Pub Med - Nov 2006

[jcc]

Irritable bowel syndrome. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17040359&itool=pubmed_DocSum) PMID: 17040359 Nov 2006


Conceptually, the irritable bowel syndrome (IBS) has been considered a brain-gut functional disorder, but this paradigm is under serious challenge. There is increasing evidence that organic disease of the gastrointestinal tract can be identified in subsets of patients who fulfil the Rome criteria for IBS. Evidence for subtle inflammatory bowel disease, serotonin dysregulation, bacterial overgrowth and central dysregulation continue to accumulate. The underlying causes of IBS remain to be adequately identified, but postinfectious IBS is a clear-cut entity. Furthermore, a genetic contribution to IBS also seems likely. Diagnosis continues to be based on the symptom profile and the absence of alarm features. A heightened awareness of coeliac disease masquerading as IBS is becoming accepted. Management remains largely based on symptomatic rather than on disease-modifying therapy, but this is likely to change in the near future. Here, recent advances in the pathophysiology and management of IBS are considered.
PMID: 17040359

[Zonulin]

That's a biggie - and it's not even November yet ;) I notice the study is from the Mayo Clinic in Rochester, where we finally got a couple of answers for my son Ted during the Summer of 2005 (after over 2 years and 22 doctors). During our many hours of waiting (between tests) at the Mayo Clinic, I happened to pick up a pamphlet on Irritable Bowel Syndrome in one of the waiting rooms published in 1998 by the International Foundation for Functional Gastrointestinal Disorders. Ted and I got a few chuckles over it - see what you think:

"IBS is not caused by an infectious agent. Lactose (milk sugar) intolerance can have similar symptoms to IBS, and while lactose intolerance and irritable bowel can occur concurrently in a person, they are different problems."

"Emotional distress can significantly influence IBS. It is incorrect and unfair for patients or care givers to characterize IBS as 'all in one's head' or IBS patients as 'emotionally disturbed.' IBS results from a complex interaction between the nerves and muscles of the bowel and an individuals (sic) emotional state. To understand IBS, one must understand that the disorder represents an unusual sensitivity of the bowel to external stressors."

I kept the pamphlet all this time because I thought it was one of the least helpful things I'd ever read ("Look for the sources of stress in your life, and see if you can do something about them.") !!!!! It harkened back to the "olden days" of the 1980s when they thought ulcers were caused by "stress," but it turns out that over 90% of ulcers are caused by the bacterium, H. pylori, which lives in the stomach lining and ultimately causes stomach cancer.

So - I'm glad to see that this pamphlet will soon be OBSOLETE :eek: :rolleyes:

Karen

[jcc]

It is so nice to have you back, Karen! I always enjoy your commentary :D !

Cara

[annelb]

We have a long way to go to get CD recognized by the majority of the doctors. We have even farther to go concerning gluten sensitivity.

I have been GF for 3 years and there is progress. Not as fast as I want, but progress is good.

Anne

[Zonulin]

Yes, progress is definitely GOOD! However, it can certainly get very STRESSful waiting for it to hurry up a little faster ;)

Karen

[jcc]

Gluten-Free Diet Impact on Leptin Levels in Asymptomatic Coeliac Adolescents: One Year of Follow-Up. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17057405&itool=pubmed_DocSum) PMID: 17057405 Oct 2006


Coeliac disease, daily more frequently diagnosed in our population, involves many organs also in oligosymptomatic patients and with an adequate nutritional regime. Possible endocrine implications include failure to thrive, pubertal delay and reproduction diseases due to deregulation of GH, FSH and LH secretion. Leptin, an adipose tissue hormone, can be decreased as well and its deficiency could be related to growth and puberty anomalies. We studied 14 asymptomatic coeliac patients in peripubertal age (7.5-13.8 years) and tested their leptin levels in order to correlate them with endocrine and anthropometric data. Before the diet was started leptinaemia (M+/-DS) was: 4.94 +/- 5.53 ng/ml. In 10/14 patients (71%) leptinaemia was </=2 DS for gender and age. In all the patients, after a period of 6-12 months of gluten-free diet, Leptin levels appreciably raised to 10.8 +/- 7.9 ng/ml, with a significant correlation to the time of the diet. Leptinaemia was actually lower in patients with a severe mucosal atrophy, and in these patients it increased more significantly after the diet was started. The removal of gluten itself may reduce immunological hit to adipose tissue and the 'malnutrition' of adipocytes: leptin can hence increase despite no significant increase of body mass index occurs. This study could partially explain the correlation between body mass index, Coeliac disease and the deregulation of puberty and fertility, mainly in patients who started the diet late. It could also explain the reversibility of this alteration if the cause is removed. Copyright (c) 2007 S. Karger AG, Basel.
PMID: 17057405

