Medscape (Medical Professionals' Continuing Ed site) Celiac Disease/Gluten Sensitivity articles
canadjineh
Posts: 5,396 Member
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.
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.
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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.
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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.
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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
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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.
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These are all really interesting thanks for posting them.1
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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
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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.
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Wow. Canadjineh you rock! Very helpful articles! Thanks0
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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 toodalansteiner wrote: »Wow. Canadjineh you rock! Very helpful articles! Thanks
)
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'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.
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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)
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Really interesting articles. Thanks for posting them canadjineh.0
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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.***
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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.0
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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.
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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.
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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."0 -
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**1 -
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.
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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.
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From my Medscape inbox - although it is a year old I hadn't noticed online before.
Current Screening Guidelines Fail to Identify Celiac Disease
Fran Lowry
January 13, 2014
Current guidelines for detecting undiagnosed celiac disease (CD) are inadequate for widespread CD screening, according to results from a study published online January 13 in Pediatrics.
Current guidelines rely on asking children about disease symptoms, but in a population-based screening study, researchers found that questionnaire data on symptoms did not differ significantly between individuals ultimately diagnosed with CD and those without the disease.
"Several studies have presented active case-finding strategies and concluded that they are effective by showing an increased incidence of CD in the group subjected to the case-finding, both in the clinical setting and at a population-based level," write Anna Rosén, MD, PhD, from Umeå University, Sweden, and colleagues. "However, these earlier studies have limitations because control groups were lacking, and the sensitivity, specificity, and predictive values of the suggested strategies therefore remain to be evaluated."
Therefore, in the current study, the authors aimed, first, to describe the symptoms and conditions associated with CD among screening-detected CD cases and children without CD as reported before CD status was known, and second, to evaluate questionnaire-based case-findings targeting the general population.
The study included children from 5 regions across Sweden who were 12 years old and in the sixth grade.
In the population-based screening, 7054 (98%) of the children and 6294 (88%) of their parents completed questionnaires on the frequency of CD-associated symptoms and conditions, which included tiredness, poor appetite, nausea, stomachache, upset stomach, abdominal gas, bloating, hard stools, loose stools, and lactose intolerance.
Parents also reported on the presence of CD-associated disorders in their child. These included anemia, type 1 diabetes, thyroid disease, rheumatic disease, inflammatory bowel disease, vitiligo, alopecia areata, dermatitis herpetiformis, trisomy 21, and Turner syndrome, as well as the presence of CD among the child's first-degree relatives.
Of 7208 children tested for tissue transglutaminase–immunoglobulin A or tissue transglutaminase–immunoglobulin G, the investigators found 192 (2.7%) with elevated levels.
Of those, 153 (2.1% of the total sample) tested positive for CD in a confirmatory small-bowel biopsy.
However, when the investigators compared questionnaire responses from children with screen-detected CD and those without, they found no significant difference in frequency (2.1% vs 2.1%; P = .930). Similarly, they found no significant difference in the frequency of CD-associated conditions (3.6% vs 2.1%; P = .07).
"Case-finding by asking for CD-associated symptoms and/or conditions would have identified 52 cases (38% of all cases) at a cost of analyzing blood samples for 2282 children (37%) in the study population," they write.
The sensitivity of this case-finding questionnaire was 38%, the specificity was 63%, the positive predictive value was 2%, and the negative predictive value was 98%.
"Our findings indicate that a questionnaire concerning symptoms cannot be used to discriminate unrecognized CD children from their non-CD peers, which is in line with a recent CD screening study in adults in the United States," the authors write.
The new study raises many questions and adds a layer of complexity to identifying children with CD, according to Dr. Baker. For example, if symptoms cannot be used to identify candidates for screening, what can be used? "With the relatively high prevalence [of CD], should all children be screened? If so, at what age? Are repeat screenings necessary because CD can present at any age, and if so, at what intervals? Is it ever justifiable to place a child with gastrointestinal symptoms on a gluten-free diet without clearly making a diagnosis of CD?"
Dr. Baker emphases that this last question is important because some experts now advocate a trial of a gluten-free diet for children with gastrointestinal symptoms.
"This study...raises important questions, suggests recommendations for screening of CD be revisited, and further suggests that care be taken in prescribing a gluten-free diet when a diagnosis of CD has not been made," she concludes."
