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PubMed2001

Current approaches to diagnosis and treatment of celiac disease: an evolving spectrum.

Celiac disease (CD) is a syndrome characterized by damage of the small intestinal mucosa caused by the gliadin fraction of wheat gluten and similar alcohol-soluble proteins (prolamines) of barley and rye in genetically susceptible subjects. The presence of gluten in these subjects leads to self-perpetuating mucosal damage, whereas elimination of gluten results in full mucosal recovery. The clinical manifestations of CD are protean in nature and vary markedly with the age of the patient, the duration and extent of disease, and the presence of extraintestinal pathologic conditions. In addition to the classical gastrointestinal form, a variety of other clinical manifestations of the disease have been described, including atypical and asymptomatic forms. Therefore, diagnosis of CD is extremely challenging and relies on a sensitive and specific algorithm that allows the identification of different manifestations of the disease. Serologic tests developed in the last decade provide a noninvasive tool to screen both individuals at risk for the disease and the general population. However, the current gold standard for the diagnosis of CD remains histologic confirmation of the intestinal damage in serologically positive individuals. The keystone treatment of CD patients is a lifelong elimination diet in which food products containing gluten are avoided.

Celiac Disease↗
PubMed2005

[Clinical picture of celiac disease in children].

UNLABELLED: During the last few years we have been observing the decreasing incidence of the symptomatic celiac disease and increasing incidence of mono- and asymptomatic disease. Various atypical symptoms and extraintestinal manifestations were observed in older children (above 7 years) and in adults. Clinical symptoms of celiac disease may appear at any age, in each of the following forms: clinical celiac disease (symptomatic), silent (oligosymptomatic) or latent, with late manifestation, being the effect of stress, pregnancy, infections or excessive dietary gluten provocation. THE AIM OF THE STUDY: The presentation the variety of clinical pictures of celiac disease in children. MATERIALS AND METHODS: We have evaluated the clinical course of celiac disease in 16 children (13 girls and 3 boys), aged between 12 months to 17 years (mean-7,5 years). The celiac disease was diagnosed on the grounds of clinical symptoms, histopathological examination of the small intestinal endoscopic biopsy and immunological examinations: serum antitransglutaminase antibodies and anti-endomysium antibodies. RESULTS: Most commonly diagnosed form was the silent, monosymptomatic celiac disease. Four children manifested with growth retardation, one with osteoporosis, and one with iron deficiency anemia resistant to treatment. Two girls (aged 16 and 17 years) presented with symptomatic celiac disease. In 3 patients despite the gastrointestinal symptoms and histopathological changes present (villous atrophy, Marsh's index > 40) we did not find any immunological markers of celiac disease (with normal IgA levels). CONCLUSIONS: School-aged children with celiac disease, in many cases have no evident clinical and functional disorders caused by gluten intake, despite to presence of considerable abnormalities in the histopathological examination.

Adolescent↗
PubMed2005

Celiac disease: from inflammation to atrophy: a long-term follow-up study.

OBJECTIVES: Celiac disease develops gradually from lymphocytosis, crypt hyperplasia and minor villous atrophy to overt villous atrophy. It IS NOT known how such minor mucosal changes predict eventual celiac disease. The aim of this study was to evaluate the role of intraepithelial lymphocytosis and marginally decreased villous height/crypt depth ratio in the development of overt villous atrophy in a long-term follow-up. METHODS: The authors evaluated 980 small bowel biopsies of children who had previously been studied and found to be histologically negative for celiac disease between 1976 and 1992. Villous height/crypt depth ratio and the number of intraepithelial lymphocytes were measured in these initial biopsies. Cases with slight biopsy changes were identified for further study and sex and age matched subjects with normal biopsies from same group were selected as controls. They all were asked to submit serum samples for gliadin, endomysial and tissue transglutaminase antibodies 8 to 28 years after the initial biopsy. Those with positive screening tests were asked to undergo endoscopy and small intestinal biopsy. RESULTS: 236 cases with slight changes were identified, and 236 with normal mucosa served as controls; 76 cases and 68 controls participated in the follow-up study. Ten individuals had positive screening test results. Two new celiac disease patients, one in each group, were found. Four patients in the case group had been diagnosed with celiac disease by routine procedures during the follow-up. Thus, five cases and one control had developed celiac disease. CONCLUSIONS: Small bowel mucosal lymphocytosis or slight reduction in villous height/crypt depth ratio are common findings in patients with suspicion of celiac disease. These findings alone are poor predictors of celiac disease.

