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PubMed1998

Significantly increased levels of nitric oxide products in urine of children with celiac disease.

BACKGROUND: Celiac disease is characterized by morphologic and functional aberrations of the small intestinal mucosa, i.e., crypt hyperplasia, villous atrophy, infiltration of intraepithelial lymphocytes, and alteration of permeability. Nitric oxide has been shown to affect mucosal permeability after ischemia-reperfusion, but little is known about the regulatory role of nitric oxide in celiac disease. The purpose of this study was to assess nitric oxide production in children with celiac disease and in control subjects. METHODS: The sum of nitrite and nitrate in the urine was measured with a colorimetric method in 137 children with a median age of 3 years, 84 patients and 53 reference children, all of whom underwent a small intestinal biopsy to confirm or overrule suspicion of celiac disease. RESULTS: Median urinary nitrite-nitrate concentration in celiac children was 3323 microM (4147 +/- 1102; mean +/- SEM) at first clinical examination and 2501 microM (2939 +/- 386) after gluten challenge, which was significantly higher than concentrations in reference children (1029 microM; 1174 +/- 116) and in children with celiac disease on a gluten-free diet (882 microM; 1369 +/- 360) (p < 0.0001). CONCLUSIONS: A gluten-containing diet is associated with an increased nitrite-nitrate secretion in the urine in children with celiac disease, presumably as a result of nitric oxide synthase activation and nitric oxide production in the diseased small intestinal mucosa.

Adolescent↗
PubMed2002

Breast-feeding protects against celiac disease.

BACKGROUND: Celiac disease, or permanent gluten-sensitive enteropathy, is an immunologic disease strictly dependent on exposure to wheat gluten or related proteins in rye and barley. OBJECTIVE: The aim of this study was to explore whether breast-feeding and the mode of introducing dietary gluten influence the risk of celiac disease in childhood. DESIGN: A population-based incident case-referent study of Swedish children, 627 cases with celiac disease and 1254 referents, was conducted; 78% of the matched sets were included in the final analyses. A questionnaire was used to assess patterns of food introduction to infants. Models were built, based on current epidemiologic and immunologic knowledge of celiac disease, to study the potential influence of dietary patterns on disease risk and were evaluated by conditional logistic regression in multivariate analyses. RESULTS: The risk of celiac disease was reduced in children aged <2 y if they were still being breast-fed when dietary gluten was introduced [adjusted odds ratio (OR): 0.59; 95% CI: 0.42, 0.83]. This effect was even more pronounced in infants who continued to be breast-fed after dietary gluten was introduced (OR: 0.36; 95% CI: 0.26, 0.51). The risk was greater when gluten was introduced in the diet in large amounts (OR: 1.5; 95% CI: 1.1, 2.1) than when introduced in small or medium amounts. In older children, these risk factors were of no or only minor importance. CONCLUSIONS: The gradual introduction of gluten-containing foods into the diet of infants while they are still being breast-fed reduces the risk of celiac disease in early childhood and probably also during the subsequent childhood period.

Adolescent↗
PubMed2001

Clinical and subclinical autoimmune thyroid disease in adult celiac disease.

Our aim was to investigate the occurrence of clinical and subclinical autoimmune thyroid disease in 79 patients with celiac disease as reflected in thyroid function, antibodies, and ultrasound. Since subclinical thyroid diseases are common in the population, 184 nonceliac controls were also studied. Normal thyroid function combined with positive antibodies and marked hypoechogenicity was considered subclinical disease. Autoimmune thyroid disease was observed in 13.9% of celiac patients and in 2.1% of controls (P = 0.0005); and subclinical disease in 10.1% and 3.3%, respectively (P = 0.048). The mean thyroid gland volume was 8.3 ml in celiac patients and 10.4 ml in controls (P = 0.007). Hypoechogenicity was found in 73% of celiac patients and in 42% of controls (P < 0.0001). Positive thyroid antibodies were associated with hypoechogenicity in celiac patients but not in controls. In conclusion, the occurrence of both clinical and subclinical autoimmune thyroid disease was increased in celiac disease; subclinical thyroid disease indicates regular surveillance.

Autoimmune Diseases↗
PubMed1997

[Bone metabolic disease associated with celiac disease].