The study was funded by the European Union; the Swedish Research Council; the Swedish Research Council for Environment, Agricultural Sciences, and Spatial Planning; the Swedish Council For Working Life and Social Research; and the County Council of Västerbotten. The authors and Dr. Baker have disclosed no relevant financial relationships.
Pediatrics. Published online January 13, 2014.
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New Article (partial quotes from a 4 page commentary)
COMMENTARY
Should We All Go Gluten-Free?
William F. Balistreri, MD
Disclosures | February 04, 2016
A recent report by Fasano and colleagues[8] reviewed the current understanding of NCGS and outlined steps to dissipate some of the confusion related to this disorder. They propose a working definition as follows: "a clinical entity induced by ingestion of gluten leading to intestinal and/or extraintestinal symptoms that resolve once gluten is eliminated." This definition requires that celiac disease and wheat allergy have been ruled out. They further propose that NCGS is associated with prevalent gluten-induced activation of innate—rather than adaptive—immune responses in the absence of detectable changes and mucosal barrier function. Gluten sensitivity was similarly defined by an international panel as the occurrence of intestinal and extraintestinal symptoms related to the ingestion of gluten-containing food in subjects without celiac disease or wheat allergy.[18-21]
Fasano and colleagues[8] emphasized a need for better understanding of the role of gluten and wheat in irritable bowel syndrome (IBS), chronic fatigue syndrome, and autoimmunity, with precise nomenclature and definitions. In the absence of intestinal injury, specific antibodies, or any other biomarker, there is a clear need for an optimal diagnostic algorithm and consensus-based diagnostic criteria.[20]
Relationship to Irritable Bowel Syndrome
Individuals with gluten sensitivity have an increased prevalence of fulfilling the Rome III criteria for IBS.[1,22] It is not uncommon for patients with IBS to report improvement in clinical symptoms when gluten intake is restricted.
A series of studies have investigated the response to gluten in patients with IBS in whom celiac disease has been excluded. Wahnschaffe and colleagues[33] noted an improvement in patient-reported outcomes following institution of a gluten-free diet, including a decrease in the frequency of bowel movements, in patients with diarrhea-predominant IBS in whom celiac disease had been excluded.
Biesiekierski and colleagues[34] also studied patients with IBS who were proven not to have celiac disease and whose symptoms were under control on a gluten-free diet. Participants in this randomized trial were asked to eat a muffin containing gluten or a placebo of identical taste and texture. They found that symptoms were present in 68% of those ingesting gluten compared with 40% of those receiving a gluten-free product.
Vazquez-Roque and colleagues[35] studied 45 patients with diarrhea-predominant IBS who had no history of gluten avoidance. They were randomly assigned to receive either a gluten-free or a regular diet. Those on the gluten-containing diet had more frequent bowel movements.
FODMAPs
Several investigators have proposed a role for poorly absorbed carbohydrates in the genesis of the clinical symptoms. Intake of fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAPs) can trigger gastrointestinal distress.[39,40] These carbohydrates are poorly absorbed from the small intestine and thus enter the colon, where they osmotically increase luminal water, produce short-chain fatty acids, and induce gas production through fermentation by colonic bacteria. This leads to luminal distension, gas, and bloating. FODMAPs may also affect the microbiota, immune function, and the barrier of the gut, which might also generate gastrointestinal symptoms.[40] A diet with reduced FODMAPs has been reported to be effective in the treatment of patients with IBS.
Nonceliac Wheat Sensitivity
Carroccio and colleagues[47] reviewed data on 276 patients diagnosed to have NCWS by means of double-blind, placebo-controlled wheat challenge. NCWS was characterized by a personal childhood history of food allergy, coexistent atopic diseases, positive serum anti-gliadin and anti-beta lactoglobulin antibodies, positive cytofluorimetric assay revealing in vitro basophil activation by food antigens, and a presence of eosinophils in the intestinal mucosa biopsies. Patients with NCWS and multiple food sensitivities showed several clinical, laboratory, and histologic characteristics that suggest they might be suffering from a non-IgE-mediated food allergy.
The current clinical approach involves ruling out celiac disease and wheat allergy, testing for additional food intolerances or gastrointestinal conditions, and providing the latest data on the benefit/unintended consequences of gluten avoidance and these evolving entities.[50] It is also important to inform patients and their families about what is not known. It may also be effective to individualize the recommended dietary strategy by eliminating certain components of the FODMAP class, wheat products, and/or gluten sequentially.
