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D Dell'Olio

Publications and source records attributed to D Dell'Olio.

At least 19 recordsLinked to original sources
PubMed1999

Gluten-induced nitric oxide and pro-inflammatory cytokine release by cultured coeliac small intestinal biopsies.

OBJECTIVES: To determine whether there was increased nitric oxide (NO) production from coeliac small intestinal biopsies cultured in vitro with gluten and whether the inhibition of NO production could prevent gluten-induced enterotoxicity. The relationship between NO production with the pro-inflammatory cytokines interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) was evaluated. DESIGN: Small intestinal biopsies from ten patients with treated coeliac disease and six controls were studied. METHODS: Small intestinal biopsies were taken from each patient and set up in culture with Frazer's fraction III (FFIII), a peptic/tryptic digest of gluten, FFIII plus L-NMMA and L-NMMA alone, culture medium alone and ovalbumin which served as a control protein. The biopsies were cultured for 20 h at 37 degrees C. The supernatants were then collected and analysed for nitrite using the Greiss reaction; cytokine levels were determined using ELISA kits. Enterocyte height was determined by microscopy using a calibrated eyepiece graticule and cryostat sections of the cultured biopsies. RESULTS: Coeliac biopsies cultured with FFIII produced significantly greater nitrite compared to culture medium alone (P< 0.05) and this could be blocked with L-NMMA (P< 0.01). A reduction in enterocyte height was seen in coeliac biopsies cultured with FFIII compared to culture medium alone (P < 0.01) and this was ameliorated but not completely blocked when FFIII was cultured with L-NMMA. These changes were not seen in the controls. There was a significant reduction in IL-1beta levels in the supernatant of coeliac biopsies cultured with FFIII compared to culture medium alone (P< 0.05), but when cultured with FFIII and L-NMMA there was a significant increase in IL-1beta levels (P< 0.05). An increase in IFN-gamma levels was also seen when coeliac biopsies were cultured with FFIII and L-NMMA (P< 0.05). This pattern was not seen with TNF-alpha. CONCLUSIONS: Increased levels of NO can be found when coeliac biopsies are cultured with gluten in an in vitro small intestinal culture system, and NO may play a role in the observed enterotoxicity as the inhibition of NO production ameliorates the enterocyte damage. The results suggest that NO is involved in the regulation of pro-inflammatory cytokines, particularly IL-1beta. This is likely to be one of many pathways leading to the observed mucosal pathology in coeliac disease and demonstrates the close interactions between them.

Adolescent↗
PubMed1998

The detection and localization of inducible nitric oxide synthase production in the small intestine of patients with coeliac disease.

OBJECTIVES: To investigate whether there are increased numbers of inducible nitric oxide synthase (iNOS) containing cells in the small intestine of patients with coeliac disease and the localization of nitric oxide synthase production. DESIGN: Small intestinal biopsy specimens from patients with coeliac disease (11 untreated, 10 treated) and nine disease controls were studied. METHODS: Histochemical staining of sections for NADPH-diaphorase activity was performed, which gives an indication of NOS activity. iNOS protein was detected with immunohistochemistry and iNOS mRNA expression was detected using in situ hybridization with an oligonucleotide probe cocktail for iNOS. Cell phenotype was detected using monoclonal antibodies to CD3 (T-lymphocytes) and CD45 (total inflammatory cell infiltrate). RESULTS: There was significantly greater NADPH diaphorase staining in the lamina propria of patients with untreated coeliac disease (P < 0.005). The same pattern was found for immunohistochemical and in situ hybridization methods of staining for iNOS in each of the patient groups (P < 0.005) but no epithelial staining was seen with any method. The pattern of iNOS staining in the lamina propria appeared in a similar distribution to that of the inflammatory cell infiltrate. At least 80% of the significantly increased total inflammatory cell infiltrate (CD45) in the lamina propria of patients with untreated coeliac disease was lymphocytic (CD3) whilst the iNOS staining cells made up less than 15% of the total inflammatory cell infiltrate. CONCLUSIONS: There is a significant increase in the number of NOS staining cells of the inducible isoform in the lamina propria of patients with untreated coeliac disease. The lamina propria and not the epithelium is the site of iNOS production in coeliac disease. It appears that inflammatory cells other than T-lymphocytes are likely to be the cellular sources of iNOS production within the lamina propria. This is the first study to demonstrate increased numbers of iNOS producing cells in the small intestine of patients with untreated coeliac disease and suggests a role for nitric oxide in the pathogenesis of the histological changes seen in coeliac disease although it may be a non-specific inflammatory response to immune activation by gluten in susceptible individuals.

