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PubMed2006

Cladribine therapy in refractory celiac disease with aberrant T cells.

BACKGROUND & AIMS: Refractory celiac disease (RCD) may be subdivided into RCD types I and II with phenotypically normal and aberrant intraepithelial T-cell populations, respectively. In RCD II, transition into enteropathy-associated T-cell lymphoma (EATL) is seen frequently. We have evaluated the effect of cladribine (2-CDA), a purine analogue inducing T-cell depletion, on clinical, histopathologic, and immunologic parameters, as well as the toxicity and side effects in a group of RCD II patients. METHODS: Between 2000 and 2005, 17 patients were included (8 men, 9 women). All patients had a clonal rearrangement of the T-cell receptor gamma gene and immunophenotyping showed an aberrant T-cell population lacking surface expression of CD3, CD8, and T-cell receptor alphabeta, in the presence of expression of surface CD103 and intracytoplasmic CD3. Treatment consisted of 2-CDA (0.1 mg/kg/day) intravenously for 5 days, given in 1-3 courses every 6 months depending on the response. RESULTS: All patients tolerated 2-CDA without serious side effects. Six patients (35.8%) showed a clinical improvement (weight gain, improvement of diarrhea, and hypoalbuminemia). In 10 patients (58.8%) a significant histologic improvement and in 6 patients (35.2%) a significant decrease in aberrant T cells was seen. Seven patients (41.1%) developed EATL and died subsequently. One patient died of progressive refractory state with emaciation. CONCLUSIONS: Treatment with 2-CDA in RCD II is feasible, well tolerated, and can induce clinical and histologic improvement as well as a significant decrease of aberrant T cells in a subgroup of patients, albeit it does not prevent EATL development. However, the earlier reported potential risk of precipitating an overt lymphoma should be taken into consideration.

Aged↗
PubMed2005

Reduced plasma ghrelin concentration in celiac disease after gluten-free diet treatment.

OBJECTIVE: Celiac disease (CD) is characterized by malabsorption, weight loss and increased energy expenditure. The aim of this study was to investigate the relationship between circulating ghrelin and leptin, which are produced at gastrointestinal level and are involved in energy balance regulation, and changes in body composition and energy metabolism in CD patients before and after gluten-free diet (GFD)-induced restoration of the intestinal mucosa. MATERIAL AND METHODS: Body composition (by dual-energy X-ray absorptiometry), resting metabolic rate and substrate oxidation rates (by indirect calorimetry) were assessed in 18 adult women with the classic form of CD (age 31.4 +/- 7.8 years, body mass index (BMI) 20.6 +/- 2.1 kg/m2) before and at least 2 years after GFD treatment and in 22 age-matched healthy women (age 33.1 +/- 7.2 years, BMI 22.9 +/- 2.1 kg/m2). Plasma leptin and ghrelin concentrations were assessed by the ELISA and RIA procedures, respectively. RESULTS: Fat-free mass was reduced before and after GFD compared to control subjects (p < 0.01), while fat mass increased after treatment (p < 0.01). Plasma leptin concentration was similar between groups and correlated only with BMI (r = 0.84; p < 0.0001) and percentage body fat (r = 0.86; p < 0.0001). Circulating ghrelin levels (pg/ml) were similar between untreated patients and control subjects, but decreased after GFD treatment (untreated CD: 282.6 +/- 55.5 versus treated 109.2 +/- 49.9; p < 0.0001 and versus control subjects 262.2 +/- 30.0; p < 0.0001) and were negatively correlated with BMI in CD patients (r = -0.32; p < 0.01). CONCLUSIONS: The low plasma ghrelin concentration found in CD patients after GFD treatment could only be partially explained by the slight increase in body-weight and fat mass. Further studies are needed to better ascertain the role played by an incomplete functional or quantitative recovery of ghrelin-producing cells in CD.

Adult↗
PubMed1988

In vitro (organ culture) studies of the toxicity of specific A-gliadin peptides in celiac disease.