Because there is no specific biomarker for NCGS, the diagnosis is "confirmed" by dietary elimination, followed by double-blind, placebo-controlled gluten-based re-challenges. This is a cumbersome, time-consuming, and difficult-to-access clinical approach. Even with this information at hand, the diagnosis of NCGS may remain unclear, raising the question of whether the salutary effects of gluten withdrawal are specifically attributed to the gluten-protein per se or to nongluten components such as fermentable carbohydrates and amylase-trypsin inhibitors.[49]
Khabbani and colleagues[51] reviewed records from 238 patients who presented for the evaluation of symptoms responsive to gluten restriction without prior exclusion of celiac disease. Of these study subjects, 42% had celiac disease and 52% had NCGS; the remainder had an indeterminate diagnosis. The majority (67%) of subjects with celiac disease presented with symptoms of malabsorption, compared with 25% of the NCGS subjects. In addition, those with celiac disease were significantly more likely to have a family history of celiac disease, personal history of autoimmune diseases, or nutrient deficiencies.
On the basis of these findings, the authors proposed a diagnostic algorithm to differentiate celiac disease from NCGS.[51] They state that subjects with negative celiac serologies (IgA tTG or IgA/IgG DGP) ingesting a gluten-containing diet are unlikely to have celiac disease. Those with negative serology who also lack clinical evidence of malabsorption and risk factors for celiac disease are highly likely to have NCGS and may not require further testing. Those with equivocal serology should undergo HLA typing to determine the need for biopsy.
Guandalini and colleagues[48] proposed assessment of the levels of gamma delta T-cell receptors in intraepithelial lymphocytes (which are specific for celiac disease) or detection of IgA anti-tissue transglutaminase antibody deposits in intestinal mucosa in order to more clearly exclude celiac disease in problematic cases.
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Reuters Health Information
D1 Biopsy Helps Spot Ultra-Short Celiac Disease
By David Douglas
February 18, 2016
NEW YORK (Reuters Health) - Additional biopsy collection from any site in the duodenal bulb (D1) increases conventional celiac disease diagnosis yield and aids detection of ultra-short celiac disease (USCD), according to U.K. and U.S. researchers.
In a paper online January 30 in Gastroenterology, Dr. Peter D. Mooney of Royal Hallamshire Hospital, Sheffield, and colleagues note that celiac disease is underdiagnosed in general and D1 may be the only site of villous atrophy in newly diagnosed celiac disease. However, this approach is not yet fully accepted for reasons including very limited experience.
To investigate further, the team prospectively studied more than 1,300 patients who underwent endoscopy. Routine duodenal biopsies were collected from D1 and the second part of duodenum (D2).
In all, 268 patients (19.4%) were diagnosed with celiac disease and 171 underwent quadrantic D1 biopsy. Of these, 65 patients (38%) were diagnosed with celiac disease.
Twenty-six patients had villous atrophy confined to D1 and were diagnosed with USCD. Of these, seven had entirely normal D2 biopsies. Collection of a single additional biopsy from any D1 site, say the investigators, increased the sensitivity of celiac disease detection by about 10%.
Patients with USCD were significantly younger, had lower titers of tissue transglutaminase antibody, and less frequently presented with diarrhea. The conventional celiac disease group were significantly more likely to have ferritin or folate deficiency than the USCD group or controls.
All patients diagnosed with USCD and conventional celiac disease received specialist dietetic advice. After a median of about 15.5 months, there was no significant difference between the median symptom improvement scores between USCD and conventional celiac disease patients on a gluten free diet.
The researchers speculate that, "Perhaps USCD represents the next step in the development of a more extensive enteropathy. Further study may identify which patients require long term follow up for now however USCD and conventional celiac disease patients should be treated as part of the spectrum of the same disease and receive standard follow up."
Commenting on the findings by email, Dr. Carolina Sousa of the University of Seville, Spain, told Reuters Health, "Patients with USCD would be prone to lack of a correct diagnosis due to concentration of findings just at the D1 portion of duodenum."
Dr. Sousa, who has conducted research in the field, added that "the authors provide evidence of potential endoscopy bias and note that its reduction could eliminate misdiagnosis. Specimens from the proximal duodenum are encouraged."
Dr. Mooney did not respond to requests for comments.
SOURCE: bit.ly/1TnGhX5
Gastroenterology 2016.
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Finally a new MedScape post in my in box that deals with celiac disease, NCGS, allergies.
