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At least 1,279 records · Page 71Linked to original sources
PubMed2004

Prospective population screening for celiac disease: high prevalence in the first 3 years of life.

BACKGROUND: Celiac disease (CD) is an autoimmune enteropathy that develops in genetically susceptible individuals exposed to gliadin. Early diagnosis of CD may reduce the risk of complications, and several studies have related the duration of gluten exposure to the risk of other autoimmune diseases. It has been proposed that silent CD be diagnosed as soon as possible to avoid potential complications. OBJECTIVES: The purpose of this study was to determine the prevalence of CD among children less than 3 years and to provide treatment to those patients diagnosed with CD. PATIENTS AND METHODS: Parents of 1100 healthy children born between October 1998 and December 1999 were asked at the time of delivery to enroll their children in a program for the early diagnosis of CD. The parents of 830 children agreed to participate. Patients in the study were examined and anti-tissue transglutaminase antibody was first measured at about 1.5 years of age. A second antibody titer was obtained at about 2.5 years of age. Patients with detectable autoantibodies underwent intestinal biopsy for confirmation of CD. RESULTS: Of the 830 children initially enrolled, 613 and 484 returned for the first and second visits, respectively. None had anti-tissue transglutaminase antibodies at the first visit, but 9 had anti-tissue transglutaminase immunoglobulins at the second visit. In 7 of these 9, intestinal biopsy confirmed the diagnosis of CD which suggests a minimum prevalence of CD of 1 per 118 healthy newborns. CONCLUSIONS: The authors observed a very high prevalence of CD, comparable to that observed in other European populations, which might even be higher if all of the children initially examined had returned for their second visit. If general screening for CD were accepted, the authors would recommend age 2-3 years as the best time for measuring tissue transglutaminase antibodies.

Autoantibodies↗
PubMed2005

High prevalence of celiac disease in autoimmune hepatitis detected by anti-tissue tranglutaminase autoantibodies.

Celiac disease (CD) may be found in association with other autoimmune diseases. We investigated the relation between autoimmune hepatitis (AIH) and CD by assessing the prevalence of IgA and IgG anti-tissue transglutaminase (tTG) antibodies in AIH, and by verifying whether the findings were associated with clinical and histological features of CD. Forty-seven consecutive patients with AIH (type I: n = 39; type II: n = 8) were studied. One hundred patients with chronic hepatitis C, and 120 healthy blood donors were also studied as controls. We analyzed sera for the presence of IgA and IgG anti-tTG antibodies using a specific human recombinant tTG immunoenzymatic assay. Anti-tTG positive patients and controls were further tested for anti-endomysium antibodies (EMA) and HLA typing, and those found positive by either of these tests underwent duodenal biopsy to confirm a possible diagnosis of CD. Three of the 47 AIH patients (6.4%) were positive for IgA anti-tTG and EMA antibodies, and were subsequently confirmed to be affected with CD by small-bowel biopsy findings. No IgG anti-tTG positivity was found in the AIH patients. None of the controls were positive for IgA anti-tTG, and only one with chronic hepatitis C had a low positive reaction for IgG anti-tTG, which resulted as a false positive. The crude prevalence rate of CD in AIH was 63.8 per 1,000 (95% CI, 13.2-186.1), and it was significantly higher than that found in the general population in Italy (4.9 per 1,000; 95% CI, 2.8-7.8). The results of this study showed a high prevalence of CD in patients with AIH. For this reason, early serological screening testing for CD is strongly recommended for all AIH patients.

Adolescent↗
PubMedDate not supplied

Erythema nodosum in association with celiac disease.

We present a 16-year-old girl with a 4-year history of chronic persistent erythema nodosum. Recurrently low serum iron values suggested the possibility of a malabsorption syndrome. The presence of antitransglutaminase and antiendomysium antibodies and the jejunal biopsy specimen findings showed an underlying celiac disease. On a strict gluten-free diet, the skin lesions resolved and the girl has since remained symptom free for 9 months. Thus celiac disease can be a triggering factor for erythema nodosum. In the chronic form of the skin lesions, serologic testing for this specific enteropathy may be justified.

Adolescent↗
PubMed2004

Proximal myopathy as an unusual presenting feature of celiac disease.

A 37-year-old woman presented with back pain, diffuse musculoskeletal pain, and muscle weakness without marked gastrointestinal symptoms. She complained of difficulty in walking and bilateral hip pain for the preceding year. Clinical examination revealed proximal muscle weakness especially in the lower extremities and a waddling gait pattern. Laboratory parameters and radiographic findings revealed the diagnosis of osteomalacia. The etiology of osteomalacia was investigated and a diagnosis of celiac disease was established. As osteomalacia symptoms may be the only presenting feature of celiac disease, it should be considered in the differential diagnosis of patients presenting with proximal muscle weakness and diffuse musculoskeletal pain.

