Biomedical subjects
Publications and source records attributed to G Oderda.
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To determine the clinical significance of Helicobacter pylori seropositivity and seronegativity in healthy blood donors, we carried out a serological evaluation of Helicobacter pylori status and endoscopy in a healthy blood donors population. In all, 1010 donors were screened for Helicobacter pylori by IgG ELISA and assessed for pepsinogen I and gastrin levels by RIA; 298 IgG seropositive and 61 seronegative subjects underwent endoscopy with biopsies. Of 359, 165 were also tested for CagA by western blotting. Of the 298 IgG seropositives, 274 were shown to be infected on biopsy testing. Endoscopy revealed 70 peptic ulcers, 41 cases of erosive duodenitis, and two gastric cancers. In all 105 seropositive donors were tested for CagA and 69 were CagA positive [34/58 gastritis (58.6%), 24/35 duodenal ulcer (68.6%) and 11/12 gastric ulcer (91.6%)]. Histologically active/chronic gastritis was associated with CagA: 88.4% vs 50% (CagA seropositive vs seronegative). Of the 61 IgG seronegatives, 59 were negative on biopsy testing. At endoscopy three had duodenitis. Of the 60/61 IgG seronegatives tested for CagA, one had a moderate reaction. Duodenal ulcer donors showed higher pepsinogen I levels than donors without duodenal ulcers (97.7 microg/ml vs 80.9 microg/ml respectively). Screening for Helicobacter pylori and anti-CagA seropositivity and pepsinogen I can identify individuals likely to have gastroduodenal pathology even in the absence of symptoms.
When trying to decide which children with Helicobacter pylori infection should be treated and at what stage they should be tested, we should take into account the fact that eradication of the infection may be useful both to induce symptom remission and to prevent later complications in adulthood. However, well designed studies to identify those infected children who are at risk of developing complications or have symptoms due to the infection are still lacking. Current literature only gives information on how to treat children with H pylori infection. Treatment regimens that include two drugs are usually more effective than in adults, and produce an eradication rate of 70-80%, but they should be given for at least two weeks, shorter treatments being less effective. Antibiotic resistance can impair eradication rate and the frequency of resistant strains in children should be studied. Combinations of antibiotics with antisecretory drugs are highly effective in adults, but triple therapy with two antibiotics and an antisecretory drug has been seldom tried in children; compliance is often poor so that the eradication rate is often similar to that produced by dual therapy. Compliance strongly influences eradication, and short simple treatment regimens that produce rapid symptom remission with few side effects are needed to optimise patient compliance. After treatment, eradication must be proved. Serological tests can help, provided that pretreatment serum is available and three to six months have passed since the treatment. A 13C-ureabreath test (13C-UBT) should be performed at least six weeks after treatment, but false negative results can occur and cut-off must be adjusted.
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An in-house enzyme-linked immunosorbent assay (ELISA) for measurement of Helicobacter pylori-specific immunoglobulin G (IgG) and IgA in saliva was evaluated by comparison with histopathologic (Giemsa staining) and biochemical (urease quick test) examination of gastric biopsy specimens obtained from 112 children referred for diagnostic gastroscopy. Serum H. pylori IgG was also measured in a subgroup of 50 children by the same ELISA. Salivary H. pylori IgG levels were significantly higher in H. pylori-positive (n = 57) than in H. pylori-negative (n = 55) children (P < 0.001). The sensitivity and specificity of the salivary IgG test were 93 and 82%, respectively; the positive and negative predictive values were 84 and 92%, respectively; and the accuracy was 87.5%. Salivary H. pylori IgA did not distinguish H. pylori-positive from H. pylori-negative children. The performance of serum H. pylori IgG was slightly (3 to 6%) better than that of salivary H. pylori IgG. The salivary IgG test can be considered a useful tool for the screening of H. pylori infection in children.
BACKGROUND: Familial clustering of Helicobacter pylori infection has been reported. We tested the hypothesis that simultaneously treating all Helicobacter pylori positive family contacts of infected symptomatic children results in lower treatment failure. METHODS: Relatives of 47 children (index) with Helicobacter pylori gastritis had endoscopy to assess prevalence of infection in first degree cohabiting relatives. Controls included 60 children with dyspepsia and Helicobacter pylori gastritis whose infected family contacts were not treated. Index children, siblings younger than 18 years of age and control children received a 2-week course of amoxicillin and tinidazole. Parents of index children and their siblings over 18 years of age received a 2-week course of Colloidal Bismuth Subcytrate and tinidazole. The eradication rate in index children and their relatives was compared to controls whose infected family contacts were not treated. RESULTS: Helicobacter pylori was found in 67% of 31 siblings younger than 18, in 82% of 22 siblings older than 18 years, and in 87% of 92 parents. Endoscopy, repeated four to six weeks after the end of treatment, showed Helicobacter pylori eradication in 94% of children and siblings younger than 18, and in 70% of parents and siblings over 18 years in the family treatment group, compared with 75% of control children (p < .01). CONCLUSIONS: The high prevalence of the infection in family members suggests that person-to-person spread of Helicobacter pylori takes place. Furthermore our results show that if (or when) required, simultaneous treatment given to the whole family results in lower treatment failure, since it may promote compliance to treatment.
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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.
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.
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.
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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.
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.
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.
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.