Key Primary Care Takeaways: Digestive Disease Week 2016
David A. Johnson, MD
Sleep Fragmentation and the Gut Microbiome
"The last study that I wanted to bring to your attention was a very fascinating study looking at the effects of sleep fragmentation on the gut microbiome.[12] You can't pick up a journal of any sort, primary care or specialty, and not see something about the gut microbiome.
This particular study looked at the effects of sleep on the gut microbiome and potential effects on immune function. This was a mouse study where they fragmented the sleep of mice and they looked at the microbiome, comparing with a control population of mice without sleep fragmentation. What is very interesting is that there is actually a circadian rhythm in the gut. In the course of the normal day, there is undulation, but a return to baseline from the day before. When they fragmented the sleep of these mice, they actually inverted this rhythm. Instead of a nice undulating clock-like mechanism, they found profound dysbiosis. We know that sleep fragmentation changes gut permeability, but we also can say that the gut is the largest immune system. They also looked at the mesenteric lymph nodes and their gene arrays that encode for the integrity of the gut wall—so, cytokines and chemokines that upregulate the integrity of the gut wall. These gene arrays were all inhibited. There was a major reduction in their viability, and they were basically downregulated.
Certainly when talking about immune function, we need to remember to talk to patients about sleep function. This is really a big wakeup call for us, as it starts to relate to gut dysbiosis and when patients are not responding to treatment. We need to take a good sleep history and talk to the patient about how they sleep and how they feel the next day when they get up. Sleep function is going to be really important as we start to tie this with the role of dysbiosis of the gut microbiome in virtually all diseases.
I wanted to give you a 30,000-foot view of the data that I thought were newsworthy from DDW 2016. You'll see more on these topics as the articles start to appear in in the literature, but I wanted to give you these updates that will hopefully steer you well in your next patient interactions."1 -
Some Non-celiac Gluten Sensitivity Patients May Have 'Celiac Lite' Disease
July 29/16
NEW YORK (Reuters Health) - A subset of patients with non-celiac gluten sensitivity (NCGS) may actually have a form of celiac disease, researchers in Spain report.
"The differential diagnosis of 'minor' forms of celiac disease and NCGS is difficult," Dr. Fernando Fernandez Banares of the University Hospital Mútua de Terrassa told Reuters Health by email. A diagnosis of NCGS requires ruling out celiac disease on the basis of negative celiac serology and a duodenal biopsy of normal villi (no villous atrophy) in a person who is currently on a diet that contains gluten, he explained. But those diagnostic criteria may need to be revisited.
Dr. Banares and colleagues conducted a small proof-of-concept study that aimed to demonstrate that gluten can trigger clinical symptoms in a subgroup of patients who currently fulfill the diagnostic criteria NCGS. Recent trials suggest that only a minority of those patients will exhibit symptoms in response to a gluten challenge, the authors note in PloS One, online July 8.
At the time of NCGS diagnosis, the 18 participants had all been on a gluten-containing diet, with lymphocytic enteritis on distal duodenum biopsy and gastrointestinal symptoms that fell within the clinical spectrum of celiac disease - but they had negative celiac disease serology. In addition, they all had genes that predispose to celiac disease (HLA-DQ2.5 and/or HLA-DQ8 haplotypes).
Other causes of lymphocytic enteritis such as parasitic infection, NSAID intake or Helicobacter pylori infection had been ruled out.
All participants also had clinical and histological remission after at least a year on a gluten-free diet.
Eleven patients were randomly assigned to take a sachet of 10 grams of gluten twice daily for six months; the other seven patients took placebo sachets twice daily.
In the gluten-challenge group, 10 patients (91%) had a clinical relapse within the first two weeks; including seven who "were prematurely withdrawn because of intolerable symptoms." By comparison, only two patients (28.5%) relapsed in the placebo group (p=0.01).
Clinical scores and quality of life worsened after gluten, but not after placebo (p<0.01).
"Since these patients (the 91%) were characterized by gastrointestinal clinical symptoms within the clinical spectrum of celiac disease, presence of HLA-DQ2/8+, Marsh stage 1 lesion (increased intraepithelial lymphocytes but no villous atrophy), and a clinical and histological response to a gluten-free diet, the question remains as to whether this condition should be considered a 'minor' or 'low-grade' celiac disease (also called 'celiac lite' by some authors) or NCGS," Dr. Banares said.