Specific peptides of known amino acid sequence were prepared from alpha-gliadin (A-gliadin) by cleavage of the protein with cyanogen bromide and chymotrypsin and purification of the resulting peptides. The three peptides derived from the cyanogen bromide cleavage spanned the complete sequence of A-gliadin (266 residues). Four peptides derived from chymotryptic digestion covered the N-terminal sequence through residue 68. These peptides were tested for toxicity in celiac disease by organ culture of biopsied small intestinal tissues taken from patients with active celiac disease. Enterocyte height was used as a measure of peptide effect on cultured tissues. Five of seven peptides tested significantly inhibited increase of enterocyte height in the cultures and were considered toxic on this basis. The largest common sequences among the toxic peptides were -pro-ser-gln-gln- and -gln-gln-gln-pro-; these sequences were absent from the nontoxic peptides. The relationship of these sequences to the damaging effect of gliadins on the small intestinal mucosa in celiac disease remains to be investigated.

Biopsy↗
PubMed1982

Celiac disease: case report with an associated arthropathy.

A case is presented of a patient with biopsy documented celiac disease who presented with an acute arthropathy along with symptoms of malabsorption. The etiology of the arthropathy could not be determined; however, the temporal relationship of the presenting manifestations (i.e., malabsorption and the arthropathy) as well as lack of further gastrointestinal of joint symptoms after 2 yr of follow-up suggest that in this case the arthropathy was related to the patient's celiac disease. Possible pathogenetic mechanisms for this heretofore unreported relationship are also presented.

Adult↗
PubMedDate not supplied

How common is celiac disease in Eastern Saudi Arabia?

BACKGROUND: In contrast to its prevalence in Europe, celiac disease (CD) is considered rare in non-Caucasian populations. We aimed to estimate the prevalence of CD in clinically suspicious celiac disease patients and in patients with disorders known to be associated with CD, such as autoimmune diseases, using serological assay for IgA-endomysial antibodies (EMA) on inexpensive human tissue substrate. PATIENTS AND METHODS: IgA-endomysial and IgA-reticulin antibodies (ARA) were evaluated by indirect immunofluorescence (IIF) study using human umbilical cord (HUC) and rat tissues, respectively, in the following groups: group 1, 145 patients with clinical suspicion of CD; group 2, 80 with autoimmune diseases; group 3, 20 patients with inflammatory bowel disease (IBD); and group 4, 100 healthy blood donors. RESULTS: Of the 145 patients with suspected CD (group 1), 11 were EMA positive with or without ARA, giving a serological prevalence of 7.6%. The histological findings of intestinal biopsy were confirmed in six of them, indicating a CD prevalence of 4%. In group 2, two EMA-positive (2.5%) with or without ARA cases were found. Both were from the 18 patients who had autoimmune thyroid disease, indicating an 11% prevalence of EMA in autoimmune thyroid disease. No positive EMA was detected in the 3rd and 4th groups, indicating 100% specificity. CONCLUSION: Our findings showed high prevalence of CD in a reference laboratory setting. This highlights the importance of keeping CD in mind and of promptly investigating suspected individuals. There is also a high prevalence of CD among patients with autoimmune thyroid diseases, and further studies are needed to elucidate the significance of this association. Test for endomysial antibodies using human umbilical cord is an inexpensive, easily available and highly specific tool for identifying patients to undergo biopsy and to screen at-risk groups of patients.

Journal Article↗
PubMed1999

Differing patterns of transforming growth factor-beta expression in normal intestinal mucosa and in active celiac disease.

