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At least 19 recordsLinked to original sources
PubMed2004

cDNA microarray analysis of gene expression in coeliac disease jejunal biopsy samples.

In coeliac disease in the jejunum of a genetically susceptible person wheat gliadin and related prolamins from rye and barley trigger an immunological reaction, which induces small-bowel mucosal transformations, villous atrophy and crypt hyperplasia. Though CD4+ specific T cells, intraepithelial lymphocytes, infiltrating plasma cells and autoantibodies are known to have an effect on the coeliac disease, the pathogenic mechanisms leading to the tissue injury remain to be elucidated. Our aim was to find novel gene transcripts, which might have a role in coeliac disease pathogenesis. The gene expression in duodenal biopsy samples from untreated coeliac patients (n=4), patients on gluten-free diet (n=4) and healthy controls (n=4) was studied by cDNA microarray analysis. The method allows monitoring of the expression of thousands of genes simultaneously. Compared to healthy controls, the expression of 156 and 60 genes was changed in untreated and treated coeliac disease, respectively. Between treated and untreated coeliac disease, 98 genes had altered expression. Of the 5184 genes or expressed sequence tags, altogether 263 were affected. Many of these genes are directly or indirectly connected to T-cell activation, B-cell maturation or epithelial cell differentiation. By the microarray method, numerous genes were found to evince altered mRNA expression in coeliac disease. The method holds promise in exploring the pathogenetic mechanisms in the small bowel and may reveal new target genes for the therapy of coeliac disease.

Adult↗
PubMed1986

[Endoscopic diagnosis of duodenal and jejunal diseases].

We presented and studied the endoscopic diagnosis of the duodenal ulcer, duodenal tumors and duodenal bleeding. Duodenal Ulcer is classified according as location, form and evolutive stage. Duodenal tumors are divided in polyps, primitive tumors, pancreas anomaly and lymphoma. Duodenal bleeding can be diagnosed according its cause (inflammatory, tumors vascular and traumatic). It is emphasized the importance of the indications and methods of the enteroscopy. We show our experience in 313 duodenal ulcers cases and 98 enteroscopic diagnosis.

Duodenal Diseases↗
PubMed1962

A study with the electron microscope of the jejunal epithelium in primary malabsorptive disease.

Jejunal biopsy specimens were obtained by means of the Crosby capsule from a normal person and from seven patients. Of these, three with primary malabsorptive disease (idiopathic steatorrhoea) had an abnormal mucosal pattern under the light microscope, and the microvilli under the electron microscope were stunted, broadened, and sparse. Two with primary malabsorptive disease had normal light microscopic appearances, and the microvilli appeared normal, while two who had appearances typical of primary malabsorptive disease under the light microscope had malignant disease of the small intestine. Of the patients with malignant disease, one had normal microvilli under the electron microscope and the other demonstrated microvilli similar to those found in primary malabsorptive disease. The former patient may have had primary malabsorptive disease in addition to the malignant change but this is uncertain, and there is no reason to believe that this was the case in the latter patient. The changes seen under the light microscope are usually of great value as an aid to diagnosis in primary malabsorptive disease but this is not always the case, and the same applies to electron microscope changes.

Celiac Disease↗
PubMed1990

Gliadin challenge-induced jejunal prostaglandin E2 secretion in celiac disease.

Jejunal prostaglandin E2 secretion in patients with adult celiac disease was studied under basal conditions and after local gliadin challenge. A newly developed tube system with occluding balloons was used to perfuse a jejunal segment. After an initial basal perfusion period of 40 minutes, an average of 12 mg +/- 3 (SEM) of crude gliadin was administered into the perfused segment. Perfusion continued for an additional 100 minutes and prostaglandin E2 was determined in the effluent with a radiometric method. Patients with histologically active celiac disease (n = 7) had higher basal jejunal secretion of prostaglandin E2, 523 +/- 229 pg.cm-1.h-1 (mean +/- SEM), than both celiac patients with normalized small bowel mucosa (n = 6), 160 +/- 44 pg.cm-1.h-1, and healthy controls (n = 18), 184 +/- 38 pg.cm-1.h-1, (P less than 0.05). After gliadin challenge of the jejunal segment, a significant increase (P less than 0.05) in prostaglandin E2 secretion was noted in patients with celiac disease (n = 10). The individual maximum increase was on average fivefold and occurred 60-100 minutes after gliadin administration. In healthy controls (n = 5), no alteration in prostaglandin E2 secretion was detected after gliadin challenge. Enhanced jejunal prostaglandin 2 synthesis may be involved in the pathophysiological processes initiated by gliadin in patients with celiac disease.