"Previous studies have shown that the intraepithelial lymphocyte (IEL) count and/or the presence of anti-transglutaminase (TG2) deposits in the mucosa are biomarkers of celiac disease," he continued. "In the present study, these tissue celiac markers were present in around 55% of patients at inclusion, despite their being on a gluten-free diet, suggesting a 'celiac lite' disease."
He added, "Previous studies of celiac disease with (villous) atrophy have shown a permanent increase in IEL, even after a gluten-free diet, (suggesting) that this marker may provide a clue for celiac disease diagnosis and offering the possibility of identifying celiac disease patients when they are on a gluten-free diet, even when histological examination of the biopsy shows recovered mucosa."
"This 'proof of concept' study suggests that there is a 'minor' form of celiac disease with negative celiac serology that should be taken into account in the differential diagnosis of NCGS. The presence of increased IEL count and/or TG2 deposits in the mucosa could be of help in the diagnosis of these patients," Dr. Banares observed.
"We are routinely using this diagnostic strategy in our outpatient clinic, and we think that the intraepithelial lymphogram study adds important information to the diagnostic work-up of these patients. Our recommendation is to use it in clinical practice," he concluded.
Commenting by email, Dr. Gina Sam, director of the Gastrointestinal Motility Center at the Mount Sinai Hospital in New York City said, "This study suggests that patients who do not have celiac disease but still have symptoms like a celiac patient (NCGS patients) do respond to a gluten-free diet. This is a groundbreaking study and supports that there is some type of inflammatory response that occurs with gluten in some patients. This is an amazing finding and suggests this is why IBS patients do well gluten free."
No commercial funding or conflicts of interest were reported.
SOURCE: http://bit.ly/2az6WmJ1 -
New post in my inbox the other day....
Passing it on as I am looking forward to getting one of these:
Reuters Health Information
Want to Detect Gluten on the Go? There's a Device for That
By Ben Gruber
August 31, 2016
SAN FRANCISCO (Reuters) - A California startup has developed a portable technology that will allow consumers to test their food for gluten on the go.
"Even when you go out and see these labeled menu items, you are still playing Russian roulette," said Shireen Yates, co-founder and chief executive of NIMA, which was founded in 2013.
Designed in San Francisco by a team from MIT, Stanford, Google and Nike, NIMA can analyze any type of food or beverage for gluten down to 20 parts per million, the Food and Drug Administration (FDA) classification for gluten-free products.
"There is still cross contamination, there is miscommunication, you just never know," Yates added.
An estimated 15 million people in the United States have some form of food allergy or sensitivity, a statistic that is on the rise, according to the Centers for Disease Control and Prevention.
Users of the device are instructed to fill a disposable cartridge with a pea-sized sample of food and then load it into the device, which is about half the size of a smartphone.
Roughly two minutes later, after the device measures the chemical reaction between antibody proteins and gluten, the screen will display a happy face if no gluten was detected.
Conversely, a wheat icon and text that reads "gluten found" will appear if any gluten is detected.
According to Yates, the antibodies bind to the presence of gluten if it is present in the sample, triggering a change that a sensor picks up on, Yates said.
To date, the company has raised $14 million in total with the help of a $9.2 million Series A round of venture capital funding earlier this year.
The funding, Yates said, will drive the company's next generation sensor, which consumers will be able to purchase as soon as 2017 if they want to detect milk and peanut allergens in their food as well.
Yates is launching an iPhone application to complement the device, allowing users to share their results.
The first orders of the gluten device, priced at $199, are expected to ship out to customers by the end of the year.
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Link to an important documentary by many MD's, oncologists, allergists, internal specialists, pediatricians, and university scientists about GMO foods and gut health - Institute for Responsible Technology's "Genetic Roulette, the Gamble of Our Lives"
Free Vimeo link until Jan 1.
action.responsibletechnology.org/signup_page/grm58
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Journal of Clinical Pathology
Is a Detailed Grading of Villous Atrophy Necessary for the Diagnosis of Enteropathy?
Federico Biagi; Claudia Vattiato; Marco Burrone; Annalisa Schiepatti; Simona Agazzi; Gregorio Maiorano; Ombretta Luinetti; Costanza Alvisi; Catherine Klersy; Gino Roberto Corazza
Disclosures
J Clin Pathol. 2016;69(12):1051-1054.