Adolescent↗
PubMed2004

A genomewide screen in a four-generation Dutch family with celiac disease: evidence for linkage to chromosomes 6 and 9.

OBJECTIVES: Celiac disease is caused by the interaction of multiple genes and environmental factors. Inheritance of the disease shows a complex pattern with a 10% sibling recurrence risk. The HLA-region is a major genetic risk locus in celiac disease, but genes outside this region are expected to contribute to the disease risk as well. The aim of this study was to identify the loci causing celiac disease in one large Dutch family with apparent dominant transmission of the disease. METHODS: The family comprised 17 patients in four generations, with possible transmission of the disease by both grandparents. Microsatellite markers evenly spread over all chromosomes were genotyped and linkage analysis was performed using both dominant and recessive disease models and a model-free analysis. RESULTS: Disease susceptibility in the family was linked to the HLA-region (lod score of 2.33) and all patients were HLA-DQ2. A dominantly inherited non-HLA locus with a maximum lod score of 2.61 was detected at 9p21-13, which was shared by 16 patients. Model-free analysis identified another possible non-HLA locus, at 6q25.3, which was shared by 14 patients (p = 0.01). Neither of these regions was detected in a genomewide screen in Dutch affected sibpairs, but the 9p21 locus has been implicated in Scandinavian families. CONCLUSIONS: Two potential non-HLA loci for celiac disease were identified in this large Dutch family. Our results provide replication of the Scandinavian 9p21 locus, and suggest that this locus plays a role in celiac disease patients from different Caucasian populations.

Adolescent↗
PubMed1986

Short stature as the major manifestation of celiac disease in older children.

Celiac disease was diagnosed by jejunal biopsy and response to gluten elimination in 11 of 23 children with short stature referred after negative endocrine evaluation. The mean age of the group was 11 years, with a range of 5-16. All had been followed for a mean of 2.5 years at a large pediatric endocrine clinic for the evaluation of growth retardation. Bone age retardation of more than 25 percent of the chronologic age was found in all children. Microcytic anemia and past history of gastrointestinal problems were typical of the celiac group but were not documented in the nonceliac patients. Stool fat excretion was a specific but insensitive test, while the 1-hour blood xylose test was of no value in differentiating between the two groups. Close cooperation between pediatric endocrinology and gastroenterology clinics may be fruitful in the identification of celiac patients, especially in a group of older children with short stature, bone age retardation, and microcytic anemia.

Adolescent↗
PubMedDate not supplied

Adult celiac disease in northern India.

OBJECTIVE: To study the presentation of adult celiac disease in a northern Indian hospital. METHODS: Case records of all patients diagnosed as having adult celiac disease in the Gastroenterology unit of this hospital during January 1996 till December 2001 were reviewed. Celiac disease was diagnosed according to the revised ESPGAN criteria. Adult celiac disease was diagnosed if disease manifestations started after 15 years of age. All patients had a minimum of one-year follow up. RESULTS: The mean duration of illness in the 96 patients (mean [SD] age 32.9 [11.4] years; 50 men) diagnosed over the 6-year study period was 7.3 (2.4) years. Diarrhea was present is 67.7% of cases; 18.7% presented with refractory iron-deficiency anemia, and 9.4% with abdominal symptoms like flatulence and distension. Three patients presented with dysphagia and anemia and were diagnosed as having Plummer-Vinson syndrome. Ulcerative colitis, non-alcoholic steatohepatitis, and aphthous ulcers were associated conditions. All patients had significant improvement in symptoms and hematological and biochemical parameters after dietary gluten restriction. CONCLUSION: Adult celiac disease is not rare and usually presents as diarrhea, abdominal distension and flatulence, and refractory anemia.

Acute Disease↗
PubMed2006

Prevalence of celiac disease in Brazilian children with type 1 diabetes mellitus.

