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PubMed1981

Immunogenetics of childhood celiac disease: the association with HDA DR3 and DR7 in unrelated patients with multiply affected families.

The association between childhood celiac disease and the histocompatibility complex was studied in five multiply affected families and 20 unrelated patients. The diagnosis of celiac disease (CD) was established by three consecutive jejunal biopsies: 1) at the initiation of the diagnosis; 2) following a gluten-free diet; and 3) after gluten provocation. The results of this study indicate that a significant association exists between celiac disease, DR3 (P less than 0.001) and DR7 (P less than 0.001). The relative risks for these antigens were 8.56 and 5.05, respectively. Segregation analysis in the families suggested that the susceptibility genes associated with the histocompatibility antigens are not inherited in either a dominant or a recessive pattern. While an intermediate type fits better into the genetic framework of CD, more than one susceptibility and protecting gene may be involved in the pathogenesis of this disease.

Adult↗
PubMed1993

Transmission electron microscopy of microvilli of intestinal epithelial cells in celiac disease in remission and transient gluten enteropathy in children after a gluten-free diet.

The structure of microvilli of intestinal epithelial cells was investigated in 70 children: 34 with celiac disease in remission, 28 with transient gluten enteropathy after a gluten-free diet, and eight controls. Transmission electron microscopy was used to determine the mean thickness of the glycocalyx layer covering the microvilli, the mean length and width of microvilli, and the number of microvilli per 1 micron length of enterocyte surface. The structure of the glycocalyx was found to be intact, but in some children with treated celiac disease the layer of glycocalyx was either thin or absent on the surface of individual cell microvilli. In children with treated celiac disease, microvilli were statistically significantly shorter than those in children with transient gluten enteropathy and controls. Microvillous width in treated celiac disease was greater as compared with that in controls. There was no difference in the number of microvilli on the enterocyte surface in the three groups.

Biopsy↗
PubMed1999

Sugar tests detect celiac disease among first-degree relatives.

OBJECTIVES: First-degree relatives of patients with celiac disease are at high risk for developing the disease themselves. Detection of serum antibodies and intestinal permeability tests have been useful to identify candidates for intestinal biopsies. Recently it was demonstrated that abnormal sucrose permeability is a very sensitive marker of active disease. Our objectives in this prospective study were (1) to assess the screening value of permeability tests, and (2) to compare the usefulness of these markers with that of the celiac disease-related serology in screening for celiac disease in a cohort of first-degree relatives of well-known patients. METHODS: We performed sugar tests in 66 first-degree relatives of probands. Subjects ingested 450 ml of a solution containing sucrose (100 g), lactulose (5 g), and mannitol (2 g). Subsequently, a complete overnight urine collection was obtained. Measurement of sugars was performed by high-performance liquid chromatography. All relatives were evaluated for antigliadin (type IgA and IgG) and endomysial antibodies and subjects positive for any test underwent intestinal biopsy. RESULTS: Twelve relatives were diagnosed as having small intestinal mucosal atrophy. Increased sucrose permeability was detected in 9 (75%) of these patients. Four false-positive determinations were found but all had gastric erosions, which is known to increase sucrose permeability independently of duodenal damage. Increased lactulose/mannitol ratios were observed in all new celiac patients. An additional nine relatives had positive results; however, four of them did not accept intestinal biopsy and the remaining five did not seem to have histological evidence of disease. Endomysial antibodies were detected in 11 of 12 patients and no false-positive cases were observed. Antigliadin antibodies were 75% sensitive and 88% specific. CONCLUSIONS: Our study demonstrated that screening using the endomysial antibody test is highly sensitive and specific for detecting celiac disease; however, almost 10% can be missed. The addition of lactulose/mannitol permeability testing to the screening protocol allowed us to detect all relatives who actually presented with evidence of gluten sensitivity. Sucrose permeability exhibited a lower sensitivity; however, it did detect other endoscopically visible lesions.

Adolescent↗
PubMed1999

Serological diagnosis of celiac disease.

In developing countries like India, unlike in the West, diagnosis of celiac disease is a dilemma because the histological changes consistent with celiac disease may not be pathognomonic of the disease. We need clarity on how to use one or more of the serological antibodies, namely IgG and IgA anti-gliadin and IgA anti-endomysial antibodies as independent disease markers or as adjuncts to clinico-histological diagnosis. In this review, various possible algorithms have been discussed. The serological antibodies can be used as reliable screening tests to decide whom to biopsy and to interpret histological changes in our settings where malnutrition and intercurrent enteric infection are common.