Adult↗
PubMed1984

Gastrointestinal regulatory peptide storage granule abnormalities in jejunal mucosal diseases.

The mucosal concentrations of seven regulatory peptides and the density properties and integrity of their storage granules have been studied in mucosal biopsies from the human jejunum in eight gastrointestinal disease states and compared with normal controls. In diseases with associated mucosal inflammation (coeliac disease, Crohn's disease with jejunal involvement, postinfective tropical malabsorption, and common variable immunodeficiency) there was a selective increase in fragility of the gastric inhibitory polypeptide (GIP) and somatostatin storage granules. The gastrin, motilin, enteroglucagon, secretin, and vasoactive intestinal polypeptide granules had normal properties in these conditions. In diseases in which diarrhoea occurred in the absence of changes in jejunal mucosal histology (irritable bowel syndrome, pancreatic insufficiency, jejuno-ileal bypass for morbid obesity, and purgative abuse) there were no abnormalities of the storage granules. Increased mucosal concentrations of all peptides except vasoactive intestinal polypeptide (VIP) were found in coeliac disease and selective increases of VIP found in Crohn's disease, motilin in the irritable bowel syndrome and gastrin and GIP in pancreatic insufficiency. It is suggested that the storage granule abnormalities in the diseases with abnormal mucosal histology are secondary to the inflammatory changes.

Gastric Inhibitory Polypeptide↗
PubMed1979

Abnormalities of jejunal mucosal enzymes in ulcerative colitis and Crohn's disease.

Jejunal mucosal function and structure was examined in 31 patients with ulcerative colitis and 29 patients with Crohn's disease with ileal, ileocolonic or colonic involvement; A significant reduction of the specific activity of disaccharidases (lactase, sucrase and trehalase) in jejunal mucosal homogenate occurred in patients with inflammatory bowel disease. Similarly, alkaline phosphatase was reduced in ulcerative colitis. Several dipeptidases such as glycyl-leucine, leucyl-glycine, glycyl-glycine and valyl-proline hydrolase activities were lower in patients with inflammatory bowel disease than in controls. Histological changes in jejunal mucosal biopsies occurred in 71% of patients with ulcerative colitis and 61% with Crohn's disease. These changes ranged from mild abnormalities of villus architecture to marked reduction of villus height. Most patients with a reduction in mucosal enzymes had concommitant morphological changes in jejunal mucosal biopsy. The results of this study indicate that functional and structural abnormalities of the jejunal mucosa frequently occur in patients with inflammatory bowel disease without radiologic evidence of proximal small bowel involvement.

Adolescent↗
PubMed1981

Protein synthesis by cultured jejunal mucosa from control subjects and patients with coeliac disease.

Jejunal biopsies from patients with coeliac disease and from controls were cultured in vitro for 24 hours with 14C-labelled leucine. The net rate of protein synthesis was found to be linear over 24 hours for mucosa from control subjects and patients with coeliac disease. Protein synthesis by mucosa from untreated coeliac patients was significantly greater than by control mucosa. Protein synthesis by treated gluten-sensitive coeliac mucosa was significantly less than that by untreated coeliac mucosa and did not differ from control mucosa. Protein synthesis by treated non-responsive coeliac mucosa was significantly less than untreated coeliac mucosa but greater than control mucosa. The differences in protein synthesis could not be accounted for by differences in the size of the enterocyte leucine pool. Analytical subcellular fractionation of cultured jejunal mucosa showed that most of the protein synthesised in vitro was found in the cytosol and endoplasmic reticulum-brush border fractions of the enterocyte.

Celiac Disease↗
PubMed1977

Jejunal mucosal immunoglobulins and complement in untreated coeliac disease.

