PubMed - 2006

[jccgf]

Celiac disease presenting with chilblains in an adolescent girl. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17014640&itool=pubmed_DocSum)
PMID: 17014640 Sep-Oct 2006

Chilblains, or pernio, are cutaneous lesions that may accompany systemic illnesses including states of malnutrition and autoimmune diseases. We report an adolescent girl in whom chilblains were the chief presenting sign of celiac disease. A gluten-free diet led to weight gain and resolution of the chilblains. We speculate that in this patient, weight loss due to celiac disease contributed to the development of chilblains.
PMID: 17014640


What are chilblains?
http://www.mayoclinic.com/health/chilblains/AN00952
http://www.dermnet.org.nz/reactions/chilblains.html

[jccgf]

Should Stored Serum of Patients Previously Tested for Celiac Disease Serology be Retested for Transglutaminase Antibodies? (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17016136&itool=pubmed_DocSum)
PMID: 17016136 Oct 2006

INTRODUCTION: Tissue transglutaminase (tTG) antibodies are currently recognized as a highly sensitive indicator of celiac disease (CD). Although a high concordance rate between tTG antibodies and anti-endomysial antibodies (EMA) has been reported up to a third of known CD patients are positive for only one of these antibodies. AIM: To determine whether in laboratories in which serum samples previously examined for CD serology markers had not been discarded, these samples should be tested for tTG antibodies. METHODS: Fifty-eight stored (frozen at -70) serum samples of patients previously found to be EMA-negative but positive for one or more of the non-EMA markers: antigliadin antibodies (AGA)-IgA, AGA-IgG, antireticulin antibodies, were tested for anti-tTG antibodies (IMMCO Diagnostics). In patients found to be tTG positive, medical charts were reviewed and patients or their physicians contacted. RESULTS: Twelve of fifty-eight (20.7%) samples were found to be anti-tTG positive. These included: group A: 3/3 samples previously positive for AGA-IgA, AGA-IgG, and antireticulin antibodies. Group B: 3/16 samples positive for AGA-IgA and AGA-IgG. Group C: 3/4 samples positive for AGA-IgA and group D: 3/35 samples positive for AGA-IgG. Of the 12 positive patients, 1 was a 2-year-old boy, 5 were lost to follow up, and 7 underwent an intestinal biopsy. In 3 of these 7 patients, the biopsy was compatible with CD; 2 of these 3 patients were from group A and 1 from group B. CONCLUSIONS: In laboratories where stored serum samples are available, EMA-negative samples previously found to be positive for at least 2 other CD markers should be retested for tTG antibodies.
PMID: 17016136

[valeriemates]

CONCLUSIONS: In laboratories where stored serum samples are available, EMA-negative samples previously found to be positive for at least 2 other CD markers should be retested for tTG antibodies.

Wow, that one is fascinating. And, come to think of it, that would apply to my four-year-old. Her first celiac test was an EMA (negative) and one of the antigliadin tests (off-the-scale positive), which made the doctor say that she didn't have celiac disease. A year and a half later, when I finally pestered her doctor into sending her to a gastroenterologist, she had transglutaminase IgA and IgG tests (and antigliadin IgA and IgG tests) that were strongly positive. I wonder what would have happened if I hadn't pestered her doctor into sending her to a GI. Would the lab have eventually dug up her old blood samples and run transglutaminase testing on it the way this article says to? Man, that would be a weird phone call to receive. "Hi, remember that negative blood test on your daughter from several years ago? Well, guess what -- it wasn't so negative after all, and she may have this disease....."

-Valerie

[jccgf]

Yep, blood tests are good but not perfect.

I used to hear in a perfect world that anti-endomysial and anti-tTG should be consistent, but they aren't always. Which is why a thorough doctor will run them all. I know in our case, only the anti-tTG was run, yet I believe it can go both ways (negative anti-tTG and positive anti-endomysial)

It is also why it makes me a little crazy that some of our major celiac centers (like a very windy one) suggest all is needed is a single anti-tTG test.

Recommendations for testing come down to picking what is considered the BEST TEST OVERALL to contain cost, but it is a shame that it comes down certain people falling through the cracks because no test is 100% accurate.

Cara

[jccgf]

Valerie,

Well, your daughter's case highlights TWO things. One is that more sensitivity is gained by running the entire panel of tests, and two is that negative testing one year can turn positive a year later. I'm glad you did pester your doctor!