[jcc]

Objective. Coeliac disease (CD) is a common disease with a strong heredity. About 10-20% of 1st-degree relatives of probands develop CD. Relatives should be screened for CD, because if not treated, CD exposes patients to numerous complications. The heterogeneity of symptoms and the lifetime-spanning risk of CD render the timing of CD antibody and/or gastroscopy screenings difficult. As CD susceptibility has been shown to be strongly associated with the HLA alleles DQA1*0501 and DQB1*0201 (together encoding the DQ2 heterodimer) and DRB1*04 (associated with the DQ8 heterodimer), our aim was to investigate whether HLA genotyping might be useful in the identification of 1st-degree relatives of CD patients who do not need further screening for CD.Material and methods. The study comprised 54 Finnish CD families including 54 CD probands and 382 living 1st-degree relatives. All subjects who were willing to participate were screened for CD (duodenal and skin biopsies; endomysial, reticulin and gliadin antibodies). The DQA1*0501, DQB1*0201 and DRB1*04 allele frequencies of CD patients and the 1st-degree relatives were determined.Results. Altogether 17.6% (5.9% of the parents, 15.7% of the siblings, 25.8% of the offspring) of the investigated 1st-degree relatives (n=245) did not carry any of the alleles studied. All of the CD patients (n=136) with the exception of one (0.7%) carried at least one of the alleles investigated.Conclusions. By using the HLA genotyping a considerable proportion of 1st-degree relatives of CD probands could be excluded from further screening for CD.
HLA genotyping is useful in the evaluation of the risk for coeliac disease in the 1st-degree relatives of patients with coeliac disease. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17060123&itool=pubmed_DocSum)
PMID: 17060123 Nov 2006


Background Coeliac disease is strongly associated with human leukocyte antigen (HLA)-DQ2 or DQ8 genotypes. The diagnosis is based on demonstrating crypt-hyperplastic villous atrophy, endomysial or transglutaminase antibodies and correlation of disease activity with gluten intake. Aim To evaluate the clinical utility of HLA-DQ typing, when coeliac disease diagnosis had previously been established solely by histology. Methods HLA-DQ alleles, endomysial and transglutaminase antibodies were investigated and histology slides reviewed in 70 patients diagnosed 2-25 years earlier by small-intestinal biopsy but without measuring endomysial or transglutaminase antibodies. Patients without DQ2 or DQ8 or without unequivocal villous atrophy were followed-up on free diet by using serology and biopsies. Results All 40 endomysial/transglutaminase antibodies positive patients carried DQ2 or DQ8, and 39 of them had severe villous atrophy. Only 56% of patients without endomysial or transglutaminase antibodies positivity had DQ2 or DQ8 (P < 0.001). Seropositivity and relapse developed in 4 of 11 DQ2 positive but in none of 15 DQ2 and DQ8 negative patients on long-term gluten exposure. Conclusions Coeliac disease diagnosis based solely on histology is not always reliable. HLA-DQ typing is important in identifying DQ2 and DQ8 negative subjects who need revision of their diagnosis, but it does not have additive diagnostic value if endomysial positivity is already known.
Diagnostic significance of HLA-DQ typing in patients with previous coeliac disease diagnosis based on histology alone. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17059521&itool=pubmed_DocSum) PMID: 17059521 Nov 2006

[jcc]

