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PubMed1995

Isolated iron deficiency: an atypical manifestation of celiac disease.

A 38-year-old woman presented with iron-deficiency anemia in 1983. Eight years later, she developed classic symptoms of celiac disease, ie, diarrhea, weight loss, and diminished appetite. New noninvasive blood tests and the ease with which small bowel biopsies can be achieved are having an impact on the clinical pattern of the disease. This report includes a discussion of anemia as the presenting sign of celiac disease and a review of the literature.

Adult↗
PubMed1998

Transthyretin: a marker for celiac disease activity.

Transthyretin (TTR), a well-established nutritional marker, was measured in patients with active and inactive celiac disease (CD) in order to assess its value as a marker of disease activity. CD activity was assessed by intestinal biopsy to determine intestinal atrophy histologically and by measuring the level of antiendomysial antibody titer. TTR was measured in 26 CD patients fed a diet containing gluten and 22 CD patients fed a gluten-free diet. The control group was composed of 65 healthy sex- and age-matched children. We compared the TTR levels to the two established markers of CD activity. TTR levels were lowest among the celiac patients fed a diet containing gluten and differed significantly from those of the other two groups (r = 0.7, p < 0.002). The TTR levels correlated inversely with both the degree of mucosal atrophy (r = 0.6, p < 0.005) and with anti-endomysial antibody titers (p < 0.005). TTR levels appear to be correlated with morphologic and serologic markers of activity in celiac patients. TTR can be used as a systemic parameter in assessing celiac patients. It can contribute information to the evaluation of children in whom celiac disease is suspected, and it can monitor patients' diet compliance.

Adolescent↗
PubMed2004

A role for bacteria in celiac disease?

The finding of rod-shaped bacteria attached to the small intestinal epithelium of some untreated and treated celiac-disease patients, but not to the epithelium of healthy controls, ignites the notion that bacteria may be involved in the pathogenesis of celiac disease. This editorial discusses this possibility in relation to the current understanding of the molecular basis of this disorder.

Adolescent↗
PubMed1982

Adult celiac disease and recurrent pericarditis.

Three patients presented with acute pericarditis. No cause was found and, in each case, the pericarditis was recurrent. Investigation revealed evidence of malabsorption due to adult celiac disease. Two of the patients responded to a gluten-free diet and cortiscosteroid therapy. The third patient responded to a gluten-free diet alone and remains well. Celiac disease is a multisystem disorder in which extraintestinal involvement is common. Recurrent pericarditis may be such a manifestation.

Acute Disease↗
PubMed2002

[Silent celiac disease: exploring the iceberg in the school-aged population].

BACKGROUND: Epidemiological studies have shown a high prevalence of silent celiac disease (CD) among unselected pediatric populations and a low ratio of diagnosed to undiagnosed CD. OBJECTIVES: To quantify the prevalence of silent CD, to assess the clinical features of subclinical CD and to determine the total prevalence of CD (silent plus symptomatic cases). METHODS: We determined total serum IgA, IgA antiendomysial antibodies (EMA) and IgG antigliadin antibodies (IgG AGA), if IgA deficiency was found, in schoolchildren aged 10-12 years from health district IX in Madrid. RESULTS: A total of 3,378 schoolchildren (47.8 % of the eligible population) were studied. Fifteen were EMA-positive and one child with IgA deficiency was IgG AGA-positive. CD was confirmed by intestinal biopsy in 12 children, representing a prevalence of undiagnosed CD of 1/281. Of these 12 children, 7 showed clinical features of CD. The most frequent symptom was iron-deficiency, followed by recurrent aphthous stomatitis and mild malnutrition. Before the start of this study, CD had been diagnosed in seven children from the same population, which would increase the total prevalence of the disease to 1/220 with an estimated ratio of diagnosed to undiagnosed CD of 1 to 3.5. CONCLUSIONS: We confirm the high prevalence of silent celiac disease among the school-aged population. This ratio is one of the highest published and could be due to a high diagnostic suspicion for CD among pediatricians in our health district. Greater awareness of the minor symptoms of CD would reduce the number of patients with undiagnosed CD.

Celiac Disease↗
PubMed2005

Role of autoimmune gastritis, Helicobacter pylori and celiac disease in refractory or unexplained iron deficiency anemia.