Jejunal immunofluorescence studies have shown that there is a significantly increased incidence of extracellular IgA and complement in the basement membrane zone and lamina propria of untreated adult coeliac patients compared to coeliac patients on a gluten-free diet. IgG was also demonstrated with complement, particularly in the untreated patients. These findings, taken together with those of other studies, suggest that a local antibody-antigen reaction involving IgA and complement may be responsible for the ongoing mucosal damage in untreated coeliac disease as well as for the acute damage following gluten challenge of the treated patient. Furthermore, consequent upon this damage there may be a secondary IgG antibody response, possibly reticulin antibody, contributing to the mucosal damage.

Adult↗
PubMed1983

Jejunal biopsy and lymphocyte co-culture in coeliac disease.

Jejunal biopsies from 13 patients with treated coeliac disease were maintained in organ culture for 24 h with and without the addition of gluten fraction III, in each case with and without autologous peripheral blood mononuclear cells. Biopsies cultured with gluten alone or with lymphocytes alone showed no significant reduction in mean enterocyte height compared with those cultured in control medium, but those cultured with both gluten and lymphocytes had significantly lower enterocyte height than control biopsies, than those cultured with gluten alone, and than those cultured with lymphocytes alone. These results demonstrate that the combination of gluten and lymphocytes is more toxic to treated coeliac mucosa in vitro than either one alone and support the suggestion that immune reactions to gluten may be important in the pathogenesis of the mucosal lesion of coeliac disease.

Adult↗
PubMed1990

Serum lipoprotein profile in children with celiac disease.

Jejunal mucosa is responsible for the absorption of triglycerides and the production of lipoproteins [chylomicrons, very-low-density lipoprotein (VLDL), high-density lipoprotein (HDL)] and apolipoproteins (B-48, A-I, A-II, A-IV, C-II). Mucosal damage is known to cause fat malabsorption and probably also affects the serum lipid profile. To determine lipoprotein production in states of enterocyte dysfunction, we compared the serum lipid profiles in a group of 12 children with untreated celiac disease (flat jejunal mucosa) with the profiles in a control group of 10 children suffering from other intestinal diseases. Statistically significant differences were found in the following parameters (celiac versus control): plasma levels of triglycerides (70 versus 119 mg/dl), cholesterol content in LDL (107 versus 67.7 mg/dl), protein content in VLDL (6 versus 10 mg/dl), and level of apoprotein A-I (112 versus 140 mg/dl). No significant differences were found between the two groups in the serum levels of total cholesterol, the cholesterol content in VLDL and HDL, the protein content in LDL and HDL, and the level of apoprotein B. Following institution of a gluten-free diet, the lipoprotein profile reverted to normal. These data suggest that the changes in the serum lipoprotein profile in celiac disease are secondary to alterations in enterocyte function and not only a reflection of fat malabsorption.

Celiac Disease↗
PubMed1986

A freeze-fracture study of the enteropathy associated with dermatitis herpetiformis: a comparative investigation with coeliac disease.

Jejunal biopsies from patients with either dermatitis herpetiformis or coeliac disease were freeze-fractured and compared with normal jejunal biopsies. The intestinal mucosa of the normal biopsies showed a normal structure, with well-developed and tightly packed microvilli; in dermatitis herpetiformis and coeliac disease degenerative changes of the intestinal mucosa occurred. These changes appeared to be segmental in dermatitis herpetiformis and diffuse in coeliac disease. Emphasis is placed on changes in the tight junctional net at the base of the microvilli, which could represent cellular damage related to increased intestinal permeability to macromolecules in these diseases. An interpretative hypothesis for these observations is presented.

Biopsy↗
PubMed1990

Binding to human jejunum of serum IgA antibody from children with coeliac disease.

Jejunal histology and the presence of serum IgA antibodies (JAB) binding to human jejunum in vitro were studied in 139 children with severe malabsorptive symptoms. Among 33 children with confirmed coeliac disease (ESPGAN criteria), 13 (93%) of 14 sampled before starting on a gluten-free diet had JAB, none of 21 sampled had JAB while on a gluten-free diet of long duration, and 90% of 30 sampled during gluten challenge had JAB. 53 children had severe jejunal villous atrophy (probable coeliac disease): 71% of those younger than 2 years and 94% of those aged 2-18 years had JAB during gluten intake. JAB could not be detected in 53 disease control patients (normal jejunal histology) and in 3 coeliac disease patients with selective IgA deficiency. Simultaneous determination of antigliadin (AGA) and antiendomysium (EMA) levels, and gliadin and tissue absorption studies, showed that JAB and AGA are different, whereas JAB and EMA are probably identical. IgA JAB could be the target-organ-related autoantibodies in coeliac disease.