Objective. The aetiopathogenesis of psoriasis is still unclear. Associations between gut and skin diseases are well known, since psoriatic patients show a high prevalence of coeliac disease. Small-bowel abnormalities can cause clinical or, more frequently, laboratory alterations that give rise to malabsorption. The aim of the study was to evaluate the prevalence of malabsorption in psoriatic patients. Material and methods. Fifty-five (29 M, 26 F, mean age 51+/-8 years) psoriatic patients in the Dermatology Centre of our hospital and 65 healthy controls (36 M, 29 F, mean age 47+/-9 years) were screened for malabsorption using a D-xylose test. Psoriatic subjects who resulted positive were further investigated in order to reach a better characterization of the malabsorption using serum antigliadin, antiendomysium and anti-transglutaminase antibodies, H2 lactulose breath test, the parasitological faecal test and colonoscopy with retrograde ileoscopy. Results. Altered D-xylose absorption was found in 60% (33/55) of psoriatic patients and in 3% (2/65) of controls. Of the former, 6% had coeliac disease, 21% had bacterial overgrowth, 3% had parasitic infections and 1 patient presented eosinophilic gastroenteritis. Conclusions. Malabsorption was more prevalent among psoriatic patients than among controls. Coeliac disease, bacterial overgrowth, parasitic infestations and eosinophilic gastroenteritis could be possible causes of malabsorption in these patients. Further studies are needed to clarify the pathogenesis and possible causative associations between gut and skin diseases.
Malabsorption in psoriatic patients: Cause or consequence? (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17060119&query_hl=2&itool=pubmed_docsum) PMID: 17060119 Nov 2006

[jcc]

Objective. Although in both adults and children with coeliac disease (CD) it is now recommended that oats be added to their gluten-free diet, there is still some controversy concerning the possible harmful effects of oats in some individuals. In this study concentrations of nitric oxide metabolites were repeatedly measured in the urine of children under investigation for CD, when on a gluten-free diet with or without oats. Material and methods. The study included 116 children, randomized to a standard gluten-free diet (GFD-std) or a gluten-free diet supplemented with wheat-free oat products (GFD-oats), over a one-year period. Small-bowel biopsy was performed at the beginning and end of the study. Morning urine samples were collected from 87 children and urinary nitrite/nitrate concentrations were monitored at 0, 3, 6, 9 and 12 months. Results. All patients were in clinical remission after the study period. There was a rapid decline in urinary nitrite/nitrate concentrations in both groups as early as after 3 months. No differences were seen between the study groups at any of the checkpoints. However, at the end of the study, the nitrite/nitrate values of 9 children in the GFD-oats group and 8 children in the GFD-std group had not normalized. Conclusions. Children with CD on a gluten-free diet with oats display a similar reduction in urinary nitrite/nitrate as those on a traditional gluten-free diet. Some children, however, still demonstrate high nitrite/nitrate excretion after one year on either diet, indicating that long-term follow-up studies of children on an oats-containing diet are needed.
Urinary nitric oxide during one year of gluten-free diet with or without oats in children with coeliac disease. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17060120&itool=pubmed_DocSum)
PMID: 17060120 Nov 2006


Background Chronic constipation is common in the general population. Some studies have shown that in children cow's milk protein hypersensitivity can cause chronic constipation unresponsive to laxative treatment. Aims To review the literature and summarize the data that point to a relationship between refractory chronic constipation and food hypersensitivity, and to discuss the hypothesis that the pathogenesis of constipation due to food hypersensitivity. Methods A search in the U.S. National Library of Medicine was performed, matching the key words 'chronic constipation, food intolerance and allergy'. Results Thirty-three papers were found but only 19 of them were related to the topic of this review. Most of the data indicated a relationship between constipation and food allergy in a subgroup of paediatric patients with 'idiopathic' constipation unresponsive to laxative treatment. There was only one study in adults that demonstrated the resolution of chronic constipation on hypoallergenic diet in four patients. Conclusions An increasing number of reports suggest a relationship between refractory chronic constipation and food allergy in children. Similar data in adults are scarce and need to be confirmed. Further studies should be performed to obtain firmer evidence for the role of allergy in constipation and clarify the pathogenetic mechanisms involved.
Review article: chronic constipation and food hypersensitivity - an intriguing relationship. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17059511&itool=pubmed_DocSum)
PMID: 17059511 Nov 2006

[annelb]

Here is another. They are looking for more grains that can be tolerated by people with CD. The testing was done on tissue in a dish, not tissue in the body. So do get too excited yet :rolleyes:
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17060124&query_hl=1&itool=pubmed_docsum
Lack of intestinal mucosal toxicity of Triticum monococcum in celiac disease patients.

