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PubMed1998

Peptide excretion in celiac disease.

BACKGROUND: In celiac disease, the mucosa in the small intestine is damaged. This study was conducted to determine whether the normal peptide and protein uptake from the gut is increased in patients with celiac disease. METHODS: The low-molecular-weight peptides were measured in urine from children and adults with untreated celiac disease. A reversed-phase technique was used. RESULTS: The excretion of peptides increased compared with that in an age- and sex-matched reference group. CONCLUSIONS: Celiac patients have hyperpeptiduria. It is possible that some of these peptides are bioactive and may mediate varying systemic effects also found in untreated celiac disease.

Adolescent↗
PubMed2002

Celiac Disease.

Individuals with celiac disease present with a wide array of symptoms and signs. Celiac disease can result in substantial injury to the small intestine, deleterious effects on other organ systems, and an overall doubling of mortality. The role of the gastroenterologist is primarily to make the diagnosis and then to ensure that patients with celiac disease receive up-to-date and accurate instructions on diet. It is our opinion that gastroenterologists should participate in the follow-up of what is in fact a form of inflammatory bowel disease. The failure to identify and treat patients with substantial problems may result in an excess of preventable morbidity and mortality. Intestinal biopsy is the definitive method of making the diagnosis of celiac disease, provided the patient has not excluded gluten from his or her diet, because exclusion of gluten results in negative serologic test results and normal small intestinal biopsy samples. The removal of gluten from the diet can result in a total recovery of gut function and a correction of most other consequences. The response is usually so complete that patients should consider themselves to be basically healthy as long as they stay away from the offending foods. However, the execution and maintenance of the "theoretically simple" exclusion of gluten is difficult. The condition is permanent and mandates adherence to a lifelong gluten-free diet; even small amounts of gluten can result in injury to the intestinal lining. The diet is restrictive and requires the patient to be careful about food choices. Therefore, patient education and motivation are crucial to a successful outcome. The correction of vitamin and mineral deficiencies may be helpful in aiding recovery; vitamin D and calcium supplementation often is recommended. No drug therapy has been proven to suppress the disease.

Journal Article↗
PubMed1988

[Radiological study of the duodenum in celiac disease in adults].

Celiac disease (CD) is the most common form of malabsorption in childhood when it presents with diarrhea and growth failure, a jejunal biopsy is considered the first diagnostic investigation by some authors. In adulthood, clinical symptoms of CD may mimic several different disease, such as peptic ulcer and IBS, and the first diagnostic investigation is an upper GI series. Radiological features of duodenum and small bowel were evaluated in twenty patients with adult onset celiac disease. Sign of duodenitis such as thickened folds, mucosal nodules, dilatation of duodenum and erosions were observed in 19 out of our 20 patients (95%); particularly, thickened folds in 17 (85%), nodularity in 16 (80%), duodenal dilatation in 12 (60%) and erosions in 4 (20%). In celiac disease the lesions are more severe in the upper part of small bowel, and duodenitis may be the unique sign of CD. Duodenitis may be part of a disease involving the entire small bowel; so, a duodenitis observed in the upper gastrointestinal tract requires the study of the entire small bowel--which seems to be very important in the case of celiac disease.

Adolescent↗
PubMed2000

[Neurological diseases associated with celiac disease].

During the period from May 1997 to October 1998, eight patients with coeliac disease or dermatitis herpetiformis and neurological disorders were admitted to the Department of Neurology, University Hospital of Bergen. The most frequent conditions were polyneuropathy (seven patients) and spinocerebellar ataxia (three patients). Other conditions were lower motor neuron disease, myelopathy, epilepsy and encephalopathy. The patients used various degrees of gluten-free diet at the time of admission. It remains unclear whether there is a shared common pathogenetic mechanism or the neurological disorder is a complication to the coeliac disease. Both vitamin depletion and immunological mechanisms may cause neurological disorder. Neurological manifestations may occur before the gastrointestinal symptoms. With reference to our patients and available literature we discuss prevalence, clinical picture, pathogenesis, treatment and prognosis. Neurologists, gastroenterologists and general practitioners should be aware that coeliac disease can cause neurological diseases, especially polyneuropathy, cerebellar ataxia and encephalopathy.

Adult↗
PubMed1992

Association of subepithelial deposition of activated complement and immunoglobulin G and M response to gluten in celiac disease.

Patients with celiac disease produce not only immunoglobulin A (IgA) but also immunoglobulin G (IgG) and M (IgM) antibodies to gluten. Intake of dietary gluten may hence induce local complement activation and mucosal damage. Jejunal tissue sections from adult patients with celiac disease were examined by immunofluorescence with monoclonal antibodies to activation neoepitopes in C3b and the terminal complement complex (TCC). Subepithelial deposition of TCC was observed in 93% of 28 untreated and in 57% of 23 partly treated study subjects. The immunofluorescence staining intensity was well correlated with the serum level of gluten-specific IgG and IgM (but not IgA), the number of mucosal IgG-producing cells, and the degree of villous atrophy. Similar immune deposits were not observed in 5 successfully treated patients with celiac disease, 5 patients with dermatitis herpetiformis without jejunal villous atrophy, and 90% of 21 control patients with histologically normal jejunal mucosa. Gluten challenge increased the amount of subepithelial TCC and produced additional C3b deposition, suggesting recent complement activation. Ingested gluten might thus, via Ig-mediated subepithelial complement activation, damage the surface epithelium in celiac disease and induce compensatory crypt hyperplasia.