Cara

[valeriemates]

I used to hear in a perfect world that anti-endomysial and anti-tTG should be consistent, but they aren't always.

The thing that bothers me about the endomysial test is that it's done by labs all over the place, but it's only accurate if it's interpreted by a highly trained special technician -- which most labs don't have. So most EMA test results are about as valid as flipping a coin. What in the world is the point of even *doing* a test that is known to be that inaccurate? Sigh....

...negative testing one year can turn positive a year later. I'm glad you did pester your doctor!

I am glad too. But I believe that my daughter had active celiac disease when they did the first test, too, and the test was only negative because the EMA is a very inaccurate test.

-Valerie

[jccgf]

The thing that bothers me about the endomysial test is that it's done by labs all over the place, but it's only accurate if it's interpreted by a highly trained special technician -- which most labs don't have. So most EMA test results are about as valid as flipping a coin. What in the world is the point of even *doing* a test that is known to be that inaccurate? Sigh....



I am glad too. But I believe that my daughter had active celiac disease when they did the first test, too, and the test was only negative because the EMA is a very inaccurate test.

-Valerie

I think you are probably right, and I'm sorry your daughter was one who fell through the diagnostic crack :(. I guess that is part of our mission... to help people understand that the diagnostic testing is not perfect and there is room for plenty of error in both false negative blood work and false negative biopsy.

Cara

[DogtorJ]

Hi Cara,

I finally got around to registering on BT2. I've been swamped recently but ready to get back to learning some more from you guys. Looks like you're still at it in a great way.

Great "seeing" you again. More later,
John

[jccgf]

Where were you when I've had all my dog questions??? :)

Well, we have a new pup coming home in 7 weeks...so its probably a little late to ask you about the breed. We lost our Golden Retreiver in July :(.

Nice to see you. I'd love to hear about that conference you were talking about last time I heard from you!

Cara

[DogtorJ]

I'm sorry to hear that about your Goldie, Cara. I've been either preparing for a speach or doing one for the past 6 months. I now do a monthly Podcast and just agreed to do another. I'm like a dyslexic slouch...I don't think I'm busy enough. LOL

The human conference (www.worldhealth.net) I did in July was interesting. I spoke on epilepsy and The G.AR.D. I'll shoot you a PM about it.

Send me a PM if you want advice on the puppy. Do you have my Email? That would be better. Starting the right diet is of paramount importance, of course...especially important in some breeds that are clearly food intolerant in a big, big way (e.g. Goldies. Labs, Rotties, Cockers/spaniels, Shih Tzus and many more).

Good to hear from you again,
John

[jccgf]

I'll shoot you an email or pm John!



This has no abstract, but I wonder a little what it says. My daughter has had both bone island and bone spurs... which makes me wonder~

[Defects in mineral density of bone tissue in patients with celiac disease] (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17019965&itool=pubmed_DocSum)PMID: 17019965 2006


Nothing earth shattering here..at least not in the abstract!
Coeliac disease: an update for pathologists (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17021129&itool=pubmed_DocSum). PMID: 17021129

Coeliac disease is the manifestation of an immune hypersensitivity reaction towards gluten and related proteins, in genetically predisposed people. Although the precise pathogenesis of this condition remains to be fully elucidated, it is probably multifactorial in origin. The diagnosis of coeliac disease has traditionally depended on intestinal biopsies alone; nowadays, the diagnosis has been expanded to include an array of serological markers. This review is intended to offer pathologists an update of the relevant history and immunopathology pertaining to coeliac disease and also to offer recommendations on the ongoing responsibilities of the pathologist in the diagnosis and reporting of coeliac disease.
PMID: 17021129

[jccgf]

Overweight in celiac disease: prevalence, clinical characteristics, and effect of a gluten-free diet. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17032202&itool=pubmed_DocSum)
PMID: 17032202 Oct 2006


Rotavirus infection frequency and risk of celiac disease autoimmunity in early childhood: a longitudinal study. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17032199&itool=pubmed_DocSum)
PMID: 17032199 Oct 2006

[jccgf]

Putting the pieces of the puzzle together - a series of hypotheses on the etiology and pathogenesis of type 1 diabetes. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17045415&itool=pubmed_DocSum) PMID: 17045415 Oct 2006


