA. This database includes all patients with a diagnosis of CeD that have received clinical care at the BIDMC Celiac Center at least once since 1990. For this study, only patients who had been on a GFD for a minimum of 5 years were included. This study was approved by the IRB.

Response to Survey

We mailed the survey to 709 subjects. At the end of the collection period, 355 (51.1%) subjects had responded to the survey. The distribution of socio-demographic and clinical variables between respondents and nonrespondents is shown in Table 1. Respondents and nonrespondents differed significantly only for having a tissue transglutaminase IgA antibody assay available around the time of the survey. They, nonetheless, did not differ significantly for frequency of serological normalisation.

Adherence to the GFD

Among the respondents, 75.5% had adequate GFD adherence (CDAT score ≤13). The mean time on a GFD was 9.9 ± 6.4 years and the mean CDAT score for all the respondents was 10.9 ± 3.7. See Figure 1 for distribution of CDAT scores. The average time on a GFD did not differ significantly between the respondents who were adequately adherent and the respondents who were inadequately adherent. Achieving serological normalisation, defined as a tTG IgA antibody around the time of the survey below 20, was significantly more frequent (P = 0.012) in patients with adequate GFD adherence (87.2%) as compared to those with inadequate adherence (66.7%).

Socio-demographic and clinical variables that were acquired through the survey and our clinical database were compared between subjects above and below the cut-off score of 13 for CDAT as reported in Table 2. The level of education differed significantly between the subjects with adequate and inadequate adherence (χ2 test, P = 0.002). Furthermore, a significant inverse correlation was found between the CDAT score and the education level (Spearman ρ = −0.1304, P = 0.0136) as illustrated in Figure 2. This finding remained significant after adjustment for median household income (P = 0.0220). No other socio-demographic variables were associated with an adequate or inadequate GFD adherence.

Patient Perception Affecting GFD Adherence

The four factors hypothesised to be correlated with adherence based on previously published reports[20–26] were: (i) the cost of a GFD, (ii) the perceived effectiveness of a GFD, (iii) the perceived knowledge of the GFD and (iv) the perceived self-effectiveness at following a GFD. A statistically significant correlation was found between all four factors and the CDAT score (Table 3). Respondents were divided regarding cost as a limiting factor in GFD adherence – nearly 40% of respondents strongly or somewhat agreed of whom 65.9% had adequate adherence. In contrast, more than 50% strongly or somewhat disagreed that cost was a factor limiting adherence of whom 83.6% had adequate adherence. Interestingly, there was a marginally significant correlation (P = 0.039, ρ = 0.1116) between agreement that cost is a barrier to GFD adherence and having a lower median household income. Over 80% (219/260, 84.2%) of the respondents that classified their knowledge of the GFD as good or excellent had adequate adherence vs. about 50% (46/91, 50.5%) of those who classified their knowledge of the GFD as fair to poor. Close to 80% of respondents considered the GFD to help with their symptoms, and over 85% of these respondents were found to have adequate adherence. In contrast, close to 20% who were unsure or felt that the GFD did not improve their symptoms, nearly 50% (49.3%) were adequately adherent.

Of these four factors, the two that showed the strongest correlation with adherence were self-effectiveness (ρ = −0.3733) and knowledge of the GFD (ρ = 0.3561). We further assessed whether the level of education was correlated with the perceived knowledge of the GFD and found this correlation to be significant (P = 0.0077, ρ = −0.1440) as illustrated in Figure 3. However, after correcting for education level, the perceived knowledge of the GFD remained correlated with the CDAT score (adjusted P < 0.001).

Discussion

When measuring adherence to a GFD, factors such as a protracted learning curve or patient's perception of increased burden of treatment could render initial measurements of adherence during the first years after diagnosis unrepresentative of lifelong adherence. Therefore, measuring adherence in the long-term is likely a more representative marker of ongoing and future adherence. No known previous US study has directly addressed the question of long-term GFD adherence, specifically, more than 5 years after CeD diagnosis.