Absorptiometry, Photon↗
PubMedDate not supplied

[Diagnosis of celiac disease in an elderly subject: description of a clinical case].

A 70-year-old woman was admitted to the hospital because of a 5-year history of weight loss, weakness, anemia, osteomalacia, pathologic fractures and pain responding only to narcotic analgesics. A diagnosis of celiac disease was made on the basis of pathologic xylose absorption test results, studies confirming the presence of antigliadin and antiendomysial antibodies, and jejunal biopsy evidencing shortened or absent villi. The detection of unusual cases of celiac disease without diarrhea is on the increase. The only observable symptoms of this pathology may be osteomalacia or persistent iron deficiency anemia despite oral iron therapy.

Aged↗
PubMed1997

Effect of celiac disease and gluten-free diet on growth hormone-binding protein, insulin-like growth factor-I, and insulin-like growth factor-binding proteins.

Failure to thrive is common in children with celiac disease. As alterations in the growth hormone-insulin-like growth factor I (GH-IGF-I) growth axis have been reported in these patients, we studied the behavior of growth hormone-binding proteins (GH-BPs I and II), IGF-I and its binding proteins in 14 children with celiac disease, either before or after a 6-month gluten-free diet. GH-BP II levels were significantly lower in patients during the active phase of the disease than after the diet or in comparison with control subjects, appropriate for age and sex. There was no difference in the GH-BP-I levels of patients and controls, nor did they change after the diet. Blood levels of IGF-I and IGFBP-3 were reduced before the diet in all patients while ligand blotting showed that IGFBP-2 and 1 were increased. All of these parameters normalized after the gluten-free diet. IGFBP-4 was not greatly influenced by the disease. Furthermore, we found a significant, positive correlation between GH-BP II and IGF-I or IGFBP-3 levels. The height standard deviation scores and body mass indices of the patients improved significantly after the diet. The body mass index significantly and positively correlated with GH-BP II, IGF-I or IGFBP-3 levels. In conclusion, our data show that celiac children had multiple alterations in the growth axis during the active phase of the disease which disappeared during the gluten-free diet.

Body Height↗
PubMed2000

The CTLA4/CD28 gene region on chromosome 2q33 confers susceptibility to celiac disease in a way possibly distinct from that of type 1 diabetes and other chronic inflammatory disorders.

The effect of the gene region on chromosome 2q33 containing the CD28 and the cytotoxic T-lymphocyte associated (CTLA4) genes has been investigated in several diseases with chronic inflammatory nature. In addition to celiac disease (CD), type I diabetes, Grave's disease, rheumatoid arthritis and multiple sclerosis have all demonstrated associations to the A/G single nucleotide polymorphism (SNP) in exon 1, position +49 of the CTLA4 gene. The purpose of this study was to investigate this gene region in a genetically homogeneous population consisting of 107 Swedish and Norwegian families with CD using genetic association and linkage methods. We found a significant association with preferential transmission of the A-allele of the exon 1 +49 polymorphism by using the transmission disequilibrium test (TDT). Suggestive linkage of this region to CD was moreover demonstrated by non-parametric linkage (NPL) analysis giving a NPL-score of 2.1. These data strongly indicates that the CTLA4 region is a susceptibility region in CD. Interestingly, of the several chronic inflammatory diseases that exhibit associations to the CTLA4 +49 A/G dimorphism, CD appears to be the only disease associated to the A allele. This suggests that the +49 alleles of the CTLA4 gene are in linkage disequilibrium with two distinct disease predisposing alleles with separate effects. The peculiar association found in the gut disorder CD may possibly relate to the fact that the gastrointestinal immune system, in contrast to the rest of the immune system, aims to establish tolerance to foreign proteins.

Abatacept↗
PubMed2006

Diagnosis of celiac disease in a patient with fecal incontinence.

BACKGROUND: A 69-year-old white woman presented to our gastroenterology department with loose stools, daily fecal incontinence and weight loss. She had a 3-year history of fecal incontinence, which had increased in frequency and severity in the year before her most recent presentation. Prior diagnostic workup included anorectal manometry, revealing global sphincter dysfunction, which improved slightly with biofeedback therapy, and colonoscopy, which proved unremarkable. At the time of referral, the patient was taking loperamide 2mg once daily. INVESTIGATIONS: Physical examination, fecal fat stain, abdominal CT scan, therapeutic trial of pancreatic enzymes, celiac disease serologic tests, and upper endoscopy with small-bowel biopsy. DIAGNOSIS: Celiac disease. MANAGEMENT: Gluten-free diet.