Patients with celiac disease present a high prevalence of osteopenia and osteoporosis which globally jeopardize the skeleton. The pathogenesis of this bone disease is related to an accelerated bone change in which catabolism predominates. The metabolic studies coincide in a negative calcium balance with consequent secondary hyperparathyroidism. Diagnosis requires evaluation of bone mineral density by precise, reliable methods to which all adult celiac patients should be submitted. Finally, specific treatment with a gluten-free diet leads to significant bone remineralization.

Bone Diseases, Metabolic↗
PubMed1995

Screening for celiac disease in first-degree relatives of patients with celiac disease by lactulose/mannitol test.

OBJECTIVES: In first-degree relatives of celiac patients, the risk of oligosymptomatic celiac disease is elevated. These individuals therefore also have a higher potential for malignancy or nutritional deficiencies. Lactulose/mannitol permeability is increased in untreated celiac patients and has been recommended to screen for celiac disease. We investigated the usefulness of a lactulose/mannitol home test kit for screening first-degree relatives home test kit for screening first-degree relatives of celiac patients. METHODS: The lactulose/mannitol test was performed at home by 111 first-degree relatives. These subjects received the test kit from celiac index patients, were instructed by an information sheet how to carry out the test, and were asked about their symptoms by questionnaire. When lactulose/mannitol permeability was abnormal, endomysial antibodies were tested by immunofluorescence. Any relatives with positive endomysial antibodies were then biopsied. To investigate the specificity of the lactulose/mannitol test for celiac disease, 40 patients with nonspecific gastrointestinal symptoms were tested. RESULTS: Lactulose/mannitol permeability was elevated in 34 (31%) relatives, but only nine (8%) of those relatives showed positive endomysial antibodies. Flat mucosa was found in all nine relatives after biopsy. The prevalence of celiac disease was much higher (42%) among 12 relatives who contacted the outpatient clinic themselves because of symptoms. Seventy-one percent of the remaining 21 relatives with elevated permeability demonstrated normal intestinal permeability at a control test within 1 yr. CONCLUSION: By combining the lactulose/mannitol test with endomysial antibody testing, we have developed a good strategy for use in screening for celiac disease among first-degree relatives.

Adolescent↗
PubMed2004

Imbalance of osteoclastogenesis-regulating factors in patients with celiac disease.

UNLABELLED: Celiac disease is an autoimmune disorder characterized by atrophy of the intestine villi triggered by ingestion of gluten in genetically susceptible individuals. The association between celiac disease and low BMD has been recognized, but the mechanisms of disturbance are poorly understood. We show imbalance of cytokines relevant to bone metabolism in celiac patients' sera and the direct effect of these sera on in vitro bone cell activity. INTRODUCTION: Celiac disease is associated with mineral metabolism derangement and low BMD. We investigated whether imbalance of serum factors in celiac patients could affect human bone cell activity in vitro. MATERIALS AND METHODS: We studied two groups of celiac patients--one on a gluten-free diet and another before the diet--both with decreased bone mass. Patients were investigated for bone turnover markers, and their sera were used for culturing bone cells from healthy donors and evaluate changes in cell activity. RESULTS: The N-terminal telopeptide of procollagen type I and interleukin (IL)-6 were higher than normal in patients not on the gluten-free diet. IL-1beta and TNF-alpha/beta were normal in all patients. IL-12 was reduced in all patients, whereas IL-18 was reduced only in patients on the diet. The RANKL/osteoprotegerin (OPG) ratio was increased in patients not on the gluten-free diet. Persistently increased osteoclast numbers were obtained from peripheral blood mononuclear cells of healthy donors on incubation with sera of patients not on the gluten-free diet versus control sera and sera from patients on the diet. In human osteoblasts from healthy individuals, IL-18 was reduced on incubation with sera from all patients, whereas OPG expression was lower when sera from patients not on the diet were used. Proliferation, alkaline phosphatase, and nodule mineralization were increased in osteoblast cultures containing sera from all celiac patients, either on or not on the gluten-free diet. CONCLUSIONS: We conclude that bone loss in celiac disease might also be caused by a cytokine imbalance directly affecting osteoclastogenesis and osteoblast activity.

