SUMMARY 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.Since the description by Warren and Marshall of S shaped spiral Gram negative bacteria in the antral mucosa of adult patients with gastritis or peptic ulcer,1 the association between Campylobacter pylori and gastritis has also been described in children,2 3 and the incidence among children undergoing endoscopy for upper gastrointestinal symptoms varies between 20 and 24%. 5 Though the relationship has not been proved to be causal, preliminary studies have shown that elimination of the organism results in improvement or healing of the gastritis,6 thereby providing indirect evidence of its pathogenic role. Eradication has been achieved in adults with courses of amoxycillin,6 or tripotassium dicitratobismuthate,7 or a combination of the two, but relapse is common.
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.In adults a strong association is now recognised between the presence of Helicobacter pylori in gastric mucosa and histologically confirmed gastritis.' H pylori has also been specifically associated with primary antral gastritis in children, and as in adults the organism is present only in the gastric mucosa with concomitant gastric inflammation.23 Raised serum pepsinogen I concentrations are found in about two thirds of adults with peptic ulcer disease,4 and are thought to be a useful subclinical marker of genetic predisposition to ulceration. Serum pepsinogen I concentrations and a high titre of antibody to H pylori have been found to be raised in children with H pylori associated gastritis.2 Moreover, it has been shown that the concentrations of serum pepsinogen I, gastrin, and IgG antibody to H pylori significantly decreased after a six week course of amoxycillin and tinidazole.'
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.
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