OBJECTIVE: Although the relationship between celiac disease and diabetes mellitus type 1 is well recognized, there are no studies of this association in Brazil. This study aims to identify the prevalence of celiac disease in a group of children with diabetes mellitus type 1 undergoing treatment in the pediatric endocrinology division of a university hospital in Minas Gerais, Brazil. METHODS: Immunoglobulin (Ig)A and IgG antigliadin antibodies (enzyme-linked immunoadsorbent assay) were measured in blood collected from 236 children and adolescents with diabetes mellitus type 1. Patients with antigliadin antibodies then had jejunal biopsy and determination of antiendomysial antibodies by indirect immunofluorescence. RESULTS: Twenty-one patients had IgA or IgG antigliadin antibodies. Nineteen underwent jejunal biopsy. Six had mucosal alterations compatible with celiac disease; four had nonspecific histologic changes; nine had normal biopsies. Thirteen antigliadin antibody-positive patients were antiendomysial antibody-negative; one antiendomysial antibody-negative patient had celiac disease. The prevalence of celiac disease was 2.6% among 234 patients. CONCLUSIONS: Measurement of antigliadin antibodies in patients with diabetes mellitus type 1 helped in the selection of patients to undergo jejunal biopsy. Antiendomysial antibodies were highly specific and moderately sensitive in predicting celiac disease. The prevalence of celiac disease was higher in diabetics than in the general population, suggesting the need for regular screening assessment of diabetic children.

Adolescent↗
PubMed2003

Celiac disease: a progress report.

Celiac disease (CD) has a wide range of clinical presentations and is being diagnosed with increasing frequency in patients in the 4th and 5th decades of life. The diagnosis of CD is confirmed by a combination of clinical, serological, and morphological findings associated with a response to a gluten-free diet. In small-bowel mucosal biopsy specimens, abnormalities range from minimal (increased villous intraepithelial lymphocytes only) to severe (complete villous blunting with crypt hyperplasia). Recognition of CD is important because appropriate therapy of this condition will obviate the risk of its severe complications.

Celiac Disease↗
PubMed2004

The global village of celiac disease.

In the last years our knowledge on epidemiology of celiac disease has increased: there is a wide spectrum of its clinical presentation (classical, atypical, silent and latent forms of celiac disease), and of its pathological mucosal intestinal features, which range from early and mild pictures to severe villous atrophy (Marsh stages). In addition, a strong genetic component, associated with the susceptibility to the disease (HLA and non HLA genes), has been found. This knowledge, together with the availability of new high sensitive and specific serological tests (antigliadin, antiendomysium and antitransglutaminase antibodies), has led us to the realization that celiac disease is the most common food intolerance in the world, involving genetically predisposed individuals consuming gluten-containing cereals in their diet. So, today it is well known that celiac disease is a common disorder not only in Europe but also in populations of European ancestry (North and South Americas, Australia), in North Africa, in the Middle East and in South Asia, where until a few years ago it was historically considered extremely rare. Therefore, celiac disease is spread worldwide as in a common "Global Village", and greater levels of awareness and attention on gluten intolerance are needed, both in the Old and in the New World.

Celiac Disease↗
PubMed2000

[Celiac disease and abortion: focusing on a possible relationship].

Celiac disease represents one of the most frequent chronic inflammatory diseases. In Italy the prevalence among school-age population has been calculated in 1:180 subjects. Along with typical forms of the disease characterized by overt symptoms and signs of malabsorption, many cases are undiagnosed because they are subclinical, atypical or even symptomless. In adults, the disease may present with infertility; in particular celiac disease may be responsible of multiple abortions. These manifestations, whose pathogenesis is unknown, are not related to the severity of the disease; the gluten-free diet strongly ameliorates the fertility. In this paper we have focused the connection between abortion and celiac disease. A better knowledge of this relationship may lead to correctly diagnose and consequently to treat the cause of some cases of abortion, previously labelled as cases of unidentified origin.

Abortion, Spontaneous↗
PubMed2002

Enterovirus infection during pregnancy is not a risk factor for celiac disease in the offspring.