BACKGROUND: Growth-inhibitory autocrine polypeptides such as transforming growth factor (TGF)-beta may play a role in the control of normal epithelial cell proliferation and differentiation. In addition, TGF-beta has a central role in extracellular matrix homeostasis and regulates the immune response at the local level. In this study immunohistochemistry was used to examine the pattern of TGF-beta protein distribution and quantitative reverse transcription-polymerase chain reaction (RT-PCR) to determine levels of TGF-beta messenger RNA expression in normal intestinal mucosa and in the flat mucosa of children with celiac disease. METHODS: Small intestinal biopsies were performed in children with active celiac disease and in histologically normal control subjects. Frozen sections were single stained using an anti-TGF-beta monoclonal antibody and were double stained for TGF-beta and T cell, macrophages, and the activation marker CD25. Total RNA was extracted from frozen specimens and competitive quantitative RT-PCR performed for TGF-beta mRNA using internal synthetic standard RNA. RESULTS: In normal intestinal mucosa, by immunohistochemistry, TGF-beta expression was most prominent in the villous tip epithelium, whereas in the lamina propria, weak immunoreactivity was present. The celiac mucosa showed weak and patchy epithelial TGF-beta immunoreactivity. In contrast, an intense staining positivity was present in the lamina propria localized mostly in the subepithelial region where T cells, macrophages, and CD25+ cells were detected by double staining. By quantitative RT-PCR, levels of TGF-beta mRNA transcripts appeared to be increased in celiac intestinal mucosa compared with that in control subjects, although the difference did not reach statistical significance. CONCLUSIONS: These observations suggest that TGF-beta expression is associated with differentiated enterocyte function. In celiac disease the lower TGF-beta epithelial cell expression could be a consequence of the preponderance of a less differentiated epithelial cell phenotype also present in the surface epithelium. In contrast, the prominent TGF-beta positivity of the subepithelial lamina propria suggests an association with the local immune and inflammatory response, as well as a potential role of these peptides in mesenchymal-epithelial cell interaction.

Antigens, CD↗
PubMedDate not supplied

Celiac disease presenting as urticaria.

Celiac sprue is a chronic malabsorptive disorder that occurs in predisposed individuals secondary to ingestion of gluten. An increase of atopic or immunologic disorders has been reported in the setting of gluten enteropathy. The incidence of urticaria and celiac sprue is unknown but appears to be rare.

Celiac Disease↗
PubMedDate not supplied

Celiac disease and type I (insulin-dependent) diabetes mellitus in childhood: follow-up study.

To ascertain the specificity of IgA and IgG antigliadin (IgA-AGA, IgG-AGA), IgA-antireticulin (R1-ARA), and antiendomysial (AEA) antibodies for the diagnosis of celiac disease, we evaluated 133 type I diabetic children aged 1.4-28.4 years (mean 14.1 +/- 6.6), with diabetes from onset to 20.5 years. Fifty-three patients were considered at onset and 49 of these also during follow-up. IgA-AGA and IgG-AGA were determined by enzyme-linked immunosorbent assay (ELISA), R1-ARA and AEA by indirect immunofluorescence. IgA-AGA were positive in 20 of 133 (15%), IgG-AGA were positive in seven of 133 (5.26%), while R1-ARA and AEA were positive in three patients. At the onset of disease we found elevated IgA-AGA in 17 of 53 (32%) patients, IgG-AGA in four (7.55%) patients, three of them with IgA-AGA as well; R1-ARA and AEA were present in three (5.66%) patients, all with high IgA-AGA levels. During 1-10 year follow-up IgA-AGA decreased to within the normal range in 13 patients, with elevated IgA-AGA at onset but without R1-ARA and AEA; in four patients with high IgA-AGA at onset, IgA-AGA remained constantly elevated as did R1-ARA and AEA in three of them; and two patients, without IgA-AGA, R1-ARA, and AEA at onset, became positive for all three antibodies. Intestinal biopsy confirmed a diagnosis of celiac disease in five of these with IgA-AGA, R1-ARA, and AEA, but not in one patient with persistent IgA-AGA but no AEA and R1-ARA, suggesting that R1-ARA and AEA are more reliable markers for the screening of celiac disease in type I diabetic patients.

Adolescent↗
PubMed2003

[Screening of celiac disease in first-degree relatives].

BACKGROUND AND OBJECTIVE: Our aim was to analyze the prevalence of celiac disease (CD) in first-degree relatives of patients diagnosed with this disorder in Cantabria (Northern Spain). SUBJECTS AND METHOD: A questionnaire was administered and a complete biologic study was performed in 184 relatives. When serum CD-related antibodies were detected, relatives were asked to undergo a jejunal biopsy to confirm the diagnosis. RESULTS: Thirteen relatives had autoantibodies yet only 4 were diagnosed with CD. The biopsy was suggestive of CD in 3 relatives who underwent it. A further relative was diagnosed with CD by the clinical and serological response to a gluten-free diet. CONCLUSIONS: The prevalence found in our study is high enough so that we recommend the screening of autoantibodies, especially anti-gliadin and anti-transglutaminase antibodies, in this risk-population of celiac disease.