Antibodies, Anti-Idiotypic↗
PubMed2001

Helicobacter pylori-negative gastric ulcerations associated with celiac disease at first presentation.

Ulcers of the small bowel have repeatedly been described as a late complication of celiac disease and they are considered a signum mali ominis. We report a case of a 53-year-old woman presenting with diarrhea, epigastric pain and abdominal distensions for a period of few weeks. At upper GI endoscopy, biopsies were taken showing complete atrophy of the villi and colonization of the small bowel mucosa. Additionally, uncommon multilocular peptic ulcers were seen in the gastric antrum. These ulcers proved to be Helicobacter pylori-negative with no evidence of Zollinger-Ellison syndrome. Biopsies of gastric ulcers showed signs of a lymphocytic gastritis with an extensive infiltration of the lamina propria by almost exclusively CD3- and CD45R0-positive T-lymphocytes. Intraepithelial T-lymphocytes were found to be increased in the antral as well as the corpus mucosa. Typing the patient for human leukocyte antigens showed a DQA1*0501 and DQB1*0201 phenotype. According to the present report, gastric peptic ulcers seem to be another phenomenon associated with celiac disease. In the case presented here, ulcers were diagnosed together with celiac disease already at first presentation of the patient.

Biopsy↗
PubMed2001

Celiac disease presenting with microcephaly.

A 15-month-old girl with celiac disease presented with microcephaly and developmental delay. Head growth resumed during a gluten-free diet. Subsequent gluten ingestion resulted in no head growth, areflexia, and increased celiac antibodies. All resolved with gluten elimination. Poor head growth may precede other clinical manifestations of celiac disease.

Celiac Disease↗
PubMed1991

[Assessment of the reparative capacity of the small intestine in celiac disease in children according to the DNA and RNA contents in enterocyte nuclei].

In 44 children suffering from celiac disease, cytophotometry was used to measure the content of DNA and RNA in enterocyte nuclei in the jejunum mucosa. The measurements were made after the diagnosis was established, 6-8 months and 1-1.5 years after administration of the agliadin diet. In celiac disease children, there was an increase of the content of DNA and RNA in enterocyte nuclei of the intestinal villi and cryptae and lack of gradient in the distribution of the amount of nucleic acids along the length of the villi, which characterized the hyper-regeneration type of small intestinal mucosa atrophy. The recovery of the crypta/villus gradient accompanied by the normalization of the content of nucleic acids, comparable with the analogous indicators of the unchanged mucosa of the small intestine, allows regarding the measurements of the content of DNA and RNA in the nuclei as an index of reparative capacity of enterocytes in children afflicted with celiac disease.

Celiac Disease↗
PubMed1999

Celiac disease associated with familial chronic urticaria and thyroid autoimmunity in a child.

An 11-year-old girl presented with chronic urticaria (CU), antithyroid antibodies, and anemia. Celiac disease was diagnosed. The family history was positive for maternally derived CU and thyroid autoimmunity in three generations. Human leukocyte antigen typing disclosed human leukocyte antigen DQA1*0501 DQB1*0201 in both mother and child. CU was unresponsive to a gluten-free diet despite clinical and laboratory resolution of celiac disease in contrast to previous reports in adults. We believe that this is the first report of this association in a child, highlighting that CU may be a part of the spectrum of autoimmune phenomenon related to celiac disease.

Autoantibodies↗
PubMedDate not supplied

Celiac disease and Turner's syndrome: patient report.

Turner's syndrome is a chromosomal disease frequently associated with autoimmune disorders including thyroid disease, inflammatory bowel disease, diabetes mellitus and juvenile rheumatoid arthritis. Recent reports have described an association of celiac disease with Turner's syndrome. We present an additional patient with Turner's syndrome associated with celiac disease. A girl aged 15- 7/12 yr was seen for the complaints of delayed growth and puberty, abdominal pain and chronic diarrhea. She was diagnosed as having celiac disease and a gluten-free diet was initiated. Despite one year of strict diet no signs of puberty were observed. She was then evaluated again for absence of puberty, and 45,XO karyotype Turner's syndrome was diagnosed.

Adolescent↗
PubMed1995

Adult celiac disease is frequently associated with sacroiliitis.