BACKGROUND AND OBJECTIVES: Conventional endoscopic and radiographic methods fail to identify a probable source of gastrointestinal blood loss in about one third of males and post-menopausal females and in most women of reproductive age with iron deficiency anemia (IDA). Such patients, as well as subjects refractory to oral iron treatment, are often referred for hematologic evaluation. DESIGN AND METHODS: Patient clinic, screened for non-bleeding gastrointestinal conditions including celiac disease (antiendomysial antibodies), autoimmune atrophic gastritis (hypergastrinemia with strongly positive antiparietal cell antibodies) and H. pylori infection (IgG antibodies confirmed by urease breath test). RESULTS: The mean age of all subjects was 39+/-18 years, and 119 of 150 were females. We identified 8 new cases of adult celiac disease (5%). Forty IDA patients (27%) had autoimmune atrophic gastritis of whom 22 had low serum vitamin B12 levels. H. pylori infection was the only finding in 29 patients (19%), but was a common co-existing finding in 77 (51%) of the entire group. Refractoriness to oral iron treatment was found in 100% of patients with celiac disease, 71% with autoimmune atrophic gastritis, 68% with H. pylori infection, but only 11% of subjects with no detected underlying abnormality. H. pylori eradication in previously refractory IDA patients in combination with continued oral iron therapy resulted in a significant increase in hemoglobin from 9.4+/-1.5 (mean +/- 1SD) before, to 13.5+/-1.2 g/ dL (p<0.001 by paired t test) within 3 to 6 months. INTERPRETATION AND CONCLUSIONS: The recognition that autoimmune atrophic gastritis and H. pylori infection may have a significant role in the development of unexplained or refractory IDA in a high proportion of patients should have a strong impact on our daily practice of diagnosing and managing IDA.

Adolescent↗
PubMed1983

[Massive hepatic steatosis disclosing adult celiac disease. Study of a case and review of the literature].

The authors report the case of a 32-year old woman admitted for hepatomegaly, weight loss, and moderate diarrhea. Liver function tests showed anicteric cholestasis with slight increase in serum level of transaminases. Liver biopsy demonstrated massive steatosis. Biological and radiological investigations of the small intestine showed a malabsorption pattern. Stool fat excretion was 54 g per day. Duodenal biopsies disclosed total villous atrophy. A ten-day treatment with metronidazole (1,5 g per day), followed by a gluten-free diet, resulted in rapid improvement of hepatic and intestinal symptoms. This case report shows that: 1) adult celiac disease may be the cause of severe steatosis; 2) anicteric cholestasis with or without hepatomegaly during the course of adult celiac disease may be secondary to steatosis, as well as primary biliary cirrhosis or malignant infiltration of the liver; 3) bacterial overgrowth should be searched and eventually treated in the case of massive fatty liver occurring in adult celiac disease.

Adult↗
PubMed2006

Bone mineral density in children with celiac disease. Effect of a Gluten-free diet.

OBJECTIVE: To assess the degree of osteopenia in children with celiac disease (CD) at the time of diagnosis and the effect of a gluten-free diet (GFD). DESIGN: Longitudinal and prospective study. SUBJECTS: In total, 24 children (18 girls, six boys) diagnosed with CD by means of an intestinal biopsy were included in the study. Mean+/-s.d. age was 4.9+/-4.3 years. In all, 16 patients were under (2.20+/-0.82 year) and eight were over the age of 4 years (10.30+/-2.90 year). The time between the first symptoms and diagnosis was 17.30+/-24.70 months (range: 2-109 months). Spine bone mineral content (BMC), area and bone mineral density (BMD) were measured by DXA at baseline and 1.17+/-0.93 years after GFD. RESULTS: Before treatment, mean+/-s.d. BMD was 0.46+/-0.13 g/cm(2), the BMD Z-score was -1.36+/-1.20, and was below -1 s.d. in 14 patients (58%). BMC, area and BMD increased significantly on GFD. BMD increased from 0.46+/-0.13 to 0.55+/-0.13 g/cm(2) (P<0.001). BMD Z-score improved from -1.36+/-1.20 to -0.23+/-1.20 after GFD. However, BMD increased more than 1 s.d. in 15 of the 16 children under the age of 4 years, a similar increase was only observed in four of the eight children aged more than 4 years, some of whom did not follow GFD strictly. Height and weight increased significantly with GFD (P<0.001) and the increase correlated positively with the increase in BMD. CONCLUSIONS: Axial BMD below -1 s.d. was found in 58% of children with celiac disease. Axial bone mass reverted to normal values in most children under the age of 4, who had low bone mass, all of whom followed GFD strictly.