Adult↗
PubMed1993

T cell receptor heterogeneity in gamma delta T cell clones from intestinal biopsies of patients with celiac disease.

In celiac disease large numbers of gamma delta T lymphocytes infiltrate the intestinal epithelia. We have isolated intestinal gamma delta T cell clones from patients with celiac disease and have analyzed their T cell receptor repertoire. T cell lines and clones were obtained from jejunal biopsies of 14 celiac patients and 12 individuals without celiac disease. These were analyzed by staining with monoclonal antibodies against CD3, alpha beta and gamma delta T cell receptor, by Southern blot with gamma- and delta-specific probes and by polymerase chain reaction using V delta-specific oligonucleotides. Intestinal gamma delta cells from patients with celiac disease differed from those of controls with normal jejunal histology in that V delta 1+ cells and V delta 1-V delta 2- cells were significantly increased. There was no evidence of the expansion of one or more clones expressing particular types of gamma delta T cell receptor.

Adolescent↗
PubMed1978

Low serum somatomedin activity in celiac disease. A misleading aspect in growth failure from asymptomatic celiac disease.

In 4 children with celiac disease, aged 7 months to 11 years, serum somatomedin activities (SMA) were consistently low: less than 0.40 U/ml (N greater than 0.50 U/ml). Basal plasma growth hormone (GH) levels were not elevated and increased normally under arginine-insulin stimulation in 3 patients. Human GH administration at a dosage which usually determines an increase of serum SMA in children with GH deficiency (4 mg/day/2 days) did not modify significantly the low serum SMA. However, in 1 child a clear-cut increase of serum SMA (0.22-0.82 U/ml) was noted under a higher dosage of human GH (8 mg/day/2 days). In 3 patients serum SMA was studied 3 weeks to 4 months after starting the gluten-free diet and was found to be normal. A limitation of the somatomedin generation unrelated to a deficit in GH secretion and probably resistant to GH appears therefore to be present in celiac disease. The rapid normalization of serum SMA under gluten-free diet suggests that the low serum SMA is induced through some unknown hormonal or metabolic signal by the protein malabsorption and/or the nutritional deficiency present in celiac disease.

Celiac Disease↗
PubMed2005

The value of wireless capsule endoscopy in patients with complicated celiac disease.

BACKGROUND: Celiac disease may be complicated by symptoms that raise the suspicion of small-intestinal malignancy. The objective is to evaluate wireless capsule endoscopy (WCE) in complicated celiac disease. METHODS: This is a prospective study at a university referral center. There were 47 patients. The indications for WCE were abdominal pain (57%), cancer surveillance (23%), blood in the stool, or persistent iron deficiency (19%). RESULTS: Findings were consistent with celiac disease in 87%: atrophy (68%), fissuring (62%), and mosaic pattern (19%), extending to the ileum in 34%. Unexpected findings were ulceration in 45% (n = 21), cancer (1), polyps (1), stricture (1), submucosal mass (1), ulcerated nodular mucosa (2), and intussusception (1) were seen in 60%. CONCLUSIONS: WCE has a high yield in complicated celiac disease, by identifying mucosal abnormalities and by excluding adenocarcinoma.

Abdominal Pain↗
PubMed2001

Small bowel permeability in diagnosis of celiac disease and monitoring of compliance of a gluten-free diet (gut permeability in celiac disease).

BACKGROUND & AIM: Celiac disease is an autoimmune disease with the damage of the intestinal barrier. The aim of study was to measure gut permeability in patients with untreated celiac disease and during treatment with a gluten free diet. METHODS: 30 patients with celiac disease before and during treatment with gluten-free diet were investigated, 30 patients without organic damage of the gastrointestinal tract served as control. Small bowel permeability was measured using lactulose/mannitol and lactulose/D-xylose ratios. The saccharides were examined in the 5 hours collected urine using capillary gas chromatography. RESULTS: Small bowel permeability (indices lactulose/mannitol and/or lactulose/xylose) increased significantly in patients with untreated celiac disease. 23 patients were followed up before and during treatment with a gluten-free diet 2-6 months after beginning of this treatment and small bowel permeability (measured as indices lactulose/mannitol and/or lactulose/xylose) significantly decreased. CONCLUSION: Small bowel permeability test is a non-invasive test suitable for the diagnosis of celiac disease and monitoring of compliance to a gluten-free diet in these patients.