Adolescent↗
PubMed1997

Detection and characterisation of anti-endomysial antibody in coeliac disease using human umbilical cord.

OBJECTIVES: To verify the effectiveness of human umbilical cord (HUC) in the detection of anti-endomysial antibodies (AEA) in coeliac disease and to characterize further these antibodies by studying tissue adsorption characteristics and antibody inhibition studies. METHODS: AEA were detected on HUC and primate oesophagus in a blind study, using sera from 46 patients with untreated coeliac disease and 108 controls. Tissue adsorption studies were performed using homogenized tissue from rodent liver, HUC, primate oesophagus and human liver. Sera were adsorbed with each of these homogenates and antibody was detected using HUC, primate oesophagus and rat kidney. In the inhibition experiments AEA was detected on HUC, and inhibition of binding was attempted by pre-incubating the sections with antibodies against collagen types I, III and IV. RESULTS: The sensitivity of AEA was 91% when detected on HUC, 89% when detected on primate oesophagus (93% and 91%, respectively, after exclusion of 1 patient with IgA deficiency). Specificity was 100% for both assays. Tissue adsorption studies showed identical results for AEA detected on both HUC or primate oesophagus, whereas antireticulin antibody was adsorbed only by rodent tissue. Blocking of the HUC with anticollagen antibodies did not prevent binding of AEA. CONCLUSIONS: HUC is an effective substrate for the detection of AEA and may be superior to primate oesophagus. The antibody detected by HUC shows identical tissue adsorption specificities to that detected on primate oesophagus.

Adolescent↗
PubMed1996

Analysis of interleukin-4 and interleukin-10 and their association with the lymphocytic infiltrate in the small intestine of patients with coeliac disease.

BACKGROUND: Concentrations of pro-inflammatory cytokines are raised in the small intestine of patients with coeliac disease after ingestion of gluten but there are equivalent data on interleukin-4 (IL-4) and interleukin-10 (IL-10) producing cells. These cytokines are known to exert important regulatory effects on pro-inflammatory cytokine production from lymphocytes and macrophages. AIMS: To investigate whether there is a primary deficiency of IL-4 and IL-10 producing cells and their site of production in the small intestine of patients with coeliac disease in relation to the changes in inflammatory cell infiltrate. PATIENTS: Jejunal biopsy specimens from patients with coeliac disease (11 untreated, 10 treated) and nine disease controls were studied. METHODS: Immunohistochemical staining of sections for IL-4 and IL-10 cytokines and the cell phenotypic markers CD3 (T lymphocytes) and CD45 (total inflammatory cell infiltrate) was carried out using monoclonal antibodies. Expression of IL-4 and IL-10 messenger RNA was detected by in situ hybridisation with oligonucleotide probe cocktails for each cytokine. RESULTS: IL-4 and IL-10 mRNA and protein were detected in the lamina propria of treated and untreated coeliac patients and disease controls but not in the epithelium. A significant increase in the number of CD45 (p < 0.005) and CD3 (p < 0.05) positive cells was found in the lamina propria of patients with untreated coeliac disease compared with treated coeliac patients and disease controls but there were no differences in IL-4 or IL-10 between these groups with either method. CONCLUSIONS: There is no primary deficiency of IL-4 and IL-10 producing cells in the small intestine of patients with coeliac disease. Detectable concentrations of IL-4 and IL-10 were found in control patients which suggests that these cytokines are involved in normal mucosal immunoregulation. The increased number of T lymphocytes but not IL-4 or IL-10 producing cells in the lamina propria of patients with untreated than in those with treated disease suggests not only that the lamina propria is the major mucosal compartment for cytokine production but that newly recruited mucosal T lymphocytes are directed to a predominant Th1 and not a Th2 cytokine response in coeliac patients on a diet containing gluten.