Abstract
Aims The utility of the 7 level Marsh–Oberhuber classification of mucosal damage in patients with coeliac disease has recently been criticised. Analysis of duodenal biopsies with dissecting microscopy is an unsophisticated method that, however, provides useful information in cases of frank villous atrophy. In the last 15 years, we have always analysed duodenal biopsies with dissecting microscopy before sending them to the pathology department for histology. If the results of dissecting microscopy and traditional histology were comparable, we feel that would be strong evidence that grading of the histological lesion would be unnecessary if not pointless in the everyday diagnosis of enteropathies.
Methods The clinical notes of all 2075 patients undergoing duodenal biopsy between September 1999 and June 2015 were retrospectively analysed. Results of duodenal mucosal evaluation with both dissecting microscopy and traditional histology were collected and statistically compared.
Results The κ statistics showed a substantial agreement of the two methods (κ statistics 0.78). Sensitivity of dissecting microscopy for detection of severe villous atrophy was 85.1% (95% CI 81.2% to 88.5%) and specificity was 95% (95% CI 93.8% to 96%).
Conclusions Although dissecting microscopy is an unsophisticated method that obviously cannot substitute traditional histology, our results suggest that in everyday clinical practice, the diagnosis of coeliac disease and other flat enteropathies does not require grading of villous atrophy.
Introduction
Coeliac disease (CD) is a chronic gluten-related enteropathy whose diagnosis requires the demonstration of a certain degree of villous atrophy and positive IgA endomysial/tissue transglutaminase antibodies in the vast majority of patients.[1]
Defining a 'certain' degree of villous atrophy could seem unclear but it is necessary because, more than 20 years ago, Marsh showed that the histological lesion, characteristic of CD, is a dynamic one that evolves from an architecturally normal mucosa with just an increased intraepithelial lymphocyte count (Marsh 1 type lesion) to a destructive one with loss of villi and hypoplastic crypts (Marsh 4 type lesion).[2]
Marsh performed these studies from a pathogenic point of view without any diagnostic aim and he clearly stated that these lesions are not specific for CD but can occur in several other enteropathies.[2] However, this classification was subsequently modified and expanded into 7 levels and almost universally adopted for the everyday diagnosis of CD.[3] We believe that this was unfortunate. Probably because of the difficult reproducibility of this classification,[4] misdiagnoses of CD are nowadays very common and often due to biopsy misinterpretation.[5–7]
Very recently, Marsh expressed his disagreement with this misinterpretation of his work and concluded that the so-called Marsh–Oberhuber classification should not be used for diagnostic purposes.[8] Using scanning electron microscopy, he showed that the surfaces of flat mucosae (Marsh 3) present 'large open basins, surrounded by raised collars, coalescing into ridges and convolutions'. Different random histological sections passing either through the collared basin or conjoined ridge would result in histological sections that are totally different and thus mimicking different degrees of villous atrophy.[8] Moreover, a Finnish group has recently shown that incorrect orientation of the duodenal biopsy could lead to very different histological patterns and misinterpretation of the biopsies. So, flat mucosae could be mistaken for normal mucosae and normal mucosae for flat ones.[9]
In our centre, whenever a duodenal biopsy is taken, we orient it and, before sending it to the pathologists, we analyse it with dissecting microscopy (DM) to verify orientation and look for frank villous atrophy. Although this is a rather unsophisticated method that offers little help in cases of mild villous atrophy, frank villous atrophy can be detected in some patients. In these cases, DM is of great help because it allows us to start a gluten-free diet almost immediately, without having to wait for the traditional histology (TH) report. Moreover, it can be of help in cases of patchy villous atrophy. Being perfectly aware of the limitations of DM, we think that the concordance between DM and TH is satisfactory.
The aim of this study was, therefore, to compare the results of DM with those of TH. If the results of these two methods were comparable, this would be a strong evidence that grading of the histological lesion would be unnecessary if not pointless in the everyday diagnosis of CD and other flat enteropathies
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Interesting new peer reviewed and published study from Jan 2017 that shows that nanoparticles of titanium dioxide (OFTEN used in the food industry as a colour additive) cause increased intestinal permeability and collect in the liver and develops micro-inflammation in the colon and spleen.
presse.inra.fr/en/Press-releases/Food-additive-E171
Another thing that can affect food reactions in our gut.0 -
Medscape Medical News
Mild Viral Infection May Trigger Celiac Disease Years Later
Ricki Lewis, PhD
April 10, 2017
science.sciencemag.org/content/356/6333/44
Infection with the relatively innocuous reovirus may interfere with tolerance to food antigens and set the stage for — if not directly cause — celiac disease in genetically susceptible individuals, data from mice suggest.