Adult↗
PubMed2006

[Is pure red cell aplasia a new extra digestive manifestation of celiac disease?].

INTRODUCTION: Celiac disease is an autoimmune enteropathy that appears on a predisposed genetic background. Its clinical presentation has been extended those last years by varied extradigestive manifestations. EXEGESIS: This is a case report of a twenty-year-old woman who presented simultaneously a celiac disease and pure red cell aplasia. The IgA and IgG antigliadin antibodies as well as antinuclear, anti-DNA, anti-SSA and anti-SSB antibodies were detected, without any clinical symptom supporting the diagnosis of systemic lupus erythematosus or Sjögren syndrome. Thoracic CT-scan reveals a thymus enlargement and biopsy concludes to thymus hyperplasia at histological examination. Pure red cell aplasia regressed after gluten-free diet, corticoid therapy and thymectomy. CONCLUSION: This observation, added to the three others paediatric cases previously published in the literature concern an uncommon association between pure red cell aplasia and celiac disease. However, they are not enough to conclude to a direct link between these two disorders. Pure red cell aplasia could represent un new dysimmune manifestation occurring in celiac disease, but this will need to be confirmed with others cases.

Adrenal Cortex Hormones↗
PubMed2007

HLA-DQB1*0201 homozygosis predisposes to severe intestinal damage in celiac disease.

OBJECTIVE: Celiac disease (CD) is a T-lymphocyte-mediated small intestinal enteropathy triggered and maintained by dietary gluten, with a strong genetic component mapping to the HLA genes encoding for the class II DQ(alpha1*0501, beta1*02) molecule. Damage of the small intestine may cause a variety of clinical signs ranging from isolated long-standing iron-deficiency anemia refractory to iron supplementation to forms of severe malnutrition that may become life threatening. However, patients carrying the typical intestinal lesions of CD and presenting no symptoms at all (silent CD) are also a common clinical observation. Since it is commonly assumed that clinical signs and symptoms tend to correlate with the severity of the intestinal damage, the purpose of this study was to investigate whether particular HLA class II genotypes might also influence the extent of intestinal damage and consequently the clinical presentation of the disease. MATERIAL AND METHODS: We retrospectively compared histological grading of celiac disease intestinal biopsies with HLA haplotype, age at onset of disease and clinical signs and symptoms. RESULTS: Our findings showed that homozygosis for the DQB1*0201 allele is associated with a higher severity of the histological score (p<0.008). Of note for the clinician, this work also suggests that the same type 3c of intestinal damage causes a different clinical syndrome, depending on the patient's age. CONCLUSIONS: The genetic predisposition at the HLA-DQB1 locus influences the severity of the mucosal damage in a dose-dependent manner, but not the clinical presentation, of celiac disease.

Adolescent↗
PubMed2004

Celiac disease.

Childhood celiac disease--gluten-sensitive enteropathy--is defined in its most salient form by malabsorption and disturbed growth in association with a specific histologic lesion of the small intestine. Celiac disease occurs in response to grain consumption in susceptible individuals. Although subtotal villus atrophy with crypt hyperplasia has, in the past, been considered essential for the diagnosis, a spectrum of histologic lesions are now appreciated. The advances in the field of diagnosis (specifically, the recent development of serologic diagnostic tests) have been instrumental in correlating the histopathology of patients with subtle clinical features of the disease. Through observations, an expansion of the clinical findings associated with the condition has evolved that has helped to unfold the pathophysiology. As a result, celiac disease is now recognized as an autoimmune enteropathy of the small intestine with a broad spectrum of clinical manifestations.

Adolescent↗
PubMed1990

Intestinal gamma/delta receptor-bearing T lymphocytes in celiac disease and inflammatory bowel diseases in children. Constant increase in celiac disease.