Absorptiometry, Photon↗
PubMed2006

A preliminary investigation of ADHD symptoms in persons with celiac disease.

OBJECTIVE: Several studies report a possible association of celiac disease (CD) with psychiatric and psychological disturbances, such as ADHD. METHOD: The authors assess 132 participants from 3 to 57 years of age (M = 19.3 years) affected by CD for the possibility of an associated ADHD-like symptomatology, using the Conner Scale Hypescheme, a behavioral scale similar to the Conners Rating Scales, before their gluten-free diet was started and 6 months later. RESULTS: The overall score improves significantly as well as most of the ADHD-like symptomatology specific features (Bonferroni-corrected, paired-sample t tests). CONCLUSION: The data indicate that ADHD-like symptomatology is markedly overrepresented among untreated CD patients and that a gluten-free diet may improve symptoms significantly within a short period of time. The results of this study also suggest that CD should be included in the list of diseases associated with ADHD-like symptomatology.

Adolescent↗
PubMed2002

TNF alpha and LT alpha gene polymorphisms as additional markers of celiac disease susceptibility in a DQ2-positive population.

TNFalpha and TNFbeta, or linfotoxin (LTalpha), are two molecules playing an important role in inflammation. Their genes map on Chromosome 6, between the HLA class II and class I loci. Polymorphisms in, or near, TNF genes have been associated with susceptibility to several autoimmune diseases. Studies of TNF genes in celiac disease (CD) have presented contradictory results. We have assessed the role of TNFalpha and linfotoxin alpha (TNFbeta) in CD and their relative value as CD markers in addition to the presence of DQ2. The TNFA -308 polymorphism and the polymorphism at the first intron of the LTA gene were typed in CD patients and healthy controls and the results were correlated with the presence of DQ2. Significant differences were found in genotype and allele frequencies for the TNFA and LTA genes between CD patients and controls, with an increase in the presence of the TNFA*2 and LTA*1 alleles in CD patients. These differences increase when DQ2-positive CD patients and DQ2-positive controls are compared. In DQ2-positive individuals, allele 2 (A) in position -308 of the promoter of TNFA and allele 1 (G) of the NcoI RFLP in the first intron of LTA are additional risk markers for CD.

Celiac Disease↗
PubMed1981

Celiac disease complicated by chronic nongranulomatous ulcerative enterocolitis, nodular lymphoid hyperplasia, and disseminated intravascular coagulation.

A patient is presented in whom celiac disease was complicated by the development of chronic nongranulomatous ulcers in the small and large intestine. In addition, he had nodular lymphoid hyperplasia in the bowel wall and mesenteric lymphoadenopathy. The terminal illness was characterized by disseminated intravascular coagulation. It is postulated that the lymphoid hyperplasia was secondary to excessive stimulation of the reticuloendothelial system by nongluten antigens and may be a precursor of the development of lymphoma in celiac disease. Nongluten antigens such as bacteria or endotoxins were probably responsible for the consumptive coagulopathy.

Celiac Disease↗
PubMed1995

The diagnostic reliability of anti-endomysial antibody in celiac disease: the north Israel experience.

Assessment of anti-endomysial antibody (EMA) for the diagnosis and follow-up of celiac disease (CD) is widely accepted, but its applicability has never been investigated in Israel. We therefore investigated EMA as a diagnostic tool in a pediatric population, residing in the northern part of Israel, with suspected celiac disease. EMA was assessed by an indirect immunofluorescence assay using monkey esophageal sections as a substrate in 22 active CD, 17 non-active CD, and 22 non-CD children. EMA titers were correlated with small bowel mucosal pathology. Sensitivity and specificity of EMA were 100%. EMA levels are diet dependent, increasing on a gluten-containing diet and decreasing with gluten withdrawal after 3-12 months. EMA is a reliable marker for the diagnosis of CD, and reflects gluten intake changes and patients' dietary compliance. In our laboratory, EMA is suitable for the diagnosis and follow-up of CD.

Atrophy↗
PubMedDate not supplied

Celiac disease presenting with chilblains in an adolescent girl.

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.