This paper presents a series of 10 hypotheses on the etiology of type 1 diabetes. We begin with the hypothesis that wheat gluten is one of the elusive environmental triggers in type 1 diabetes. Habitual consumption of wheat gluten increases the intestinal synthesis of dipeptidyl peptidase IV. This enzyme helps to shape the repertoire of peptides released into the small intestine following the ingestion of wheat gluten by catalyzing the release of X-Pro dipeptides from the N-terminus of the proline-rich glutenins and gliadins in wheat gluten. The release of gluten-derived peptides causes the tight junctions of the small intestine to open through a zonulin-dependent mechanism, which allows these peptides to enter the lamina propria where they get presented as antigens by HLA-DQ, -DR and CD1d molecules. Binding of one or more gluten peptides by CD1d leads to abrogation of oral tolerance, and a marked increase in peripheral immune responses to wheat proteins. Furthermore, it is our contention, that in response to beta cell apoptosis during normal remodeling of the pancreas and CCL19/CCL21 expression within the pancreatic lymph nodes (PLNs), gluten-loaded dendritic cells migrate from the small intestine to the PLNs. These dendritic cells present gluten-derived antigens on the surface of the PLNs, which leads to migration of CD4(-)CD8(-) gammadelta and CD4(-)CD8(+) alphabeta T cells to the pancreas where they mediate Fas and perforin dependent cytotoxicity. We also hypothesize that at least one of the type 1 diabetes associated HLA-DR molecules that bind and present wheat-derived peptide(s) also bind and present an islet cell antigen(s), activating plasma cell synthesis of islet cell autoantibodies and irrevocable, complement-dependent destruction of islet cells. Our final two hypotheses state that type 1 diabetes morbidity is reduced in those areas of globe where genetically susceptible individuals get adequate amounts of vitamin D, in the diet and/or through exposure to sunlight, and in areas where people are exposed to bacterial, viral, or parasitic infections in early childhood.
PMID: 17045415

[jccgf]

[Dermatitis herpetiformis : A clinical chameleon.] (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17051408&itool=pubmed_DocSum)
PMID: 17051408 Oct 2006

Celiac disease is a genetically determined bowel disease also influenced by exogenous factors in which exposure to grain components triggers a chronic immune response with intestinal symptoms. Dermatitis herpetiformis represents the cutaneous manifestation of celiac disease. While intense pruritus is the characteristic symptom, clinical signs can be highly variable, ranging from grouped papulovesicles with excoriations or eczema-like lesions to minimal variants of discrete erythema and digital purpura. Diagnosis depends on direct fluorescence studies of perilesional skin displaying granular IgA deposits in dermal papillae. Suspecting and then searching for dermatitis herpetiformis is often clinically challenging, as the disease is a true chameleon with many clinical faces. Dapsone therapy alleviates the cutaneous symptoms and signs, but does not prevent the systemic complications of celiac disease; thus, strict adherence to a gluten-free diet is strongly advisable.

[jccgf]

Coexistence of megaloblastic anemia and iron deficiency anemia in a young woman with chronic lymphocytic thyroiditis. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17050198&itool=pubmed_DocSum) PMID: 17050198 Oct 2006

Pernicious anemia is a megaloblastic anemia caused by vitamin B12 deficiency, and is the end-stage of autoimmune gastritis that typically affects persons older than 60 years. It is the most common cause of vitamin B12 deficiency. Pernicious anemia can also be diagnosed concurrently with other autoimmune diseases. We report the occurrence of megaloblastic anemia in a 22-year-old woman with chronic autoimmune thyroiditis for 10.5 years. Recently, she presented with microcytic anemia, and iron deficiency anemia was diagnosed initially. After administration of ferrous sulfate, macrocytic anemia was revealed and vitamin B12 deficiency was detected. Pernicious anemia was highly suspected because of the endoscopic finding of atrophic gastritis, and high titer of antigastric parietal cell antibody, as well as elevated serum gastrin level. After intramuscular injections of hydroxycobalamine 100 mug daily for 10 days, and monthly later, her blood counts returned to normal.
PMID: 17050198



Do you suppose they ran the celiac antibody tests?

My thyroid disease and B12 deficiency dx came 10 years apart, too.