Aged↗
PubMed1998

Whole-body protein metabolism assessed by leucine and glutamine kinetics in adult patients with active celiac disease.

To assess the effect of increased renewal of intestinal epithelial cells on leucine and glutamine (Gln) turnover, 4-hour intravenous infusions of L-[1-(13)C]leucine and L-[2-(15)N]Gln were administered to five adult patients with active celiac disease in the postabsorptive state. There was a 35% increase in leucine flux (micromoles per kilogram per hour) in patients (117 +/- 17) compared with healthy controls (96 +/- 11, P < .03). Gln flux was increased by 13% in patients (377 +/- 35) versus controls (335 +/- 16, P < .04). These results suggest that active celiac disease, characterized by villous atrophy and crypt cell hyperplasia, is associated with a dramatic increase in whole-body protein breakdown as assessed by 13C-leucine, which may contribute per se to the protein malnutrition status of the patients. The increase in Gln utilization as assessed by L-[2-(15)N]Gln was moderate, but may have been offset due to the villose atrophy and ensuing reduced intestinal epithelial cell mass. The results are consistent with the concept that increased renewal of intestinal epithelial cells represents a sizable fraction of whole-body protein turnover and that Gln is an important fuel for epithelial intestinal cells in vivo.

Adult↗
PubMed2000

Intestinal alphabeta T cells of symptomatic celiac disease patients show oligoclonal TCRBV repertoire but polyclonal rearrangement patterns.

Celiac disease is an immunological disease provoked by some cereal proteins in HLA-DQ-mediated susceptible individuals. The role of intestine infiltrating alphabeta T cells in the pathogenesis of the disease has been functionally established. In the present report, we have studied the repertoire of TCRBV genes, spectratype distribution, and CDR3 sequences of intestinal T cell populations isolated from three CD patients at diagnosis and two normal control biopsies. Oligoclonal TCRBV usage was observed both in CD and control samples. However, a much more restricted TCRBV usage was evident in normal mucosa. The use of BV gene families was linked to no dominant rearrangements in CD, while apparent oligoclonal patterns were found in normal biopsies. Only 3 out of 73 sequenced transcripts derived from preponderant TCRBV genes in the three celiac samples were obtained twice. In contrast, only 13 different rearrangements were found out of 32 analyzed in control samples. In spite of the polyclonal behavior of T cells in CD mucosa, some conserved motifs in the CDR3 region were noticed among rearrangements derived from different TCRBV genes and patients. The lack of expanded T cell clones in the damaged tissue could be explained in terms of antigen diversity or by non-specific immunological responses in the symptomatic phase of the disease.

Celiac Disease↗
PubMed1979

An association between primary biliary cirrhosis and jejunal villous atrophy resembling celiac disease.

A 76-year-old female presented with malabsorption and was subsequently shown to have jejunal villous atrophy. There was only partial clinical and histologic recovery with gluten withdrawal, but this was thought to be due to poor adherence to the diet. The findings were considered to be consistent with adult celiac disease. During the course of investigations, she was also found to have primary biliary cirrhosis. This is the fifth recorded instance of this association and the first from North America. Because these are uncommon conditions, it is postulated that this is unlikely to be a chance association. The recognition of this coexistence is of practical importance in the investigation and treatment of patients with primary biliary cirrhosis and celiac disease.

Aged↗
PubMed2005

Nasal septal perforation in a patient with subclinical celiac disease: a possible new association.

A female patient presented with nasal septal perforation that did not respond to conventional therapeutic management. Later, because of a malabsorption problem in one of her children, she underwent analytic tests and distal duodenal biopsy, which revealed that she was suffering from subclinical/silent celiac disease. The treatment, a gluten-free diet, unexpectedly resulted in the cessation of the destructive nasal process. Four years later, the patient remains asymptomatic. Nasal septal perforation might constitute a new entity associated with celiac disease hitherto not described in the literature.

Adult↗
PubMed1994

Celiac disease and epilepsy in pediatric patients.