Adolescent↗
PubMed2000

Selective expansion of intraepithelial lymphocytes expressing the HLA-E-specific natural killer receptor CD94 in celiac disease.

BACKGROUND & AIMS: Celiac disease is a gluten-induced enteropathy characterized by the presence of gliadin-specific CD4(+) T cells in the lamina propria and by a prominent intraepithelial T-cell infiltration of unknown mechanism. The aim of this study was to characterize the subset(s) of intraepithelial lymphocytes (IELs) expanding during active celiac disease to provide insights into the mechanisms involved in their expansion. METHODS: Flow-cytometric analysis of isolated IELs and/or immunohistochemical staining of frozen sections were performed in 51 celiac patients and 50 controls with a panel of monoclonal antibodies against T-cell and natural killer (NK) receptors. In addition, in vitro studies were performed to identify candidate stimuli for NK receptor expression. RESULTS: In normal intestine, different proportions of IELs, which were mainly T cells, expressed the NK receptors CD94/NKG2, NKR-P1A, KIR2D/3D, NKp46, Pen5, or CD56. During the active phase of celiac disease, the frequency of CD94(+) IELs, which were mostly alphabeta T cells, was conspicuously increased over controls. In contrast, the expression of other NK markers was not modified. Furthermore, expression of CD94 could be selectively induced in vitro by T-cell receptor activation and/or interleukin 15, a cytokine produced by intestinal epithelial cells. CONCLUSIONS: The gut epithelium favors the development of T cells that express NK receptors. In active celiac disease, there is a specific and selective increase of IELs expressing CD94, the HLA-E-specific NK receptor that may be related to T-cell receptor activation and/or interleukin 15 secretion.

Adult↗
PubMed1998

Osteomalacia secondary to celiac disease, primary hyperparathyroidism, and Graves' disease.

Primary hyperparathyroidism is seldom associated with other autoimmune disorders. The presence of normocalcemia in primary hyperparathyroidism should prompt the physician to look for vitamin D deficiency. This observation concerns a 34-year-old vegetarian woman with combined primary hyperparathyroidism, Graves' disease, and celiac disease. The patient presented with severe bone deformities; she was unable to walk, and had severe muscular weakness and weight loss. Biochemical findings revealed severe hyperparathyroidism with normocalcemia, hypophosphatemia, very low urinary calcium, and low 25-hydroxy vitamin D level. Thyroid tests showed hyperthyroidism with positive thyroid receptor antibodies, confirming the presence of Graves' disease. Positive antigliadin and antireticulin antibodies and complete villous atrophy on duodenal biopsy established the presence of celiac disease. The patient underwent a near-total thyroidectomy, with the removal of a parathyroid adenoma. To our knowledge, this observation is the first finding of an association between celiac disease, Graves' disease, and primary hyperparathyroidism. It emphasizes the need to rule out intestinal malabsorption in the case of normocalcemic hyperparathyroidism.

Adenoma↗
PubMed1998

Detecting celiac disease in your patients.

Celiac disease is a genetic, immunologically mediated small bowel enteropathy that causes malabsorption. The immune inflammatory response to gluten frequently causes damage to many other tissues of the body. The condition is frequently underdiagnosed because of its protean presentations. New prevalence data indicate that symptomatic and latent celiac disease is present in one of 300 people of European descent. Age of onset ranges from infancy to old age. Symptomatic presentations include general ill-health, as well as dermatologic, hematologic, musculoskeletal, mucosal, dental, psychologic and neurologic diseases. Celiac disease has a 95 percent genetic predisposition and, thus, it is frequently associated with autoimmune conditions such as diabetes mellitus type 1 and thyroid disease. Untreated patients have an increased incidence of osteoporosis and intestinal lymphoma. Excellent diagnostic screening tests are now available, including those that detect antigliadin and antiendomysial antibodies. Therapy with a gluten-free diet is effective, resulting in complete resolution of symptoms and secondary complications in almost all patients. Local and national celiac-sprue associations facilitate care of patients with celiac disease and support dietary compliance.

Celiac Disease↗
PubMed2000

Gluten-dependent diabetes-related and thyroid-related autoantibodies in patients with celiac disease.

Patients with celiac disease are at high risk of having autoimmune disorders. Moreover, untreated patients with celiac disease have been found to have a higher than expected prevalence of organ-specific autoantibodies. In a prospective study of 90 patients with celiac disease, we found that the prevalence of diabetes and thyroid-related serum antibodies was 11.1% and 14.4%, respectively. Like antiendomysium autoantibodies, these organ-specific antibodies seem to be gluten-dependent and tend to disappear during a gluten-free diet.

Case-Control Studies↗