Cara

[jccgf]

Passing this along...thanks, Anne! I can't WAIT until this is proved and accepted ~

Systemic autoimmune disorders in celiac disease (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17053448&query_hl=8&itool=pubmed_docsum). PMID: 17053448 Nov 2006


Fasano A.Center for Celiac Research and Mucosal Biology Research Center and Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
PURPOSE OF REVIEW: Celiac disease is an immune-mediated disorder clinically characterized by a multitude of symptoms and complications. The comorbidity between celiac disease and other autoimmune disorders has been clearly established. RECENT FINDINGS: Two main theories have been postulated to explain this comorbidity: (1) linkage disequilibrium between the genes responsible for celiac disease and those responsible for the coexpressed autoimmune diseases or (2) untreated celiac disease leading to the onset of other autoimmune diseases. This article reviews the current literature supporting either theory and places the current knowledge in the field within the context of the most recent data on the pathogenesis of celiac disease. SUMMARY: The current literature did not clearly establish which of the two theories explain the comorbidity between celiac disease and other autoimmune disorders. There is, however, growing evidence that the loss of the intestinal barrier function typical of celiac disease could be responsible of the onset of other autoimmune disease. This concept implies that the autoimmune response can be theoretically stopped and perhaps reversed if the interplay between autoimmune predisposing genes and trigger(s) is prevented or eliminated by a prompt diagnosis and treatment.
PMID: 17053448

[jccgf]

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

[jccgf]

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

[jccgf]

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

[jccgf]

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

[jccgf]

CD8-positive T cell-induced liver damage was found in a patient with polymyositis. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17043378&itool=pubmed_DocSum)
Intern Med. 2006;45(18):1059-63. Epub 2006 Oct 16.
PMID: 17043378

Just curious on this one...would love to know if they checked for antigliadin or other antibodiesin this person with RA, liver damage, and polymyositis.

[jccgf]

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

[jccgf]

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


I'm not sure I have this in TGF before either! But if I don't... it will be added.

[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

[jccgf]

Not sure I understand all this, but I think it is supporitive of IgG allergy, right?

Changes in humoral responses to beta-lactoglobulin in tolerant patients suggest a particular role for IgG4 in delayed, non-IgE-mediated cow's milk allergy. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=16925689&itool=pubmed_DocSum)
PMID: 16925689 Sept 2006


The major cow's milk allergen beta-lactoglobulin (beta-LG) is relatively resistant to enzymatic degradation and may therefore be involved in non-immunoglobulin (Ig)E-mediated cow's milk allergy (CMA) with delayed gastrointestinal symptoms. Serum levels of beta-LG-specific IgG(1), IgG(4), IgE, and IgA were compared in clinically reactive and tolerized IgE-mediated and non-IgE-mediated CMA with delayed gastrointestinal symptoms (n = 29) and controls (n = 10). Tolerance was associated with decreased beta-LG-specific IgE, IgG(1), and IgG(4) levels in both patient groups. However, the significantly increased beta-LG-specific IgG(4) levels in clinically reactive non-IgE-mediated CMA patients, and its median 36-fold reduction in tolerant patients, suggested a possible immunopathological role for IgG(4) in delayed CMA. Similarly, the significantly increased beta-LG-specific IgE levels in IgE-mediated CMA patients were decreased 44-fold in tolerant patients. The tolerant patients had apparently shifted the humoral immune response from a beta-LG-specific IgE- and/or IgG(4)-dominated immune response to an IgA-dominated immune response as the IgA/IgE or IgA/IgG(4) ratios increased 90- and 15-fold in tolerant IgE-mediated-, and non-IgE-mediated CMA patients, respectively. Thus, the marked difference in beta-LG-specific Ig ratios suggested a tolerance-induced inhibition of a Th(2)-type of immune response with significantly increased IgA dominance in both CMA patient groups.
PMID: 16925689

[jccgf]

Out of India~

Results: Of the 63 siblings of 48 index cases studied, 15 tested positive for anti-tTG; of these 13 had celiac disease. Three tested borderline for anti-tTG; none of them had CD. Of the 45 anti-tTG-negative subjects, two agreed to undergo biopsy; one of these had features of CD. Overall, 14 of 63 (22%) siblings had CD, including 8 who had no symptoms suggestive of CD. Conclusions: CD is common among siblings of patients with CD in Punjab and may be asymptomatic.
Prevalence of celiac disease among siblings of celiac disease patients. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17090839&itool=pubmed_DocSum) PMID: 17090839 Sept 2006

[jccgf]

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

[jccgf]