Adolescent↗
PubMed1990

Secretory immunity in celiac disease: cellular expression of immunoglobulin A subclass and joining chain.

Two-color immunofluorescence staining in situ demonstrated increased proportions of immunoglobulin A2 subclass-producing cells in jejunal mucosa from adult patients with untreated (47%, P less than 0.01) or treated (37%, P less than 0.05) celiac disease compared with controls (28%). Costaining was also performed for joining chain, which is a key factor in the epithelial transport of secretory antibodies; its expression by immunoglobulin A2 cells was only marginally reduced in untreated patients (96%) compared with treated patients and controls (98%). Also, immunoglobulin A1 cells showed similar joining chain positivity (89%) in all three groups. Considering the expanded total jejunal immunoglobulin A-cell population and the subclass-associated joining chain expression, it could be calculated that the potential of immunoglobulin A2 cells for contribution to secretory immunity was increased 3.9 times in untreated (P less than 0.01) and 1.8 times in treated (P less than 0.05) patients and that of immunoglobulin A1 cells was increased 1.7 times in untreated (P less than 0.05) but remained unaltered in treated patients. The estimated relative contributions of locally produced immunoglobulin A2 to secretory immunoglobulin A would thus be 51% and 37% in the two patient categories, respectively, compared with 31% in the controls. These data suggested enhanced secretory immunity in celiac disease and might reflect a protective, possibly antimicrobial, immune response. It could not be excluded, however, that increased generation of secretory immunoglobulin A at the same time contributes to the gluten-induced pathogenesis of celiac disease.

Adult↗
PubMed1996

IgA antigliadin antibodies as a screening method for nonovert celiac disease in children with insulin-dependent diabetes mellitus.

One hundred forty-one children with insulin-dependent diabetes mellitus were screened for serum immunoglobulin A (IgA) antigliadin antibodies by means of an enzyme-linked immunosorbent assay (ELISA) method. None of them had gastrointestinal symptoms, and no major nutritional disturbances were detected except for a girl with moderate growth delay. Twelve patients with positive IgA antigliadin antibodies on two or more consecutive measurements underwent a small intestinal biopsy; four of them had a subtotal villous atrophy, and celiac disease was diagnosed; in another patient, a partial villous atrophy was observed. Children suffering from both diabetes and celiac disease showed an onset of diabetes at a younger age than did nonceliac patients. Prevalence of celiac disease in the screened population is 2.85%, which is higher than in the general population of the Comunidad Valenciana (one in 2,500 live births).

Adolescent↗
PubMed2006

Abnormalities of serotonin metabolism and their relation to symptoms in untreated celiac disease.

BACKGROUND AND AIMS: Serotonin (5-hydroxytryptamine [5-HT]) is a key modulator of gut function that in excess causes nausea, vomiting, and diarrhea. We recently showed that patients with post-infective irritable bowel syndrome have increased postprandial release of 5-HT associated with low-grade T-cell mediated inflammation. Celiac disease is another common disease in which a T-cell enteropathy is associated with increased mucosal 5-HT levels. Our aim was to determine how this inflammatory lesion influenced 5-HT bioavailability and how changes in 5-HT related to the symptoms of nausea, vomiting, and diarrhea seen in untreated celiac patients. METHODS: Fasting plasma and platelet 5-HT and postprandial plasma 5-HT levels were measured after a high-carbohydrate meal in celiac patients (n = 18) and healthy controls (n = 18) using high-pressure liquid chromatography. Dyspepsia was assessed during the postprandial period using a questionnaire. Finally, we compared the histology and mucosal 5-HT levels in duodenal biopsy specimens from celiac patients and controls. RESULTS: Celiac patients had increased 5-HT-containing enterochromaffin cell numbers and significantly higher peak plasma 5-HT levels (P = .0002), postprandial area under the curve (P = .0006), and platelet 5-HT stores (P = .031) than controls. Peak 5-HT levels correlated significantly with postprandial dyspepsia scores (P = .005). Celiac patients had higher duodenal 5-HT levels (P = .007) than controls. CONCLUSIONS: Celiac disease is associated with increased mucosal 5-HT content and enhanced 5-HT release from the upper small bowel, which correlates with postprandial dyspepsia. Serotonin excess may mediate dyspeptic symptoms in untreated celiac disease.