* Pizzuti D,
* Buda A,
* D'Odorico A,
* D'Inca R,
* Chiarelli S,
* Curioni A,
* Martines D.

Department of Surgical and Gastroenterological Sciences.

Objective. The treatment of celiac disease is based on lifelong withdrawal of foods containing gluten. Unfortunately, compliance with a gluten-free diet has proved poor in many patients (mainly due to its low palatability), emphasizing the need for cereal varieties that are not toxic for celiac patients. In evolutionary terms, Triticum monococcum is the oldest and most primitive cultivated wheat. The aim of this study was to evaluate the toxicity of T. monococcum on small intestinal mucosa, using an in vitro organ culture system.Material and methods. Distal duodenum biopsies of 12 treated celiac patients and 17 control subjects were cultured for 24 h with T. aestivum (bread) gliadin (1 mg/ml) or with T. monococcum gliadin (1 mg/ml). Biopsies cultured with medium alone served as controls. Each biopsy was used for conventional histological examination and for immunohistochemical detection of CD3 + intraepithelial lymphocytes (IELs) and HLA-DR. Secreted cytokine protein interferon-gamma (IFN-gamma) was measured in the culture supernatant using an enzyme-linked immunoadsorbent assay.Results. Significant morphological changes, HLA-DR overexpression in the crypt epithelium and an increased number of CD3 + IELs, found after bread gliadin exposure, were not observed in celiac biopsies cultured with T. monococcum gliadin. In contrast, with bread gliadin, there was no significant IFN-gamma response after culture with monococcum gliadin. Similarly, biopsies from normal controls did not respond to bread or monococcum gliadin stimulation.Conclusions. These data show a lack of toxicity of T. monococcum gliadin in an in vitro organ culture system, suggesting new dietary opportunities for celiac patients.

PMID: 17060124 [PubMed - in process]

[halsgluten]

"Evidence for ... >serotonin dysregulation<, ... continue to accumulate."

See associations with ADHD, Bipolar, and Schizophrenia. symptoms.

Hal

[annelb]

We all know there is a significant number of people with DM type 1 who also have CD. We know that all children with T1DM should be screened for CD. What is interesting is that this abstract says they found an incidence of 12.3%. That is higher than found in other studies. I need to check out articles looking for CD in adults. Most of the articles about CD and DM are about children.

What is the incidence of children with T1DM who have elevated Zonulin levels.
Anne

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17065683&query_hl=1&itool=pubmed_docsum


Diabetes Care. 2006 Nov;29(11):2452-6. Links
Clinical Benefit of a Gluten-Free Diet in Type 1 Diabetic Children With Screening-Detected Celiac Disease: A population-based screening study with 2 years' follow-up.

* Hansen D,
* Brock-Jacobsen B,
* Lund E,
* Bjorn C,
* Hansen LP,
* Nielsen C,
* Fenger C,
* Lillevang ST,
* Husby S.

Department of Pediatrics, Odense University Hospital, Sdr. Boulevard 29, 5000 Odense C, Denmark. dorte.hansen@dadlnet.dk.

OBJECTIVE: This study was performed to 1) determine the prevalence of celiac disease in Danish children with type 1 diabetes and 2) estimate the clinical effects of a gluten-free diet (GFD) in patients with diabetes and celiac disease. RESEARCH DESIGN AND METHODS: In a region comprising 24% of the Danish population, all patients <16 years old with type 1 diabetes were identified and 269 (89%) were included in the study. The diagnosis of celiac disease was suspected in patients with endomysium and tissue transglutaminase antibodies in serum and confirmed by intestinal biopsy. Patients with celiac disease were followed for 2 years while consuming a GFD. RESULTS: In 28 of 33 patients with celiac antibodies, an intestinal biopsy showed villous atrophy. In 5 patients, celiac disease had been diagnosed previously, giving an overall prevalence of 12.3% (95% CI 8.6-16.9). Patients with celiac disease had a lower SD score (SDS) for height (P < 0.001) and weight (P = 0.002) than patients without celiac disease and were significantly younger at diabetes onset (P = 0.041). A GFD was obtained in 31 of 33 patients. After 2 years of follow-up, there was an increase in weight SDS (P = 0.006) and in children <14 years old an increase in height SDS (P = 0.036). An increase in hemoglobin (P = 0.002) and serum ferritin (P = 0.020) was found, whereas HbA(1c) remained unchanged (P = 0.311) during follow-up. CONCLUSIONS: This population-based study showed the highest reported prevalence of celiac disease in type 1 diabetes in Europe. Patients with celiac disease showed clinical improvements with a GFD. We recommend screening for celiac disease in all children with type 1 diabetes.