Epilepsy and Celiac Disease: Favorable Outcome With a Gluten-Free Diet in a Patient Refractory to Antiepileptic Drugs. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17122729&itool=pubmed_DocSum)
PMID: 17122729 Nov 2006


BACKGROUND:: There is a well-documented relationship between epilepsy and celiac disease, including a syndrome characterized by epilepsy, occipital calcifications, and celiac disease. REVIEW SUMMARY:: We report the case of a 23-year-old woman with an 11-year history of refractory epileptic seizures and newly diagnosed biopsy-proven celiac disease with increased antiendomysium immunoglobulin A antibodies. The patient showed a dramatic improvement after starting a gluten-free diet. CONCLUSION:: This case emphasizes the need to include celiac disease in the differential diagnosis when investigating the etiology of epilepsy in refractory patients.
PMID: 17122729



Malignant lymphomas in autoimmunity and inflammation: a review of risks, risk factors, and lymphoma characteristics. (http://neurotalk.psychcentral.com/Malignant%20lymphomas%20in%20autoimmunity%20and%20 inflammation:%20a%20review%20of%20risks,%20risk%20 factors,%20and%20lymphoma%20characteristics.) PMID: 17119030 Nov 2006

Not sure what I think about this one :rolleyes:.

[Treatment and Management of Celiac Disease.] (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17115359&itool=pubmed_DocSum)
PMID: 17115359 Nov 2006

In most patients the clinical course of celiac disease is unproblematic after the diagnosis has been made and a strict gluten-free diet is established. However, in rare cases complications like refractory sprue or lymphoma can occur. Individual management is required since the clinical presentation of celiac disease can be very heterogeneous. For example, it is a matter of controversy if asymptomatic patients, who have the same typical histological changes in their small bowel like patients with symptomatic celiac disease, should adhere to a gluten-free diet. A major problem is the compliance and the unintentional intake of gluten. A 100 % gluten-free diet is not possible since most food components are contaminated with trace amounts of gluten. Fortunately most patients tolerate these contaminations. Furthermore, the threshold for gluten contamination can differ highly among patients. One central point in patient care is the monitoring of a gluten-free diet and the timely recognition of complications. Therefore, the role of antibodies and duodenal histology in monitoring the course of the disease will be discussed.
PMID: 17115359


[Type 1 diabetes and celiac disease] (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17112164&itool=pubmed_DocSum)
PMID: 17112164 Sept 2006

Celiac disease is more prevalent in type 1 diabetic patients than in the general population. The exact reason for this association remains unknown. Two hypotheses are taken into consideration: either a common genetic background or an immune response against Langerhans islets triggered by celiac disease. This review presents recent data about this association and its consequences in clinical practice.
PMID: 17112164


Occurrence of overt celiac disease in the elderly following total thyroidectomy. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17114916&itool=pubmed_DocSum) PMID: 17114916 Oct 2006

We report the case of a female patient in whom gluten-induced entheropathy was revealed at the age of 71 yr by resistance to treatment with levothyroxine (L-T4), calcium carbonate and alfacalcidol. Hypothyroidism and hypoparathyroidism were the consequence of a total thyroidectomy performed at the age of 65 yr for a large multinodular goiter. Six months after thyroid ablation the patient started to complain of abdominal pain, diarrhea and weight loss. Following, anemia and osteopenia were documented. A progressive increase of replacement therapy for hypothyroidism and hypoparathyridism was necessary. The clinical presentation suggested a malabsorption syndrome: celiac disease (CD) was diagnosed by serological markers and duodenal biopsy. Following gluten-free diet a normalization of clinical and serological findings was observed, bone mass density improved and a reduction of L-T4, calcium and vitamin D requirements was observed.
PMID: 17114916

[jccgf]

Another from Hadjivassiliou, et al.

Myopathy associated with gluten sensitivity. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17143894&query_hl=2&itool=pubmed_docsum)
PMID: 17143894 Dec 2006

