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Biomedical subjects

G Oderda

Publications and source records attributed to G Oderda.

At least 37 records · Page 2Linked to original sources
PubMed1996

Serum pepsinogen I in childhood Helicobacter pylori gastritis: its relation to mucosal peptic activity.

Serum pepsinogen I (PG I) levels are raised in children with Helicobacter pylori gastritis. To ascertain if this is due to increased production or to increased secretion of pepsin by chief cells, we measured mucosal peptic activity in antrum and gastric body mucosal homogenates and correlated it to serum PG I levels in 122 children with and without H. pylori gastritis. In patients infected with H. pylori, mucosal peptic activity was decreased when compared to control and to children with non H. pylori gastritis. Serum PG I levels were increased (P < 0.001) and were inversely related to mucosal peptic activity (P < 0.01). These findings suggest that H. pylori can promote a leakage of pepsinogen into the circulation.

Adolescent↗
PubMed1995

[Rare causes of gastrointestinal bleeding in childhood. A clinical case of von Willebrand's disease].

von Willebrand type I disease is an hereditary coagulation disorder characterized by a deficiency of the factor VIII complex: VIII: C, vWF:Ag, vWF:RCoF. The clinical features of this disease are spontaneous bleeding and mucosal or cutaneous bleeding following minimal injuries. The authors describe a case of a 4-year girl with recurrent episodes of gastrointestinal bleeding due to von Willebrand disease.

Child, Preschool↗
PubMed1994

An alternative approach to the assessment of gamma delta T-cell clonality in celiac disease intestinal lesions through cDNA heteroduplex analysis of T-cell receptor VJ junctions.

We have investigated the clonality of the gamma delta T lymphocytes infiltrating the intestinal mucosa of CD patients and control subjects by means of a simple and powerful method based on the heteroduplex analysis of the TCR VJ junctions. Each V-specific TCR chain, amplified either from fresh biopsy material or intestinal T-cell-line cDNA, is denatured and renatured to allow the random reshuffling of the various strands carrying different junctional sequences, coamplified in the same reaction. The mismatched chains (heteroduplexes) are separated from the matched ones (homoduplexes) through polyacrylamide gel electrophoresis, and whenever one or more T-cell clones are emerging over the polyclonal background, discrete bands are visible by ethidium-bromide staining. Through this method, we have estimated the diversity of the V delta 1-3 chains and a newly described V gene (V delta 8) whose homologue in mice is abundantly expressed in gamma delta iLs. We demonstrate that the well-documented expansion of V gamma 1+ gamma delta lymphocytes in the jejunum of CD patients is polyclonal. Overall, the heteroduplex analysis on fresh intestinal and peripheral blood lymphocytes from both healthy and affected subjects shows a polyclonal pattern of all the V delta+ subsets. In contrast, most intestinal T-cell lines produce oligoclonal patterns, suggesting a dramatic in vitro selection effect. The cell expansion in culture is generally not required for the TCR heteroduplex analysis, which can therefore be applied to rapidly monitor the T-cell response in a variety of physiologic and autoimmune reactions, substituting the standard approach of TCR cloning and multiple VJ sequencing.

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↗
PubMed1994

Evaluation of a commercial ELISA kit for the serological diagnosis of Helicobacter pylori infection.

H. pylori infection can be diagnosed serologically. We evaluated an ELISA kit (Helicobacter pylori IgG, DIESSE) prepared using a glycine extract of an autoctonous H. pylori strain which produced the highest biologically active urease titre out of five strains tested. The kit was tested with serum samples from H. pylori-infected and uninfected adults and children. The Western Blot technique was used as reference method for the H. pylori infective status. Based on the results obtained by immunoblotting with serum samples from H. pylori negative subjects, two different cut-off values were considered for adults and children. Sensitivity and specificity were respectively 95% and 100% for adults, 95.6% and 97.8% for children. In conclusion, the clinical accuracy of this commercially available ELISA kit proved to be very good; the adoption of two different cut-off values for adults and children also improved its parameters of reliability.

Adolescent↗
PubMed1993

T cell receptor heterogeneity in gamma delta T cell clones from intestinal biopsies of patients with celiac disease.

In celiac disease large numbers of gamma delta T lymphocytes infiltrate the intestinal epithelia. We have isolated intestinal gamma delta T cell clones from patients with celiac disease and have analyzed their T cell receptor repertoire. T cell lines and clones were obtained from jejunal biopsies of 14 celiac patients and 12 individuals without celiac disease. These were analyzed by staining with monoclonal antibodies against CD3, alpha beta and gamma delta T cell receptor, by Southern blot with gamma- and delta-specific probes and by polymerase chain reaction using V delta-specific oligonucleotides. Intestinal gamma delta cells from patients with celiac disease differed from those of controls with normal jejunal histology in that V delta 1+ cells and V delta 1-V delta 2- cells were significantly increased. There was no evidence of the expansion of one or more clones expressing particular types of gamma delta T cell receptor.

Adolescent↗
PubMed1993

Endoscopic and histologic findings in the upper gastrointestinal tract of children with coeliac disease.