Adolescent↗
PubMed1998

Gluten stimulation induces an in vitro expansion of peripheral blood T gamma delta cells from HLA-DQ2-positive subjects of families of patients with celiac disease.

The intestinal gluten sensitivity formally known as celiac disease (CD) is characterized by an evident involvement of local immune response and it is associated with the expression of HLA-DQ2 allele. The major role in the disease seems to be played by the T lymphocyte population bearing gamma delta T cell receptor (T gamma delta cells) which are increased both in peripheral blood and intestinal mucosae of celiac patients. In this paper data on the effects of in vitro gluten stimulation on lymphocytes expressing the T gamma delta phenotype are reported. Gluten seems to be able to induce the expansion of the T gamma delta cell population both in CD patients and their HLA-DQ2-positive asymptomatic relatives, in spite of the absence of clinical evidence of the disease. In addition, the evaluation of gluten-induced cytokine production shows that interleukin-4 could be implied in the early phases of pathogenesis of CD.

Adolescent↗
PubMed2006

Celiac disease and risk of liver disease: a general population-based study.

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.

Adolescent↗
PubMed2005

[Celiac disease in close family members].

OBJECTIVES: To investigate the presence of celiac disease (CD) in close family members of celiac patients, and the possible clinical differences between family members diagnosed and their respective index cases. DESIGN: Descriptive, observational study based on a series of cases. SETTING: Health centre and hospital. PARTICIPANTS: Family members of celiac patients registered with the Association of Celiacs of Andalusia, based in Sevilla. MAIN MEASUREMENTS: Patients and family members were interviewed and 2 questionnaires were filled in. The first, aimed at celiacs, recorded details of their disease and the second recorded personal details, current illnesses, personal history and the family members of all participants. IgA endomysium antibodies were determined only in family members. RESULTS: 56 of 215 families recorded took part, with 239 participants. Of the 56 patients, 1 per family, presentation at the moment of diagnosis was malabsorption syndrome. Of 165 family members studied, 11 cases with positive IgA endomysium antibodies were found and 5 actually with CD. One of these was asymptomatic, three presented with atypical forms of CD and another was diagnosed with herpetiform dermatitis. CONCLUSIONS: That CD was most commonly found among close family members, along with its asymptomatic or atypical clinical presentation, justifies the active search for cases. Primary care doctors should question family members as to whether they have been tested for the disease. If not, adults should be checked for the antibodies referred to and children should be referred to their paediatricians for this purpose.

Adolescent↗
PubMed1999

CD28/CTLA4 gene region on chromosome 2q33 confers genetic susceptibility to celiac disease. A linkage and family-based association study.

Celiac disease (CD) is a common small intestinal injury caused by sensitivity to gliadin in genetically-predisposed individuals. The only susceptibility locus established is the HLA-DQ. We tested whether the chromosomal region of the CD28/CTLA4 genes on 2q33 is linked to CD. These genes encode receptors regulating the T-lymphocyte activation. Recently, this gene region was reported to be linked to the susceptibility to many autoimmune diseases, including insulin-dependent diabetes (IDDM12locus). It is thus an obvious candidate locus also for CD, since the intestinal injury is mediated by the immune system. Genetic linkage between seven marker loci in this gene region and CD was studied in 69 Finnish families. In the multipoint linkage analysis, the highest non-pararametric linkage score (NPL) was 1.75 (P=0.04) for D2S116, suggesting weak linkage for this candidate locus. To evaluate this finding, an additional 31 families were typed for all markers. In the combined set of 100 families the NPL score for marker D2S116 was 2.55 (P=0.006) and for other markers 1.90-2.47 (P=0.029-0.007), supporting genuine linkage at this region. Significantly, locus D2S116 also showed a clear allelic association in these 100 families (P=0.0001). The transmission/disequilibrium test (TDT) for locus D2S116 gave preliminary evidence for preferential maternal non-transmission of allele *136 to patients (TDTmax=8.3; P<0.05). No paternal deviation was found suggesting that the effect of the locus might be mediated by a sex-dependent factor protective against CD. Our results indicate that the CD28/CTLA4 gene region can contain a novel susceptibility locus for CD and support the hypothesis that CD has an immune system-mediated component. Like the HLA, the CD28/CTLA4 genes appear to be associated with genetic susceptibility to various autoimmune diseases.

Abatacept↗