Ataxia and peripheral neuropathy are the most common neurological manifestations of gluten sensitivity. Myopathy is a less common and poorly characterized additional neurological manifestation of gluten sensitivity. We present our experience with 13 patients who presented with symptoms and signs suggestive of a myopathy and in whom investigation led to the diagnosis of gluten sensitivity. Three of these patients had a neuropathy with or without ataxia in addition to the myopathy. The mean age at onset of the myopathic symptoms was 54 years. Ten patients had neurophysiological evidence of myopathy. Inflammatory myopathy was the most common finding on neuropathological examination. One patient had basophilic rimmed vacuoles suggestive of inclusion-body myositis. Six patients received immunosuppressive treatment in addition to starting on a gluten-free diet; five improved and one remained unchanged. Among seven patients not on immunosuppressive treatment, four showed clinical improvement of the myopathy with a gluten-free diet. The improvement was also associated with reduction or normalization of serum creatine kinase level. The myopathy progressed in one patient who refused the gluten-free diet. Myopathy may be another manifestation of gluten sensitivity and is likely to have an immune-mediated pathogenesis. A gluten-free diet may be a useful therapeutic intervention. Muscle Nerve, 2006.
PMID: 17143894

[jccgf]

Coeliac disease and primary hyperparathyroidism: an association? (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17148709&itool=pubmed_DocSum)
PMID: 17148709 Dec 2006


Primary hyperparathyroidism may present with non-specific symptoms, and this may be one reason why patients with coeliac disease fail to improve despite compliance with a gluten-free diet. Seven case reports of primary hyperparathyroidism due to sporadic adenoma occurring in a series of 310 patients with coeliac disease are presented, highlighting the importance of looking for this condition in this population group. A prevalence of primary hyperparathyroidism of 2.3% in this series suggests a significant association between hyperparathyroidism and coeliac disease; most studies have indicated a prevalence of 3 in 1000 in the general population, although one study found that it may be as high as 21 in 1000 in women aged 55-75 years. The average age of patients in our series was 59 years and all but one were women. Further studies are needed to establish a possible association between primary hyperparathyroidism and coeliac disease.
PMID: 17148709

[NancyM]

Well what a funny coincidence, I just ran into something else about hyperparathyroidism: http://heartscanblog.blogspot.com/2006/12/vitamin-d-new-miracle-drug.html

[jccgf]

Thanks for posting that Nancy! I love that these forward thinking doctors are starting to blog! And this one, in Milwaukee :), just 30 minutes away. I will know who to look for next time I need a cardiologist. I need to have my Vitamin D tested. I hate that many doctors think you are nuts to ask for nutritional deficiency testing.

Cara

[NancyM]

That's great, Cara! I've been enjoying his blog.

Well, today by another weird coincidence I turned on the TV and it was on the local university's channel and there was a Internist/Professor giving a lecture on hyperparathyroid. And they did mention how taking too much Vitamin D can cause that, in addition to adenomas.

I'd really love to find out how MUCH vitamin D my body needs because I really don't get any sun, I'm photosensitive from the drugs I take and have really pale skin anyway. But I'm also afraid of over-doing it too.

[jccgf]

Celiac Disease and Risk of Liver Disease: A General Population-Based Study. (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17161656&itool=pubmed_DocSum) PMID: 17161656 Dec 2006


BACKGROUND & AIMS: Celiac disease (CD) is an important cause of hypertransaminasemia. CD might also be associated with severe forms of liver disease. We investigated the risk of liver disease in 13,818 patients with CD (1964-2003) and 66,584 age- and sex-matched reference individuals from a general population cohort. METHODS: We used Cox regression to estimate hazard ratios (HRs) for later liver disease and conditional logistic regression to estimate the risk of CD in individuals with liver disease before study entry. RESULTS: CD was associated with an increased risk of acute hepatitis (HR, 5.21; 95% confidence interval [CI], 1.88-14.40; P = .001), chronic hepatitis (HR, 5.84; 95% CI, 2.89-11.79; P < .001), primary sclerosing cholangitis (HR, 4.46; 95% CI, 2.50-7.98; P < .001), fatty liver (HR, 6.06; 95% CI, 1.35-27.16; P = .018), liver failure (HR, 3.30; 95% CI, 2.22-4.88; P < .001), liver cirrhosis or liver fibrosis (HR, 2.23; 95% CI, 1.34-3.72; P < .001), and primary biliary cirrhosis (HR, 10.16; 95% CI, 2.61-39.49; P < .001). There was no increased risk of liver transplantation (HR, 1.07; 95% CI, 0.12-9.62; P = .954). Adjustment for socioeconomic index or diabetes mellitus had no notable effect on the risk estimates. Prior liver disease was associated with a statistically significant 4-fold to 6-fold increased risk of later CD. CONCLUSION: This study suggests that individuals with CD are at increased risk of both prior and subsequent liver disease.