Adolescent↗
PubMed2003

The HLA-DQ2 gene dose effect in celiac disease is directly related to the magnitude and breadth of gluten-specific T cell responses.

In patients with celiac disease, inflammatory T cell responses to HLA-DQ2-bound gluten peptides are thought to cause disease. Two types of HLA-DQ2 molecules exist, termed HLA-DQ2.5 and HLA-DQ2.2. Whereas HLA-DQ2.5 predisposes to celiac disease, HLA-DQ2.2 does not. We now provide evidence that the disease-associated HLA-DQ2.5 molecule presents a large repertoire of gluten peptides, whereas the non-disease-associated HLA-DQ2.2 molecule can present only a subset of these. Moreover, gluten presentation by HLA-DQ2 homozygous antigen-presenting cells was superior to presentation by HLA-DQ2/non-DQ2 heterozygous antigen-presenting cells in terms of T cell proliferation and cytokine secretion. Gluten presentation by HLA-DQ2.5/2.2 heterozygous antigen-presenting cells induced intermediate T cell stimulation. These results correlated with peptide binding to the antigen-presenting cells. Finally, we demonstrate that HLA-DQ trans dimers formed in HLA-DQ2.5/2.2 heterozygous individuals have properties identical with HLA-DQ2.5 dimers. Our findings explain the strongly increased risk of disease development for HLA-DQ2.5 homozygous and HLA-DQ2.2/2.5 heterozygous individuals, and they are indicative of a quantitative model for disease development, where HLA-DQ expression and the available number of T cell-stimulatory gluten peptides are critical limiting factors. This model may have important implications for disease prevention.

Antigen-Presenting Cells↗
PubMed2003

Risk of duodenal adenoma in celiac disease.

BACKGROUND: There is a 60- to 80-fold increased risk of small-bowel adenocarcinoma in patients with celiac disease. While the adenoma-carcinoma sequence appears to operate in the small bowel as in the large bowel, the risk of duodenal adenomas in celiac patients is unknown. METHODS: The records of 381 patients (245 F, 136 M) with biopsy-proven celiac disease were reviewed to determine the prevalence of duodenal adenoma found during esophagogastroduodenoscopy (EGD). We conducted an extensive literature review to find data for estimates of the prevalence of duodenal adenoma in a comparable general population; we used data from a study at another New York City medical center of 7346 EGDs conducted between 1976 and 1982 (Ghazi et al., 1984). We estimated the relative risk, expressed as a standard morbidity ratio (SMR), by calculating the observed to expected (O/E) ratio. RESULTS: Duodenal adenomas were found in 3 celiac patients (0.78%), with 24 adenomas (0.33%) in the reference population, giving an SMR of 2.39 (95% CI 0.67-8.48). CONCLUSION: We did not find a significantly increased risk of duodenal adenoma in celiac patients compared to a non-celiac endoscoped population. Thus, despite the previously described elevated risk of small-bowel adenocarcinoma in these patients, routine endoscopic examination of the duodenum may not be adequate for screening.

Adenoma↗
PubMed1983

[State of regenerative processes in the mucosa of the small intestine in celiac disease in adults (gluten enteropathy)].

Biopsies of the small intestine mucosa were studied in 60 patients among which celiac disease was diagnosed in 35 after clinico-morphological examinations and chronic enteritis in 25. Apart from histological and histochemical methods, autoradiography of biopsies with 3H-thymidine was used. The study showed that atrophy of the small intestine mucosa in celiac disease in adults was of hyperregeneratory nature which was manifested by deepening of the crypts and increased number of DNA-synthesizing enterocytes. Due to enhanced proliferation incompletely differentiated cells appear on the villae which are incapable of completely performing the functions of membrane digestion and absorption. These enterocytes are histochemically similar with crypt epithelium and, like the latter, are more stable to autolysis. Functionally, the presence on the villae of incompletely differentiated epithelium is more significant than villi atrophy. Treatment with aglutenic diet eliminates the syndrome of disturbed absorption despite persisting atrophy. The processes of cell renewal become normalized as proved by the appearance of high epithelium on the villae and decreased label index.

Adult↗