Adult↗
PubMed1995

[What do celiac children eat? Dietary analysis of a group of children with celiac disease on a diet].

A diagnosis of Coeliac Disease (CD) indicates a lifelong compliance to a gluten-free diet (GFD), which implies a change in deeply ingrained dietary habits and may cause dietary imbalances. We studied the dietary intake in a group of children with CD on GFD. CD was diagnosed according to Espgan criteria. Strict compliance to GFD was ascertained by Hydrogen breath-test. For each patient a thorough dietary history was obtained; the Recommended Dietary Allowances (RDA) 1986/1987--Istituto Nazionale della Nutrizione were used as reference measurements. 71.3% of our patients had a daily calorie intake lower than recommended (mean +/- 1SD = -110 +/- 389 kcal/day). Calorie deficiency was mainly due to a low carbohydrate intake (50.2 +/- 7% of daily calorie intake vs. 59% RDA; difference = -4.7 +/- 7%). Fast absorbed simple carbohydrates exceeded by 46% the recommended 10% ratio to complex carbohydrates. Daily fat intake was higher than RDA (+7.7%) in 94.1% of our patients, who obtained from fat 35.7 +/- 5.2% of their daily calorie intake vs 28% recommended. Saturated to unsaturated fat ratio was unbalanced towards saturated fat intake (2.3 +/- 1.1 vs 0.33 recommended). Coeliac children on a GFD have low caloric and carbohydrate intakes and a high fat intake. An unbalance towards simple sugar and saturated fat ingestion was detected. A lifelong protraction of these dietary habits may favour the onset of metabolic diseases in mature age.

Adolescent↗
PubMed1994

[Hydrogen breath test in celiac disease: relationship to histological changes in jejunal mucosa].

Hydrogen concentration in expired breath depends on the fraction of ingested carbohydrates unabsorbed by the small intestinal mucosa which reach the large intestine and are fermented by the colonic flora. The aim of this study is to assess whether in coeliac children breath hydrogen excretion reflects the histological changes in the jejunal mucosa. Hydrogen breath test was performed on 40 children (15 males 25 females) divided into three groups. Group I (controls): 9 children with symptoms suggestive of coeliac disease who, after the appropriate workup, were found to suffer from other gastrointestinal disorders and had abnormal jejunal mucosa. Group II: 14 children who had been diagnosed as coeliacs according to the ESPGAN criteria, were kept on a gluten free diet for a minimum of 6 months and had a normal jejunal mucosa. Group III: 17 coeliac children who ate small quantities of gluten or were on a normal diet. At histology, 10 of them showed a total and 7 a partial atrophy of the jejunal mucosa. Breath hydrogen levels were measured both at baseline and after ingestion of a 2% sorbitol solution in water, at 30 minute intervals for four hours. The peak hydrogen level and the total surface area under the hydrogen excretion curve were also assessed. Coeliac children on a gluten containing diet excrete significantly more H2 than controls or coeliacs on a gluten free diet. Patients with more severe histological lesions had higher peak H2 levels and greater total excretion areas. In coeliac children, sorbitol breath H2 test represents a simple noninvasive technique to detect impaired jejunal function and it should have an important role as a screening test and in assessing dietary compliance.

Adolescent↗
PubMed1993

Prostaglandin E2 in gastric mucosa of children with Helicobacter pylori gastritis: relation to thickness of mucus gel layer.