BACKGROUND: There is a strong genetic influence on the susceptibility to celiac disease but it is also evident that environmental factors play a role in the development of the disease. Diverging studies about adenovirus infection as a possible triggering factor in the pathogenesis have been reported. Our study was undertaken to determine whether enterovirus infection during pregnancy is a risk factor for the development of celiac disease later in childhood. METHODS: Cord blood from 76 mothers whose children developed celiac disease before 15 years of age were analyzed for IgA, IgG, and IgM antibodies for enteroviruses and Ig-A endomysium antibodies. The control group comprised cord blood from 327 mothers with children without known celiac disease. RESULTS: There were no significant differences in antibody titers for enterovirus between the two groups. IgA-endomysium antibodies were elevated in 3 of the 76 mothers, whereas none had known celiac disease. CONCLUSION: This study does not show that enterovirus infection during pregnancy is associated with the development of celiac disease in childhood. Of the mothers whose children developed celiac disease, 4% had Ig-A endomysium antibodies, which may reflect a silent celiac disease.

Adolescent↗
PubMedDate not supplied

Serum carnitine and selenium levels in children with celiac disease.

BACKGROUND AND AIM: Celiac disease (CD) is a gluten-induced enteropathy that results in malabsorption of nutrients. We studied the serum levels of carnitine and selenium in children with CD. METHODS: Serum levels of free carnitine and selenium were studied in 30 children (mean age 8.1 [4.4] years) with CD and 30 age- and gender-matched healthy children. All patients had type 3 duodenal lesions. The mean (SD) serum levels of free carnitine and selenium were lower among patients with CD (24.5 [7.7] micromol/mL and 52.1 (12.9) micromol/mL, respectively) than among healthy controls (29.4 [9.2] and 65.1 [17.2] micromol/mL; p < 0.05 each). Levels were similar in children with and without diarrhea. CONCLUSIONS: Serum carnitine and selenium levels are decreased in children with CD, probably due to malabsorption.

Adolescent↗
PubMed1999

Small bowel intussusception in celiac disease.

Intussusception is not a widely recognized complication of celiac disease and yet it is not rare. The authors report on 3 children with spontaneously resolving small bowel intussusception in association with celiac disease. Small bowel intussusception in a child with suspected celiac disease initially should be managed expectantly rather than by early surgical reduction. The finding of transient small bowel intussusception, either by contrast radiology or sonography, should prompt investigation for celiac disease.

Celiac Disease↗
PubMed2000

Histopathology of celiac disease.

The diagnosis of celiac disease (CD) is based upon histologic findings in duodenal or jejunal biopsies. In the past few years it has turned out that the development of CD lesion in the small bowel is a dynamic process which may present in various histologic forms. At one end of the spectrum is a mucosa with normal architecture and an increase in intraepithelial lymphocytes (IEL), at the other end is the classical flat mucosa. Histologic features supporting the diagnosis of CD are architectural changes of the villi and/or crypts, an increase in lamina propria cell density and an increase in IEL counts. For diagnostic purposes and for monitoring CD patients an exact histologic classification of the histologic findings has to be given. This has become possible by using a modified Marsh classification. In the present paper the histologic presentation of CD is presented as well as the modified Marsh classification.

Celiac Disease↗
PubMedDate not supplied

[Reproductive aspects of celiac disease].

In the past, celiac disease (CD), or intolerance to gluten, was considered a rare disease of infancy characterized by chronic diarrhea with malabsorption and delayed growth. Besides the overt enteropathy, there are other clinic and subclinical forms which appear later in life. Target organs are not limited to the gut, but include liver, thyroid, skin and female and male reproductive systems. CD interference on reproduction is related to the multifactorial nature of the disease, whose pathological manifestations can be modulated, besides gluten, by different concurrent genetic and environmental factors. CD induces malabsorption with consequent deficiencies of micronutrients such as iron, folic acid and vitamin K, which are essential for organogenesis, and fat-soluble vitamins important for spermatogenesis. Regarding endocrine disorders, the deficiencies of specific trace elements on ovarian function could explain its involvement in the increased risk of female osteoporosis in CD patients. Affected males show a picture of tissue resistance to androgens; the increases of follicle-stimulating hormone and prolactin, not associated with infertility, may indicate an imbalance at hypothalamus-pituitary level, with general effects on health. Since reproductive alterations are reversible, adoption of a gluten-free diet supported by early diagnosis is important. Therefore, the detection of early biomarkers, such as deficiencies of vitamins and/or iron and andrological or endocrinological dysfunctions, should trigger timely strategies for prevention and treatment.