No data are available on the presence and frequency of peripheral or central joint disease, routinely determined by bone scintigraphy with 740 MBq of [99mTc]MDP, in adult celiac disease. Bone scintigraphy was carried out to detect early acute inflammatory lesions in 22 adult celiac patients (15 females and seven males; mean age 36.72 years, range 17-63). Bone scintigraphy was positive for sacroiliitis in 14 cases (63.6%). Except in the case of one patient suffering from rheumatoid arthritis, laboratory data were normal. Our data suggest that as in other chronic intestinal diseases, celiac disease in adults, is frequently associated with central joint disease. This high incidence of sacroiliitis, the joint disease most frequently found in our patients, has not been previously reported in other series. We believe, therefore, this difference could be explained by the different methodology used for the screening of joint disease.

Adult↗
PubMed1984

[Gallbladder atony and celiac disease in adults. Radiographic and echographic study of 15 cases].

Gallbladder emptying was evaluated in 15 adult celiac disease patients by oral cholecystography or ultrasonography, after fatty meal or cholecystokinin stimulation. Gallbladder inertia was found in 13 cases. Our study agrees with previously reported results; however it is the first one in which this abnormality was demonstrated by ultrasonography. Our findings may suggest that gallbladder inertia is due to duodenal release of an inactive endogenous cholecystokinin. Control studies demonstrates that gallbladder inertia is reversible after gluten-free diet, recurs with relapse, and thus represents a true celiac disease sign, and not an associated condition. Finally, our cases suggest that gallbladder inertia may be radiologically evident before clinical features of malabsorption become apparent. Awareness of this possibility may persuade the radiologist to research in this condition an occult celiac disease.

Adult↗
PubMed2001

Update on immunologic basis of celiac disease.

During the past few years several seminal studies have greatly expanded our knowledge on celiac disease pathogenesis. This review focuses on aspects that have been most properly addressed and where substantial new information has been gathered include. Topics covered include (a) the identification of T-cell epitopes in gluten and the mechanisms of specific T-cell response in celiac disease small intestine; (b) the mechanisms of induction of mucosal lesion; and (c) the putative role of non-T-cell factors in driving mucosal response to gliadin. After discussing a brief history of the "quest for the cause of celiac disease," we examine the development of the typical celiac lesion (the crypt hyperplastic mucosal atrophy) as it generally unfolds: the increased entry of dietary antigens; the early changes, linked to specific components of the innate immunity rather than to its adaptive branch; the most thoroughly investigated subsequent response, involving a strong T-cell response and cytokines; and the factors responsible for enterocytes' death. The emerging pattern is that of a complex interaction of factors, although far from being completely understood, but fascinating as it opens an incredible window of knowledge on an autoimmune disorder whose environmental factor is known, whose autoantigen is known, whose autoantibodies are known: a truly unique situation in medicine.

Journal Article↗
PubMed2002

Update on immunologic basis of celiac disease.

During the past few years several seminal studies have greatly expanded our knowledge on celiac disease pathogenesis. This review focuses on aspects that have been most properly addressed and where substantial new information has been gathered include. Topics covered include (a) the identification of T-cell epitopes in gluten and the mechanisms of specific T-cell response in celiac disease small intestine; (b) the mechanisms of induction of mucosal lesion; and (c) the putative role of non-T-cell factors in driving mucosal response to gliadin. After discussing a brief history of the "quest for the cause of celiac disease," we examine the development of the typical celiac lesion (the crypt hyperplastic mucosal atrophy) as it generally unfolds: the increased entry of dietary antigens; the early changes, linked to specific components of the innate immunity rather than to its adaptive branch; the most thoroughly investigated subsequent response, involving a strong T-cell response and cytokines; and the factors responsible for enterocytes' death. The emerging pattern is that of a complex interaction of factors, although far from being completely understood, but fascinating as it opens an incredible window of knowledge on an autoimmune disorder whose environmental factor is known, whose autoantigen is known, whose autoantibodies are known: a truly unique situation in medicine.

Journal Article↗
PubMed2000

Celiac disease in older people.

In recent years, there has been increasing recognition that the classical textbook presentation of celiac disease with a malabsorption syndrome and a flat jejunal mucosa is only part of a broad spectrum of clinical and histological features associated with gluten sensitivity. Diagnosis of this treatable condition is often delayed or missed because of a failure to appreciate that celiac disease can present at any age and that symptoms are often subtle and not clearly related to gastrointestinal disease. Nonspecific symptoms and nutritional deficiencies are especially common in older patients and may not always be investigated thoroughly. Use of serological screening tests has improved ease of detection of celiac disease in patients without classical symptoms.