AIMS: To evaluate the changes in mucus gel layer thickness and prostaglandin E2 (PGE2) content caused by Helicobacter pylori infection in the antral mucosa of children: to assess whether decreased mucus gel thickness is related to PGE2 production. METHODS: Antral biopsy specimens were taken at endoscopy from 153 children. H pylori gastritis was evident in 45 and normal mucosa in 59. The other 49 children were studied one month after antibiotic treatment that eradicated the infection in 37 of them had been stopped. One antral specimen was immersed in ice-cold saline, put under an inverse microscope with an eyepiece graticule. Mucus gel thickness was measured and then the processed for histological examination; another specimen was weighed and processed for in vitro prostanoid generation. RESULTS: Mucus gel layer thickness was significantly decreased in children with H pylori gastritis (90 (SD) 29) microns v 120 (58) microns in controls, p < 0.01) but returned to control values after H pylori had been eradicated. PGE2 generation was significantly increased in children with H pylori gastritis (1022 (811) ng/g v 641 (473) ng/g in controls, p < 0.01). One month after treatment PGE2 generation significantly decreased in children without infection (880 (534), p < 0.01), but was still high where infection persisted. A significant inverse correlation was found between PGE2 generation and mucus gel layer thickness (p < 0.05). CONCLUSIONS: These data suggest that H pylori damages the mucus gel layer, and that the gastric mucosa increases generation of PGE2 in response to back diffusion of acid and pepsin.

Adolescent↗
PubMed1991

[Clinical data on celiac disease with an early or late onset].

Typical symptoms in celiac disease (CD) are usually associated with early onset of the disease, whereas an atypical symptomatology has more often a later onset. The aim of this study was to evaluate the prevalence of some clinical signs and symptoms in children whose CD started before one year of age ("early onset" 135 children, M/F 50/85, mean age at onset 6.9 +/- 1.9 months) and in children whose disease started later ("late onset", M/F 14/26, mean age at onset 26.3 +/- 26.7 months). We analyzed: a) time lapse between gluten introduction and onset of symptoms, b) prevalence of patients with gastrointestinal symptoms alone and that of patients with gastrointestinal plus extraintestinal symptoms, c) frequency of each symptom. We then evaluated the influence of breast feeding and age of gluten introduction on time lapse. Our results showed that typical gastrointestinal symptoms, like diarrhea anorexia and abdominal distension prevailed both in children with early and late onset; whereas failure to thrive was significantly more frequent in children with an early onset CD (p < 0.01). Breast feeding delayed onset of symptoms: time lapse was significantly longer in children breast fed for a longer time (p < 0.001). On the contrary, age at first gluten ingestion seemed to have no influence on age at onset, since it was similar in both groups.

Adolescent↗
PubMed1990

Serum pepsinogen I and gastrin concentrations in children positive for Helicobacter pylori.

Serum pepsinogen I, serum gastrin concentration, and inflammatory scores were measured in a population of 71 children undergoing upper gastrointestinal endoscopy for investigation of upper abdominal pain. Forty four were initially colonised with Helicobacter pylori. The indices were measured before treatment (in 71 children), one month (in 41 children), and six months (in 21 children) after stopping treatment. Before treatment there was a significant correlation between serum pepsinogen concentration, total inflammatory score, and H pylori state, but no correlation between serum gastrin concentrations and H pylori state. Similarly, the total inflammatory score and serum pepsinogen concentrations were significantly correlated. There was no such correlation in children negative for H pylori. After treatment the inflammatory score improved in those patients in whom H pylori had been eradicated. There was also a significant fall in serum pepsinogen I and serum gastrin concentration in those patients in whom H pylori had been eradicated. These results were similar to those found six months after treatment had been stopped. These findings suggest that the serum pepsinogen I concentration could be considered a useful marker for gastritis and can be used as an index of severity of gastritis in H pylori positive subjects. The measurement of serum gastrin concentrations does not give useful information.

Adolescent↗
PubMed1990

Treatment of childhood peptic oesophagitis with famotidine or alginate-antacid.