Abortion, Spontaneous↗
PubMed1998

Similar IL-5, IL-3, and GM-CSF syntheses by eosinophils in the jejunal mucosa of patients with celiac disease and dermatitis herpetiformis.

Celiac disease (CD) and dermatitis herpetiformis (DH) are gluten-sensitive diseases with different clinical features that can initiate similar intestinal changes. The flat-destructive stage corresponds to severe lesions involving activated T-cells. However, other inflammatory cells such as eosinophils are also abundant. The mechanisms for the intestinal recruitment of eosinophils in patients with CD and DH remain unknown. Eosinophil recruitment and activation are induced in vitro by three main cytokines: interleukin-3 (IL-3), interleukin-5 (IL-5), and granulocyte-macrophage colony-stimulating factor (GM-CSF). In this study, IL-3, IL-5, and GM-CSF were detected by immunohistochemistry in all patients with CD and DH but not in the control group. By ultrastructural immunogold staining, these three cytokines had the same subcellular localization in the granule matrix of eosinophils. This result suggests that eosinophils may be involved in the immune response at the flat-destructive stage of both CD and DH.

Adolescent↗
PubMed2001

Genomewide linkage analysis of celiac disease in Finnish families.

Celiac disease (CD), or gluten-sensitive enteropathy, is a common multifactorial disorder resulting from intolerance to cereal prolamins. The only established genetic susceptibility factor is HLA-DQ, which appears to explain only part of the overall genetic risk. We performed a genomewide scan of CD in 60 Finnish families. In addition to strong evidence for linkage to the HLA region at 6p21.3 (Z(max)>5), suggestive evidence for linkage was found for six other chromosomal regions--1p36, 4p15, 5q31, 7q21, 9p21-23, and 16q12. We further analyzed the three most convincing regions--4p15, 5q31, and 7q21--by evaluation of dense marker arrays across each region and by analysis of an additional 38 families. Although multipoint analysis with dense markers provided supportive evidence (multipoint LOD scores 3.25 at 4p15, 1.49 at 5q31, and 1.04 at 7q21) for the initial findings, the additional 38 families did not strengthen evidence for linkage. The role that HLA-DQ plays was studied in more detail by analysis of DQB1 alleles in all 98 families. All but one patient carried one or two HLA-DQ risk alleles, and 65% of HLA-DQ2 carriers were affected. Our study indicates that the HLA region harbors a predominant CD-susceptibility locus in these Finnish families.

Adult↗
PubMed2005

High prevalence of celiac disease in patients with lactose intolerance.

BACKGROUND/AIMS: Acquired lactase deficiency is a common cause of gastrointestinal symptoms but its etiology remains unclear. Celiac disease could lead to lactase deficiency and is much more common than previously suspected. Several studies have highlighted the prevalence of lactose intolerance in celiac disease, but studies assessing the prevalence of celiac disease in lactose intolerance are lacking. We evaluated the prevalence of celiac disease in patients with a positive H2-lactose breath test compared to a control group. METHODS: This retrospective study included 54 patients (15 males/39 females; mean age 37.8 +/- 7 years) from southern Italy, referred to the Gastroenterology Unit for bloating and diarrhea after the introduction of milk or dietary lactose. They had a positive H2-lactose breath test and a negative H2-glucose breath test. 50 blood donors were drawn from a similar population, matched for sex and age, and enrolled as a control group. All patients were screened for possible celiac disease by measuring the serum level of IgA antibodies to endomysium, anti-transglutaminase and total IgA. Patients positive for at least one of these markers were submitted to upper gastrointestinal endoscopy. RESULTS: None of the patients had a IgA deficiency. 24% of the patients showed positivity of celiac disease antibodies compared to 2% in the control group (p < 0.001). Histologic samples of these patients showed villous atrophy (53.8% Marsh type IIIa, 38.4% Marsh IIIb, and 7.6% with Marsh type IIIc) confirming the celiac disease, while in the control subjects duodenal biopsies were normal. CONCLUSIONS: A high prevalence of celiac disease was observed in patients with a positive H2-lactose breath test compared to healthy controls. In these subjects lactase deficiency seems to be the only manifestation of celiac disease. We suggest serologic screening for celiac disease in all patients with a positive H2-lactose breath test before beginning a milk-exclusion diet.

Adult↗