PMID: 17065683 [PubMed - in process]

[jcc]

So...this is October, but I'm not sure its been posted.

Coeliac disease and risk of mood disorders - A general population-based cohort study. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17030405&query_hl=3&itool=pubmed_docsum)
PMID: 17030405 Oct 2006


BACKGROUND: Earlier research has indicated a positive association between coeliac disease (CD) and some mental disorders. Studies on CD and depression have inconsistent findings and we know of no study of CD and the risk of bipolar disorder (BD). METHODS: We used Cox regression to investigate the risk of subsequent mood disorders (MD); depression and BD in 13,776 individuals with CD and 66,815 age- and sex-matched reference individuals in a general population-based cohort study in Sweden. We also studied the association between prior MD and CD through conditional logistic regression. RESULTS: CD was associated with an increased risk of subsequent depression (Hazard ratio (HR)=1.8; 95% CI=1.6-2.2; p<0.001, based on 181 positive events in individuals with CD and 529 positive events in reference individuals). CD was not associated with subsequent BD (HR=1.1; 95% CI=0.7-1.7; p=0.779, based on 22 and 99 positive events). Individuals with prior depression (OR=2.3; 95% CI=2.0-2.8; p<0.001) or prior BD (OR=1.7; 95% CI=1.2-2.3; p=0.001) were at increased risk of a subsequent diagnosis of CD. LIMITATIONS: Study participants with CD and MD may have more severe disease than the average patient with these disorders since they were identified through a hospital-based register. CONCLUSIONS: CD is positively associated with subsequent depression. The risk increase for CD in individuals with prior depression and BD may be due to screening for CD among those with MD.
PMID: 17030405


This one from Dec 2005, but I think I must have been Christmas shopping and let is slip past. Least it wasn't in TGF.


[Diagnosis of coeliac disease in patients with isolated neuropsychological symptoms. Cases reports] (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16922014&itool=pubmed_DocSum)
PMID: 16922014 Dec 2005


INTRODUCTION: After first report of Cooke e Smith, numerous are the reports of Coeliac Disease (CD) and neuropsychological symptoms association. The neuropsychological symptoms may precede or follow the diagnosis of CD, representing sometimes the only clinic manifestations (atypical forms). It's seem that frequency of unknown CD in patients with neuropsychological symptoms is about 16% and in a recent study about 7% of new cases of CD was diagnosed in order of neuropsychological disorders. To explain this clinical association various are the hypothesis proposed. CASE REPORTS: We report n degrees 4 cases (middle age 11 years and 2 months) come to our clinic for neuropsychological symptoms; all had diagnosis of CD (by serologic screening and intestinal biopsy); nobody had nutritional deficit, sideropenic anaemia or thyroid deficits. In all patients the introduction of dietetic therapy resolved the symptoms. CONCLUSION: These cases represent atypical forms of CD manifested in childhood only by neuropsychological disorders. To make an early diagnosis and to improve the disease prognosis, the literature and our clinic experience shown that is useful screen the CD in all patients with neuropsychological disorders such as epileptics foci in the parietal-occipital region and/or occipital calcification, headache (mostly if there isn't familiarity), spinocerebellar ataxia, neuromuscular disease of unknown aetiology, Down syndrome, behavioural disorders and some psychiatric troubles.
PMID: 16922014

[jcc]

Frequency and prognostic value of IgA and IgG endomysial antibodies in recurrent aphthous stomatitis. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16874419&itool=pubmed_DocSum)PMID: 16874419 2006