Among 783 patients referred to our institute with different types of seizures as presenting symptom, systematic evaluation of antigliadin and antiendomysial antibodies in the serum has identified nine in whom jejunal biopsy has subsequently confirmed the diagnosis of celiac disease (CD). In three of them brain imaging showed the presence of calcified areas in the occipital region. They had complex partial seizures (CPS), associated in two with transient episodes of blindness. In another patient with CPS and generalized tonic-clonic seizures (GTCS) progressive multifocal cerebral calcifications were noted. In the other six patients with CPS and/or GTCS cerebral calcifications were absent. Symptoms of CD in all these cases were either not previously taken into account, or they were very mild or completely absent. In a group of 36 patients with clinically manifest CD, regular follow-up, and good compliance with the dietary regimen, no clinical seizures were reported. The pathogenetic mechanism and the relationship between epilepsy and an early diagnosis and treatment of celiac disease are discussed.

Adolescent↗
PubMed1991

Serum IgG and IgA anti-gliadin antibodies as markers of mucosal damage in children with suspected celiac disease upon gluten challenge.

Serum anti-gliadin antibodies (AGAs) of the IgG and IgA isotypes were determined in 17 children (mean age of 5.6 years) by means of an enzyme-linked immunosorbent assay (ELISA). All children were suspected of celiac disease. They had been on dietary treatment for at least 10 months before they were challenged with gluten. Based on jejunal biopsy findings, 10 of the 17 children had to be considered positive. The sensitivity of the measurement of AGA at 6 weeks after gluten challenge was found to be 90% for IgG, 100% for IgA, and 100% for IgG/IgA combined. The specificity for IgG, IgA, and the IgG/IgA combination was 100, 71, and 100%, respectively. Twelve weeks after gluten challenge, the sensitivity as well as the specificity of AGA determination for IgG, IgA, and IgG/IgA were 100%. It is concluded that testing both IgG AGA and IgA AGA in children suspected of celiac disease is valuable in monitoring the course of the diagnostic provocation protocol and that jejunal biopsies can be abolished. This inexpensive tool can be useful in reducing the number of intestinal biopsies.

Adolescent↗
PubMed2001

T cells from celiac disease lesions recognize gliadin epitopes deamidated in situ by endogenous tissue transglutaminase.

Celiac disease is an HLA-DQ2-associated disorder characterized by intestinal T cell responses to ingested wheat gliadins. Initial studies used gliadin that had been subjected to non-enzymatic deamidation during pepsin/trypsin digestion to enrich for the gliadin-specific T cells in small intestinal celiac biopsies. These T cells recognized synthetic gliadin peptides only after their deamidation in vitro by purified tissue transglutaminase (tTG). However, as these studies used a deamidated antigen for re-stimulation prior to testing for antigen specificity, this raised the possibility that T cells specific for native epitopes had not been expanded in vitro and had thus been overlooked. To address this possibility and to look for more direct evidence that endogenous tTG mediates deamidation of gluten in the celiac lesions, we have here used a minimally deamidated chymotrypsin-digest of gliadin to challenge biopsies and then investigated the specificity of the T cell lines derived from them. Interestingly, these T cell lines only barely responded to the chymotrypsin-digested gliadins, but efficiently recognized the in vitro tTG-treated variants of the same gliadins. Moreover, the addition of a tTG-inhibitor during the gliadin challenge often resulted in T cell lines with abolished or reduced responses to deamidated gliadin. These data demonstrate that DQ2-restricted T cells within adult celiac lesions predominantly recognize deamidated gliadin epitopes that are formed in situ by endogenous tTG.

Amides↗
PubMed2003

Proteomics identification of acyl-acceptor and acyl-donor substrates for transglutaminase in a human intestinal epithelial cell line. Implications for celiac disease.

Transglutaminase (TG)-catalyzed cross-linking of both intracellular and extracellular proteins is an important biochemical event. However, increased concentrations of cross-linked proteins have been observed in many disorders. Moreover, TG-catalyzed modification of proteins might generate new self-antigens responsible for the autoimmune response, as in celiac disease. The identification of available substrates may offer an understanding of how the TG-catalyzed post-translational modification has an impact on physiology and disease. We used a proteomic approach to identify TG-modified protein targets in human intestinal epithelial cells to determine the extent to which transglutaminase specifically contributes to celiac disease. Two probes were used for endogenous TG activity: 5-(biotinamido)pentylamine, which represents the acyl-acceptor, and a biotinylated glutamine-containing peptide, which represents the acyl-donor. This approach identified >25 proteins, which range from 30,000 to 300,000 Daltons and can serve as acyl-acceptor and/or acyl-donor for transglutaminase. Some of them were known transglutaminase substrates, whereas others had not been previously identified. These targets include proteins involved in cytoskeletal network organization, folding of proteins, transport processes, and miscellaneous metabolic functions.

Animals↗