Our study is, to the best of our knowledge, the largest long-term GFD adherence study in the USA. We found an adequate adherence rate of 75.5% with 24.5% not adhering closely to the diet. Our adequate adherence rate is consistent with rates of 75.8% in a prior study with our institution's Celiac Center patients.[26] Canadian population studies in adult patients with CeD have found adherence rates between 68% and 90%, consistent with our study's findings.[13] However, in the literature, the adherence rates vary from 33.7%[22] to 95%.[23]

This study explored a number of key factors correlated with GFD adherence. The issue of cost as a barrier to GFD adherence has been described previously. A US study in 2007 found that on average a standard gluten-free 'product basket' was 240% more expensive than its gluten-containing counterpart. A similar study in the UK in 2011 found that 11 of 19 gluten-free products studied were significantly more expensive than their gluten-containing counterparts. Also, the price of the gluten-free products was at least 2% but as high as 518% more expensive than their gluten-containing counterparts.[24,25]
**see my comments in italics concerning this earlier in the article**

Our patient population is almost evenly divided on whether they consider cost to be an obstacle to adherence. The cohort of respondents that considered cost to be a limiting factor for adherence have significantly higher CDAT scores and lower rates of adequate adherence. Nevertheless, respondents with an adequate adherence did not have significantly different median annual household income as compared to respondents with inadequate adherence. This finding raises the question of whether perception of cost vs. actual economic limitation is an obstacle to GFD adherence.

Another key factor that was explored in this study was education and the perception of knowledge of the gluten-free diet as factors in adherence. A higher education level was correlated with better adherence independent of median household income. A higher education level was also associated with better self-perceived knowledge of the GFD. Nonetheless, respondents' perceived knowledge of the GFD remains independently correlated with better adherence even after correcting for education level. These findings may translate into clinical practice by providing patients with self-perceived poor or fair knowledge of the GFD with increased dietary counselling regardless of the patient's education level.

Our findings of a higher proportion of serological normalisation in patients with adequate adherence as compared to those with inadequate adherence are consistent with previous findings[27] that support that adherence to the diet is key for serological normalisation or clinical improvement. However, serology cannot be reliably used as a marker of adherence to a GFD in patients with CeD.

Factors such as patient age, gender, time on a GFD and median household income were not associated with GFD adherence. These findings bring to light the challenge of designing proven, cost-effective strategies to improve long-term GFD adherence in the poorly adherent population. Future studies should focus on developing and testing interventions for this non-adherent group. Such interventions might target increased knowledge of the GFD and perceptions of the importance of close adherence.


**I've left out details of Data Collection & Statistical Analysis as it was not needed unless you are designing a study yourself**

canadjineh

Reuters Health Information

Overweight Not Unusual in Kids With Celiac Disease

By Laura Newman
November 09, 2015

NEW YORK (Reuters Health) - Celiac disease can't be automatically ruled out in children who are overweight or obese, Italian researchers confirm.

They found that 7.8% of kids with celiac disease in their cohort were overweight at diagnosis.

"Being overweight/obese shall not induce clinicians to exclude CD without testing," Dr. T. Capriati, from the Gastroenterology and Hepatology Unit, Children's Hospital, Rome and colleagues wrote in a paper online October 28 in the European Journal of Clinical Nutrition.

Furthermore, a gluten-free diet (GFD) was not linked to a significant rise in overweight/obesity at follow-up. Gender differences were also identified, with boys having a much higher rate of overweight/obesity than girls. Overweight/obese children in the study tended to be significantly older and had significantly lower levels of tissue anti-transglutaminase-IgA (tTG-IgA) antibodies.

In the study, Dr. Capriati and colleagues reviewed the charts of 445 consecutively diagnosed CD patients, including 156 boys, with a median age of six years. At diagnosis, overweight/obese kids had a median age of 6.8 years versus 3.3 years for kids with normal BMI, and significantly lower levels of tTG antibodies (101 vs. 279).

After patients were put on a gluten-free diet, very few became overweight during follow-up - an additional 2% from baseline. "Thus, GFD is not associated with the risk to develop overweight or obesity in the medium long-term of the follow-up," the authors wrote.

Dr. John Leung, Director of the Food Allergy Center at Tufts Medical Center in Boston, wasn't surprised by the findings.

"I do not disregard overweight patients and I have a very low threshold to screen for celiac disease," he said. "I screen if I see GI symptoms and do not overlook overweight patients."

The authors reported no disclosures and did not respond to a request for comment.

SOURCE: http://bit.ly/1XV4zZo

Eur J Clin Nutr 2015.

mmebouchon

Your articles are very informative. Thank you so much for continuing to post them. I wish my doctor had know even half of this info years ago.