Age Distribution↗
PubMed2002

[Selenium plasma concentrations in children with celiac disease in different stages of diagnosis].

Selenium is an important nutritional factor of human diet. Epidemiological and experimental data indicate that low selenium level can be associated with increased risk of cancer. On the other hand there are some evidence that patients with celiac disease can present selenium deficiency and increased risk of certain malignancies. Therefore the aim of study was to evaluate plasma selenium levels in children with celiac disease. The level of selenium was estimated by flame atomic absorptiometry method according to Whiteside. Celiac disease was diagnosed according to ESPGHAN criteria. Obtained results indicate that in celiac disease low plasma selenium levels are especially marked at preliminary stage of diagnosis and following low compliance to the gluten free diet. Children with this sickness may need supplementation of their diet with selenium.

Adolescent↗
PubMed2003

Tissue transglutaminase expression in duodenal mucosa of patients with celiac disease and of normal subjects.

BACKGROUND/AIMS: Our aim in the present study was to investigate tissue transglutaminase expression by immunohistochemistry in duodenal mucosa of patients with celiac disease. METHODS: A total of twelve patients with celiac disease were examined. The patients had different clinical and histopathologic degrees of severity and responded to gluten withdrawal with clinical improvement. Ten subjects with various unrelated diseases served as controls. Serum endomysium antibodies were measured by an indirect immunofluorescence method using a commercial kit. Duodenal biopsy specimens were stained with hematoxylin and eosin. Immunohistochemical staining for anti-tissue transglutaminase antibodies was performed using commercial kit. RESULTS: Serum endomysium antibodies and evaluation of small bowel biopsy specimens were normal in all control subjects. However, serum endomysium antibodies were positive in all of the celiac patients. Immunohistochemical staining pattern of duodenal biopsy specimen performed using anti-tissue transglutaminase antibodies was similar in celiac patients and control subjects. CONCLUSION: Tissue transglutaminase expression by immunohistochemical methods in untreated celiac mucosa is not suitable for diagnosis of celiac disease.

Adult↗
PubMed1996

[Diabetes and celiac disease: a study related to the association of the two pathologies].

In subjects afflicted with insulin dependent diabetes mellitus, celiac disease is more diffuse than in normal people. The study has been done to a group of 93 diabetic children and teenagers who had undergone determination of antigliadine and antiendomysial antibodies. In the study the result of the celiac disease exceeds the data reported in the literature. The motivations of this result is discussed and the necessity to do immunological screening for celiac disease is requested. A possible intestinal biopsy of all diabetes in the beginning of the disease is recommended.

Adolescent↗
PubMed2006

Peripheral neurological disturbances, autonomic dysfunction, and antineuronal antibodies in adult celiac disease before and after a gluten-free diet.

Thirty-two consecutive adult celiac disease (CD) patients (pts), complaining of peripheral neuropathy (12 pts), autonomic dysfunction (17 pts), or both (3 pts), were evaluated to assess the presence of neurological damage (by clinical neurological evaluation and electrophysiological study) and antineuronal antibodies and to assess the effect of a gluten-free diet (GFD) on the course of the neurological symptoms and on antineuronal antibodies. At entry, 12 of 32 (38%) pts showed signs and symptoms of neurological damage: 7 of 12 (58%), peripheral neurological damage; 3 of 12 (25%), autonomic dysfunction; and 2 (17%), both peripheral neurological damage and autonomic dysfunction. The overall TNS score was 105 at entry. Anti-GM1 antibodies were present in 5 of 12 (42%) pts: 3 showed peripheral neurological damage and 2 showed both peripheral neurological damage and autonomic dysfunction. One year after the GFD was started, histological lesions were still present in only 10 of 12 (83%) pts. TNS score was 99, 98, 98, and 101 at the 3rd, 6th, 9th, and 12th month after the GFD was started, so it did not improve throughout the follow-up. None of the pts showed disappearance of antineuronal antibodies throughout the follow-up. We conclude that adult CD patients may show neurological damage and presence of antineuronal antibodies. Unfortunately, these findings do not disappear with a GFD.

Adolescent↗