We studied the numbers of T-cell receptor alpha/beta- and gamma/delta-bearing lymphocytes in 27 jejunal specimens from 19 celiac patients, 27 rectal and colonic specimens from 14 ulcerative colitis patients and four patients with Crohn's disease, and 24 control specimens. MAb and a three-layer peroxidase staining method were used. Only low numbers of gamma/delta + cells were seen in normal jejunum and rectum of controls, as well as in the specimens of patients with inflammatory bowel diseases. In the lamina propria of celiac patients, the mean number of gamma/delta + cells was significantly higher than in the controls before treatment, during gluten-free diet, and after the gluten challenge. Within the jejunal epithelium, the number of gamma/delta + cells was elevated before and during gluten elimination and after the challenge test. The absolute number of intraepithelial gamma/delta + cells remained constant during gluten elimination and provocation. We infer that the constantly elevated population of gamma/delta + T cells in the epithelium of celiac patients may play an important role in the pathogenesis of celiac disease.

Celiac Disease↗
PubMed2005

Inflammatory bowel disease in patients with celiac disease.

BACKGROUND: Several case reports and series report an association between celiac disease and inflammatory bowel disease (IBD); however, there is no current data assessing this association. We therefore studied the occurrence of these conditions in a cohort of patients with celiac disease seen at a referral center. METHODS: A database of patients with celiac disease seen between 1981 and 2002 was analyzed. Only biopsy-proven adults were included. Patients who had endoscopic and pathologic evidence of IBD were identified, and their pathology was reviewed. Age- and sex-adjusted prevalence rate ratios were determined by comparing results with population-based prevalence data. RESULTS: Among 455 patients with celiac disease, IBD was identified in 10 (5 had ulcerative colitis and 5 had Crohn's disease). This represented an age- and sex-adjusted prevalence rate ratio for ulcerative colitis of 3.56 (95% confidence interval, 1.48-8.56) and for Crohn's disease of 8.49 (95% confidence interval, 3.53-20.42). CONCLUSION: Within our cohort of patients with celiac disease, IBD was significantly more common than in the general population.

Adult↗
PubMed1992

Scanning electron microscopy of the small intestine during gluten-challenge in celiac disease.

The celiac disease syndrome is characterized by structural and ultrastructural alterations of the small intestine mucosa. According to criteria by European Society of Paediatric Gastroenterology and Nutrition, the conclusive diagnosis of celiac disease in children depends on the demonstration of histological relapse of the mucosa after reintroduction of gluten in the diet, as this syndrome is a permanent condition of gluten intolerance. Under these diseased conditions, the structure of the intestinal villi has been studied by light microscopy; morphological alterations were revealed only when the gluten challenge induced a clinical relapse. Scanning electron microscopy analyses of the intestinal mucosa in celiac diseased patients showed a strikingly uniform destruction of the villi with changes in their dimensions and arrangement. At high magnification the enterocytes were irregular in size and shape with a decrease and disruption of the glycocalyx. Reductions in length and density of microvilli were also clearly identified. Although these scanning electron microscopy findings could not demonstrate a relationship between the degrees of mucosal atrophy and the duration of the gluten challenge, they nevertheless revealed early stages of fine villous alterations that cannot be detected by the presently employed low resolution light microscopic techniques.

Autopsy↗
PubMed1998

Lack of correlation between genotype and phenotype in celiac disease.

BACKGROUND: Celiac disease has a wide range of clinical features. The goal of this study was to evaluate whether specific HLA genotypes are associated with particular clinical appearances. METHODS: One hundred forty-five patients with confirmed celiac disease were oligotyped for DR and DQ HLA genes. Clinical notes, physical examination, and a questionnaire provided their personal data. Patients were grouped into nine genotypic categories, according to the presence of the specific DQ heterodimer DQA1*0501-DQB1*0201 (hence termed alpha0beta0), in single or double dose, and the presence of the DRB4 antigen. RESULTS: Age at first symptoms and age at beginning of gluten-free diet were not significantly different in the nine groups. The initial symptoms of the disease had a similar distribution in all groups. In twenty-seven patients, disease was diagnosed by family screening: they shared a similar HLA genotype with those who had relevant symptoms. The actual growth status-evaluated by standardized height, percentage of median weight for age, and percentage of median weight for height--was not different in the nine groups. Presence of unusual health complaints was not associated with a specific genotype. CONCLUSIONS: There is no evidence that clinical features of celiac disease are associated with different HLA genotypes. Genes outside the HLA may play a relevant role.

Body Height↗