Recurrent aphthous stomatitis is a common disease of the oral mucous membranes. Currently a hypothesis is being discussed that it might be pathogenetically related to coeliac disease. We evaluated the frequency of coeliac disease anti-endomysial (or anti-transglutaminase) antibodies in patients with recurrent aphthous stomatitis. Blood samples from 42 patients were evaluated and 2/42 (4.7%) were IgA- and IgG-endomysial antibody-positive. None of the 42 persons in the control group had antibodies, which was not statistically different from the patient group. The two antibody-positive patients had episodes of mild gastrointestinal symptoms only, but histopathology of duodenal mucous membranes confirmed coeliac disease. All symptoms related to aphthous stomatitis responded well to a gluten-free diet. We conclude that every patient with recurrent aphthous stomatitis should be asked about a history of gastrointestinal complaints and screened for markers of coeliac disease, since recurrent aphthous stomatitis may in some cases respond to a gluten-free diet.
PMID: 16874419

[annelb]

This isn't much information. Will have to get the complete article. Quality of life issues was discussed at the International Celaic Symposium. One interesting chart showed that men with CD perceived they had a better quality of live when compared to women with CD.
Anne

Postgrad Med J. 2006 Nov;82(973):705-712. Links
Complications of coeliac disease: are all patients at risk?

* Goddard CJ,
* Gillett HR.

St John's Hospital, Howden Road West, Livingston, West Lothian EH54 6PP, UK. helen.gillett@wlt.scot.nhs.co.uk.

Coeliac disease is a common condition that is increasingly being recognised as a result of the development of sensitive and specific serology. The diagnosis of coeliac disease and its subsequent treatment with a gluten-free diet have implications for the patient, not just for symptom control but also for the possible effect on quality of life and risk of complications. Whether the mode of presentation of coeliac disease has an effect on survival or risk of complication is yet unclear. This article reviews the available evidence regarding these issues.

PMID: 17099088 [PubMed - as supplied by publisher]

[annelb]

In order to determine the incidence of CD in a population, it must be tested. Until Dr. Fasano came to the US from Italy, the US had an incidence of 1:5000(or was it 50,000). The more they test, the more they find.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17101572&query_hl=26&itool=pubmed_docsum

1: Scand J Gastroenterol. 2006 Dec;41(12):1414-20.Click here to read Links
Population screening for coeliac disease in a low prevalence area in Italy.

* Menardo G,
* Brizzolara R,
* Bonassi S,
* Marchetti A,
* Dante GL,
* Pistone C,
* Marenco D,
* Rabellino V,
* Buscaglia S,
* Scarso R,
* Murialdo M,
* Venturino E,
* Marino CE,
* Descalzi D,
* Minetti F,
* Bagnasco M,
* Pesce G.

Medicina Interna II ASL2 Savona, Ospedale S.Paolo, Savona, Italy.

Objective. A screening program was proposed for the village of Carcare (population 5700), located in a region of Italy with an apparently low prevalence of coeliac disease (CD): only 1 patient diagnosed out of 2557 inhabitants. The study group comprised 1002 individuals (568 F, 434 M, age range 13-90 years) recruited from blood donors, secondary school pupils and people referred to the local outpatient facilities for routine blood chemistry. Material and methods. Total IgA, IgA anti-tissue transglutaminase (tTG) (ELISA, recombinant human antigen) and IgA antiendomysium (EMA) (IFI, umbilical cord substrate) antibodies were measured in the serum of all participants. All patients with IgA deficiency were investigated for IgG tTG antibodies, and in the case of disagreement between tTG and EMA, they were typed for HLA DQ2-DQ8 haplotypes. Results. Thirteen subjects were positive and 988 negative for autoantibodies (3/988 had IgA deficiency). One serum sample was positive for tTG antibodies but negative for EMA. Ten out of 13 positive subjects consented to undergo duodenal biopsy, which invariably produced evidence of CD despite the absence of clinical signs/symptoms. A post-diagnostic clinical investigation provided evidence showing mild iron deficiency (4 subjects) and osteoporosis (2 subjects). After counselling, all subjects accepted a gluten-free diet. Conclusions. The prevalence of CD in the study group was 1:100 (1.0%; 95% CI: 0.5-1.8%): this indicates that CD is largely underdiagnosed in Carcare. Our results suggest that the low prevalence of CD observed in some regions is likely to be due to underdiagnosis.

PMID: 17101572 [PubMed - in process]

[jcc]

Can't really interpret this ...but thought someone might be interested.

