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Biomedical subjects

N Ansaldi

Publications and source records attributed to N Ansaldi.

At least 37 records · Page 2Linked to original sources
PubMed1990

Increased tight junction width in two children with Ménétrier's disease.

Protein-losing enteropathy (PLE) and edema are usually the most prominent clinical features in children with Ménétrier's disease. However, the changes in gastrointestinal mucosa that can cause PLE have not been described yet in children. We studied by electron microscopy the mucosa of the gastric fundus, which is the site where macroscopic changes are most prominent, in two children with Ménétrier's disease. We found that tight junction width was increased to 10.5 +/- 0.94 nm (mean +/- 1 SD) in one child and to 9.7 +/- 0.7 in the other. Tight junction width returned to normal when PLE and edema subsided. These ultrastructural changes were similar to those described in adults with the disease, although the clinical course of Ménétrier's disease is very different in adults and in children. Both patients showed evidence of cytomegalovirus (CMV) infection, as indicated by increasing IgG antibodies against the virus or recovery of the virus in the urine. Although Helicobacter pylori was found in the antral mucosa of one patient, the clinical course of the disease was not related to this microorganism. We conclude that increased tight junction width plays a role in PLE seen in Ménétrier's disease in children and that CMV, rather than Helicobacter pylori, is associated with the disease.

Adolescent↗
PubMed1990

HLA in juvenile dermatitis herpetiformis: clinical heterogeneity correlated with DNA and serological polymorphism.

A group of 30 Italian children affected by Dermatitis Herpetiformis (DH) was analysed for HLA region polymorphisms with both serological and DNA methods. Serological typing was performed on HLA-A, B, C, DR, DQ antigens and C4A, C4B, Bf polymorphisms. DNA RFLPs obtained with TaqI enzyme were investigated with cDNA probes specific for DR beta, DQ alpha and DQ beta genes. The results were correlated with intestinal involvement and age at onset of the disease. The following observations were made: (1) the intestinal biopsies revealed a direct correlation between degree of lesions and age at onset of DH; (2) a significantly increased relative risk (RR) was found for the following HLA antigens: A1 (RR = 2.2), B8 (RR = 6.2), Cw7 (RR = 3.9), C4AQ0 (RR = 7.4), DR3 (RR = 5.2), DR7 (RR = 4.4), DRw53 (RR = 4.7), DQw2 (RR = 6.0); (3) B8 and DR3 were significantly more frequent in patients with severe intestinal lesions; and (4) of the two DR3 subtypes revealed by RFLP typing, only 3.1 showed an increased frequency in DH patients (RR = 8.4). It is suggested that the susceptibility to Juvenile DH is determined by the same genes, within the HLA region, that are associated with Coeliac Disease.

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

Amoxycillin plus tinidazole for Campylobacter pylori gastritis in children: assessment by serum IgG antibody, pepsinogen I, and gastrin levels.

32 children (mean age 12 years, range 6-18) with non-specific abdominal pain and Campylobacter pylori positive gastritis received a six week course of daily oral amoxycillin (50 mg/kg) and tinidazole (20 mg/kg). Before treatment and one month after stopping treatment, endoscopic biopsy samples were taken from the antral mucosa and serum C pylori IgG antibody, pepsinogen I, and gastrin levels were measured in fasting blood samples. One month after treatment 30 children (94%) were cleared of C pylori and gastritis had resolved in 27 (84%) and was improved in the remaining 5. Serum IgG, pepsinogen I, and gastrin levels were significantly decreased after treatment. Of 12 children assessed at six months, 9 remained free of C pylori. Increases or decreases in IgG level indicated clearance or recurrence, respectively, of C pylori.

Administration, Oral↗
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↗
PubMed1989

Serum pepsinogen I and IgG antibody to Campylobacter pylori in non-specific abdominal pain in childhood.

A consecutive series of 51 children (mean age 11 years) who presented with recurrent abdominal pain were investigated by upper gastrointestinal endoscopy including three antral biopsies for microscopy, culture and urease testing. Serum IgG, IgA, and IgM antibodies to Campylobacter pylori (C pylori) were measured by the ELISA technique. Serum pepsinogen I was also measured. Thirty two children showed histological evidence of gastritis. All had C pylori on microscopy and or culture. Nineteen children showed no histological gastritis nor evidence of C pylori on microscopy, culture and/or urease testing. The IgG and IgA antibody levels to C pylori were significantly higher in C pylori positive children than in the negative group (p less than 0.001). Serum pepsinogen I concentrations were also significantly higher in C pylori positive children than in negative (p less than 0.001). Measurement of IgG antibody levels, combined with serum pepsinogen I estimation, predict the presence of C pylori associated gastritis in children with a sensitivity and specificity of up to 95%. It may be used therefore to predict gastritis and even peptic ulceration in children presenting with non-specific upper abdominal pain.

Abdomen↗
PubMed1989

[Dental changes in children with malabsorption].

The paper reviews existing reports on relations between pathologies leading to malabsorption and dental lesion in children. The following dental alterations are reported in the literature: delayed eruption of deciduous teeth, hypoplasia of enamel and dental caries. These lesions have been observed in gastrointestinal pathologies, for example, coeliac disease, chronic diarrhea and recurrent vomiting, intolerance of cow's milk protein, Crohn's disease and salmonellosis. The delayed eruption of deciduous teeth and hypoplasia of the enamel are certainly correlated to malabsorption and maldigestion, especially if these are protracted over time. Dental caries may be due to poor oral hygiene, poor diet and to the presence of modified calcification. Only a comparative study with a control group will enable the effective prevalence to be assessed.

Child↗
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↗
PubMed1987

HLA and antigluten antibodies in children with celiac disease.

IgG and IgA antigluten antibodies (Gab) were assayed in 83 celiac disease (CD) patients typed for HLA and Gm markers. Their titer and frequency were lower when a gluten-free diet was given than in active CD; these were significantly correlated, whereas no correlation was found between titer and serum Ig. Persistence of high titers was mainly confined to HLA-DR3 negative females (45% vs 6.7% of DR3 positive females and 19.3% of males). No association was found with any Gm allotype, in contrast with the previously reported involvement of the "fnb" haplotype with both CD susceptibility and Gab persistence in patients on a gluten-free diet. A technical and/or genetic explanation could be given for these differences.

Celiac Disease↗