Both antacids and H2 receptor antagonists have a potential role in treating peptic oesophagitis associated with acid reflux. The aim of this study is to assess the efficacy and tolerability of famotidine and alginate-antacid in children with endoscopically documented peptic oesophagitis. We compared clinical, endoscopic and histological response to alginate-antacid (1 tablet to be chewed 30 min after each meal and at bed time) or famotidine (1 mg/kg before supper at 7 pm) in 49 children (mean age 9 years, 34 males). Twenty-four of them were randomly allocated to alginate-antacid treatment (group A), twenty-five to famotidine (group B). Both treatments were protracted for six months and endoscopy was then repeated. Symptoms disappeared in 43.4% and improved in 47.8% of children of group A and disappeared in 91.6% of those of group B (p less than .05). Mean time for symptom disappearance was 17 weeks for group A and 5 weeks for group B (p less than .01). After six months, at endoscopy oesophagitis was healed in 43.4% in group A and in 41.6% of group B, the difference between the two groups was not significant, however the improvement of endoscopic grades induced by famotidine was significantly better (p less than .05). Histology showed a healed peptic oesophagitis in 52.2% of the children in group A and in 70.8% of group B (p less than .001). No toxicity was observed with either treatment. We conclude that famotidine is superior to alginate-antacid in treating peptic oesophagitis associated with acid reflux, since it induces a better symptomatic response and a greater improvement of endoscopic lesions.

Adolescent↗
PubMed1989

Campylobacter pylori gastritis: long term results of treatment with amoxycillin.

To evaluate the efficacy of amoxycillin in eradicating Campylobacter pylori, endoscopic biopsy specimens were taken from the antral mucosa of 40 children with gastritis before, immediately after, and (in 30 patients) three months after treatment. Immediately after treatment 34 patients (85%) no longer had the organism in the mucosa, and the gastritis had healed in 23 (58%). Three months later the infection had recurred in 22 of 30 patients (73%), and the gastritis had relapsed in all of them. Significantly more children in whom C pylori recurred had family histories of peptic ulcer disease. The results suggest that amoxycillin alone is ineffective in the long term treatment of C pylori gastritis.

Adolescent↗
PubMed1987

Duodenitis in children: clinical, endoscopic, and pathological aspects.

In a retrospective study of 320 gastroduodenoscopies performed on children in the last 2 years, 32 cases of duodenal damage, either isolated or associated with esophagitis, gastritis, or both, were selected. Twenty matched children with dyspeptic symptoms but an endoscopically normal duodenum were chosen as controls. Histological sections of fiberoptic biopsy specimens were submitted to double-blind examination by two observers: only four fulfilled accepted criteria for histological duodenitis. The concordance between endoscopic and histological results in our patients was 13.8%. No changes of duodenal endoscopic appearance predictive of duodenitis were identified. In 8 more cases (6 patients and 2 controls) the histological examination showed an isolated lymphocyte and plasma cell infiltration of the lamina propria without any additional damage. We called this picture "minimal change duodenitis" and considered it as a variation of normal. In 17 patients and 11 controls, basal and maximal acid outputs were calculated and no significant differences were found. We concluded that duodenitis in children may be present, although rare, and its diagnosis requires histological examination of duodenal mucosa.

Adolescent↗
PubMed1985

Bethanechol versus antiacids in the treatment of gastroesophageal reflux.

To compare the efficacy of bethanechol in the treatment of gastroesophageal reflux with that of antiacids, a prospective, cross-over study was undertaken, in which 20 affected infants and children were randomized into two groups on 6-week alternate bethanechol and antiacids oral medication. Patients were evaluated clinically and by esophageal pH-metry before and after each treatment. Clinical score amelioration was achieved earlier than reflux number reduction and with similar incidence in both groups of patients, irrespectively to the initial medication; moreover, the differences in the degree of improvement between the two groups after either treatment were not found to be significant. These results fail to show that bethanechol is more effective than antiacids in controlling gastroesophageal reflux; moreover, bethanechol is more difficult to administer and offers a higher rate of undesired side effects.

Aluminum Hydroxide↗