Genome-wide linkage analysis of 160 North American families with celiac disease. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17136122&query_hl=2&itool=pubmed_docsum)
PMID: 17136122 Nov 2006


Celiac disease (CD) is a common autoimmune disease caused by exposure to the protein gliadin in wheat, and related prolamins in barley and rye. The prevalence of the disease in the US is 1:133. The aim of this study was to identify non-human leukocyte antigen (HLA) loci that predispose to CD. A genome-wide search of 405 microsatellite markers was performed on DNA samples from 160 families with a minimum of two cases of CD. Multipoint, parametric and non-parametric linkage (NPL) analyses were performed. Locations on chromosomes 1q, 3q, 6p, 6q, 7q, 9q and 10q showed linkage statistics (NPL scores or heterogeneity logarithm of the odds (HLOD) scores) of approximately 2.0 or larger. The greatest evidence for linkage outside of chromosome 6 was on 7q and 9q. An NPL score of 2.60 occurred at position 151.0 on 7q and a HLOD score of 2.47 occurred at position 144.8 on 9q under a recessive model. As expected, there was highly significant linkage to the HLA region on 6p, with NPL and HLOD scores exceeding 5.50. In conclusion, this genome-wide linkage analysis represents one of the largest such studies of CD. The most promising region is a putative locus on 7q, a region reported independently in previous genome-wide searches.Genes and Immunity advance online publication, 30 November 2006; doi:10.1038/sj.gene.6364361.
PMID: 17136122

[annelb]

Cara, I did not understand that abstract either.

This one is not about CD but since people with IBD often have gluten intolerance I decided to post it here. My message is get your vitamin D level checked. Winter is here and you need a good store to get you through the cold months.

This study used <15ng/ml as the low and found 34.6% were deficient. I wonder what percent would have been deficient if a cutoff of 30ng/ml was used. Some researchers think that the cutoff should be 30 and some think that 50-60ng/ml should be the optimal.
Anne

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17079566&query_hl=1&itool=pubmed_docsum

Pediatrics. 2006 Nov;118(5):1950-61. Links
Vitamin D status in children and young adults with inflammatory bowel disease.Pappa HM, Gordon CM, Saslowsky TM, Zholudev A, Horr B, Shih MC, Grand RJ.
Center for Inflammatory Bowel Disease, Division of Gastroenterology and Nutrition, Children's Hospital Boston, 300 Longwood Ave, Boston, MA 02115, USA. helen.pappa@childrens.harvard.edu

OBJECTIVES: Previous studies of vitamin D status in pediatric patients with inflammatory bowel disease have revealed conflicting results. We sought to report (1) the prevalence of vitamin D deficiency (serum 25-hydroxy-vitamin D concentration < or = 15 ng/mL) in a large population with inflammatory bowel disease, (2) factors predisposing to this problem, and (3) its relationship to bone health and serum parathyroid hormone concentration. PATIENTS AND METHODS: A total of 130 patients (8-22 years of age) with inflammatory bowel disease, 94 with Crohn disease and 36 with ulcerative colitis, had serum 25-hydroxy-vitamin D, intact parathyroid hormone, and lumbar spine bone mineral density (using dual-energy x-ray absorptiometry) measured at Children's Hospital Boston. RESULTS: The prevalence of vitamin D deficiency was 34.6%. Mean serum 25-hydroxy-vitamin D concentration was similar in patients with Crohn disease and ulcerative colitis, 52.6% lower among patients with dark skin complexion, 33.4% lower during the winter months (December 22 to March 21), and 31.5% higher among patients who were taking vitamin D supplements. Serum 25-hydroxy-vitamin D concentration was positively correlated with weight and BMI z score, disease duration, and serum albumin concentration and negatively correlated with erythrocyte sedimentation rate. Patients with Crohn disease and upper gastrointestinal tract involvement were more likely to be vitamin D deficient than those without it. Serum 25-hydroxy-vitamin concentration was not associated with lumbar spine bone mineral density z score or serum parathyroid hormone concentration. CONCLUSIONS: Vitamin D deficiency is highly prevalent among pediatric patients with inflammatory bowel disease. Factors predisposing to the problem include having a dark-skin complexion, winter season, lack of vitamin D supplementation, early stage of disease, more severe disease, and upper gastrointestinal tract involvement in patients with Crohn disease. The long-term significance of hypovitaminosis D for this population is unknown at present and merits additional study.

PMID: 17079566 [PubMed - indexed for MEDLINE]