The findings, published April 6 in Science, may have implications for preventing celiac disease.
"During the first year of life, the immune system is still maturing, so for a child with a particular genetic background, getting a particular virus at that time can leave a kind of scar that then has long term consequences. That's why we believe that once we have more studies, we may want to think about whether children at high risk of developing celiac disease should be vaccinated," said senior author Bana Jabri, MD, PhD, from the University of Chicago Celiac Disease Center in Illinois, in a university news release.
Celiac disease arises from a highly specific autoimmune reaction to peptides derived from dietary gluten proteins. It affects 1 in 100 people worldwide who have human leukocyte antigen DQ2 or DQ8 variants, which can direct an inflammatory T helper 1 (TH1) immune response against gluten proteins in wheat. Only 3% to 4% of people with these genotypes who eat gluten develop celiac disease.
The recent increase in prevalence of celiac disease and food sensitivities and allergies has suggested that an environmental factor might link the two. In addition, the fact that genetically similar populations can have wildly different incidences of celiac disease supports an environmental hypothesis.
Epidemiological studies have associated several familiar viruses with later development of celiac disease, including hepatitis C virus, adenovirus, enteroviruses, and rotavirus. Timing suggests a role for an environmental influence too: children typically begin to eat cereal at about age 6 months, a time when maternal immune protection wanes and the child's immune system encounters a world of viruses.
The new investigation takes a long-needed experimental approach that links the common but little-known reovirus, which causes few if any symptoms, to later celiac disease. The mechanism that Romain Bouziat, PhD, a postdoctoral researcher at the University of Chicago, and colleagues deduced from experiments in mice supports the epidemiological association of viral infections with later celiac disease in humans.
The researchers scrutinized the immune responses of mice fed gluten and infected with either of two reoviruses that differ in several respects, including tropism to the small intestine. Strain 1Lang (T1L) naturally infects the intestine. A second strain (type 3 Dearing, or T3D) does not naturally infect the intestine, but the investigators engineered a variant of T3D that does (T3D-RV).
Both viral strains evoked a TH1 response in Peyer's patches, as well as an antibody response, but T1L had a stronger effect and altered gene expression in the dendritic cells that are involved in tolerance to dietary antigen.
Further experiments in the mice confirmed that interaction between the T1L strain of reovirus and the immune system blocks tolerance to dietary antigens on gluten peptides, and instead launches a pathogenic TH1 autoimmune response.
To examine the possible link in humans, the researchers compared 160 people with celiac disease, some of whom followed a gluten-free diet, with 73 control patients. People with the disease had significantly higher antireovirus antibody titers than those without celiac disease.
In addition, individuals with celiac disease who were on a gluten-free diet and had high antireovirus antibody titers also had elevated levels of interferon regulatory factor 1, which induces dendritic cells to produce the cytokines that evoke the misplaced TH1 immunity. Although the increase in levels of the antibodies and interferon regulatory factor 1 was not linear, the researchers hypothesize that interferon regulatory factor 1 serves as a "permanent mark" on the immune system that reveals increased risk for celiac disease.
The investigators conclude that "viruses eliciting proinflammatory immune responses to dietary antigen alter immune homeostasis and in particular endow DCs with proinflammatory properties at sites where oral tolerance is induced." They call for identification of other viruses that can affect oral tolerance of food antigens and development of a vaccine to prevent celiac disease, and perhaps other autoimmune conditions.
A perspective by Elena F. Verdu, MD, PhD, and Alberto Caminero, PhD, from McMaster University places the findings in the context of information about the human microbiome. "The study of Bouziat et al. highlights the importance of microbial components as additional environmental triggers in the development of chronic inflammatory and autoimmune disorders," they write.
Dr Verdua and Dr Caminero also outline the "three factors responsible for the development of adverse reactions to dietary antigens: the antigen that triggers the maladaptive im¬mune response, the microbial milieu, and the genetic milieu."
The editorialists and the investigators call for special attention to common viral infections considered harmless because their effects are subclinical, as these viruses may set the stage for future celiac disease and perhaps other autoimmune conditions.
The researchers and commentators have disclosed no relevant financial relationships.
Science. 2017;356:29-30, 44-50. Article abstract, Perspective extract1