Frequency of mucosal damage to the esophagus, stomach, and duodenum was investigated in 176 children with coeliac disease (CD) during 230 upper GI endoscopies performed to obtain duodenal biopsy specimens and was compared with findings in 230 age-matched children who underwent endoscopy for upper GI complaints without CD (non-CD patients). To evaluate a possible association with gluten ingestion, we then compared frequency of mucosal damage in patients on a gluten-containing diet and those on a gluten-free Diet (GFD). In children with CD, frequency of esophageal damage seen at endoscopy and of peptic esophagitis shown by histology were significantly lower than in non-CD patients (p < 0.01) due to the very low frequency of mucosal damage in CD children on GFD; however, frequency of columnar metaplasia was significantly higher (p < 0.05). At endoscopy, CD children had a significantly lower frequency of gastric abnormalities, but histology showed a higher prevalence of superficial chronic gastritis (SCG; p < 0.01). SCG was associated with gluten ingestion, since its frequency in CD children on GFD was similar to the frequency in non-CD patients. At endoscopy, frequency of duodenal mucosal damage was similar in CD and non-CD patients. In addition to villous atrophy, histology showed a significantly higher frequency of duodenitis in CD children on a gluten-containing diet (p < 0.001 vs. non-CD patients; p < 0.05 vs. CD children on GFD). Our findings show that the mucosa of the whole upper GI tract can be damaged in CD patients and that the prevalence of some changes is higher with a gluten-containing diet.

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↗
PubMed1993

Occupational and environmental exposures reported to poison centers.

This analysis of 25,368 occupational and 7,565 environmental exposure cases characterizes the occupational and environmental exposures reported to the American Association of Poison Control Centers Toxic Exposure Surveillance System. Compared with other poisonings, occupational and environmental exposures were predominantly inhalation exposures rather than ingestions, were more often subacute or chronic, and demonstrated greater morbidity, mortality, and increased use of health care resources. As regional poison centers evolve to fill a critical information void in the management and assessment of environmental and occupational exposures, the American Association of Poison Control Centers Toxic Exposure Surveillance System provides an important, untapped passive surveillance mechanism.

Air Pollutants↗
PubMed1992

Eighteen month follow up of Helicobacter pylori positive children treated with amoxycillin and tinidazole.

Sixty three children with dyspepsia (mean age 12 years, range one to 18, M/F 41/22) were Helicobacter pylori positive by histology of gastric antral biopsy specimens and were treated with a six week course of amoxycillin (50 mg/kg) and tinidazole (20 mg/kg). The endoscopic diagnoses were: normal (16), nodular gastritis (19), oesophagitis (four), duodenal ulcer (13), and gastric ulcer (11). H pylori was eradicated in 54 (87%) and histological gastritis resolved in 51 and was improved in the other three. Repeat investigation was offered at six monthly intervals. Reinfection was found in three of 34 (9%) at six months, in none of 22 at 12 months, and in two of 18 (11%) at 18 months, yielding an 18 month cumulative relapse rate of 20%. Children with persisting infection despite treatment remained positive during follow up. Serum H pylori IgG concentrations fell after treatment (p < 0.001), and for individual children during follow up there was a progressive decline, but an increased concentration indicated recurrence. After eradication of H pylori by combined amoxycillin and tinidazole treatment, only a minority of children relapse during the ensuing 18 months.

Adolescent↗
PubMed1992

Mucosal peptic activity during Helicobacter pylori infection in pediatric patients.

Intramucosal peptic activity may participate in the genesis of acute and chronic superficial gastritis. The proteolytic activity of homogenates of gastric mucosa (antrum and body) and duodenum were measured at pH 2.0 (total peptic activity) after exposure to pH 8.0 (pepsinogen) and the activated pepsinogen (pepsin) was calculated in pediatric patients investigated for the presence of Helicobacter pylori (H pylori), 122 antral, 77 stomach body, and 74 duodenal biopsies were examined in 43 H pylori positive patients, 51 controls, and 28 H pylori negative gastritis patients. Activated pepsinogen was significantly reduced in the stomach of H pylori positive patients only. Pepsinogen values were similar in all the anatomical areas tested in all patients. In 13 H pylori positive patients reinvestigated three months after antibiotic therapy, antral mucosal activated pepsinogen activity increased significantly (mean pretreatment 1.56 (1.0) U/mg protein versus mean post-treatment 2.72 (1.7) U/mg protein) and reached values comparable with controls. The decreased activated pepsinogen activity in association with normal pepsinogen content observed in the antrum of H pylori positive gastritis patients indicate local pepsin inactivation or alternately enhanced removal into the gastric lumen or backflow into the circulation.

Adolescent↗
PubMed1991

Helicobacter pylori in children with peptic ulcer and their families.

Little is known about the source and spread of Helicobacter pylori, but transmission from infected family contacts has been suggested. We have therefore investigated 15 children with peptic ulcer and their first-degree relatives for H. pylori. Serum anti-H. pylori IgG, pepsinogen I, and gastrin levels were measured. Endoscopy was carried out on the children and relatives, and biopsies were taken from the gastric antrum for histology, microbiology, and urease testing. Six of 11 children with duodenal ulcer (55%) and two of four children with gastric ulcer (50%) were positive for H. pylori. Fourteen of 16 parents (87%) and eight of 13 siblings (61%) of H. pylori-positive children with peptic ulcer were also infected compared with eight of 14 parents (57%) and none of four siblings of H. pylori-negative children with peptic ulcer (P less than 0.10, greater than 0.05, and NS, respectively). The children with H. pylori-negative peptic ulcer and negative siblings combined were younger than positive children with peptic ulcer and positive siblings (P less than 0.001). The reliability of serum anti-H. pylori IgG level as a screening test for infection was confirmed. These findings call into question a pathogenetic role for H. pylori in some childhood peptic ulceration, but do suggest that person-to-person spread of infection occurs.

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↗