Adolescent↗
PubMed1987

Timing of infiltration of T lymphocytes induced by gluten into the small intestine in coeliac disease.

Jejunal biopsy was performed on control subjects and patients with treated and untreated coeliac disease. Monoclonal antibodies to T lymphocyte surface markers were used to quantify T cell phenotypic subsets in the jejunal mucosa. The patients with untreated coeliac disease had significantly more of both suppressor/cytotoxic and helper/inducer T cells in the surface epithelium than either the control subjects or the treated patients. Serial jejunal biopsy specimens were taken from five treated coeliac patients for six hours after a gluten challenge. In four of these five infiltration of the surface epithelium by both T cell phenotypes, together with deterioration in the villus architecture, had occurred both within two hours of having started the challenge. This suggests that T lymphocytes may have a role in the pathogenesis of coeliac disease.

Adolescent↗
PubMedDate not supplied

Spiral CT demonstration of hypervascularity in Crohn disease: "vascular jejunization of the ileum" or the "comb sign".

OBJECTIVE: To report spiral CT imaging features of the vascular alterations observed in active, early, or recurrent Crohn disease of the small bowel and colon. METHODS: Spiral CT examinations of the abdomen and pelvis following oral and intravenous contrast were performed in two cases of active Crohn disease. RESULTS: Spiral CT features of hypervascularity involving the mesenteric vessels of affected segments of bowel include vascular dilatation, tortuosity, and conspicuous prominence and wide spacing of the vasa recta (the "comb" sign). This is attributed to the factors of increased flow and the fibrofatty proliferation in the mesentery and serosa of the affected bowel. CONCLUSION: Clinical application of these observations may enhance the diagnosis of Crohn disease presenting initially or as an acute recurrence in the differential diagnosis from other conditions.

Adult↗
PubMed1983

Bacterial overgrowth in jejunal and ileal disease.

The number of bacteria recovered in anaerobic cultures of jejunal secretions was significantly higher in a group of 10 patients with jejunal disease and stagnation of gut content in the proximal small bowel than in a group of 10 patients with similar conditions in the distal ileum. Some overlap in bacterial numbers occurred between patients with jejunal disease, ileal disease, and healthy controls, whereas production of fermentation gas in anaerobic media supplemented with glucose occurred only in cultures from the patients with jejunal disease. The 14C-glycocholic acid test showed increased output of breath 14CO2 in both patient groups, whereas faecal 14C was significantly increased only in patients with ileal disease. Increased breath hydrogen excretion after glucose ingestion was recorded in 8 of 10 patients with jejunal disease only. Breath methane excretion, previously found in 44% of healthy subjects, was absent in all of 28 patients with Crohn's disease of the small, indicating that these patients have a gut flora that is different from that of the healthy population.

Adolescent↗
PubMed1977

Celiac disease with jejunal ulceration.

A patient with celiac disease with ulceration of the jejunum, an infrequent association, is reported. Patient underwent surgery for resection of the ulcerated segment. The frequency of such an association, possible complications and an approach to therapy is reviewed.

Adult↗
PubMed1976

Cellular infiltrate of the jejunum after re-introduction of dietary gluten in children with treated coeliac disease.

Jejunal lamina propria plasma cells and eosinophils and intraepithelial lymphocytes were raised in coeliac children on gluten-containing diets, but only intraepithelial lymphocytes were increased in patients on gluten-free diets. In contrast, lamina propria lymphocytes were reduced in children with coeliad disease on gluten-containing diets but were normal in paitents on gluten-free diets. In children with coeliac disease who were studied serially, lamina propria plasma cells and eosinophils and intraepithelial lymphocytes increased, and lamina propria lymphocytes decreased, within three months of the reintroduction of gluten to the diet. These observations are essentially similar to those made in the adult form of the disease and suggest that more than one type of immunological reaction is involved in the pathogenesis of the jejunal lesion.

Adolescent↗