33 Efficacy of Helicobacter pylori (HP) eradication treatment is influenced by the primary resistance rate of the infecting strains. In a previous study over a 9-year period, we found 119/401 (30 %) strains resistant to at least one antibiotic before any treatment, steadily increasing in the last 4 years. Although the treatment regimen can be adapted to the results of the antibiogram, failure of eradication can be due to secondary resistance acquired during treatment. Aim: to evaluate the effect of secondary resistance on the eradication rate of HP strains in children. Methods: through 1993-97, in a series of 294 children (mean age 12.5 ± 5.3 years) with HP gastritis, 244 children were treated with several combinations of antibiotics according to the indications of an antibiogram and the efficacy of the treatment duly checked with the non invasive 13C-urea breath test. A second endoscopy with biopsies for culture and antibiogram was proposed before commencing a second treatment. Results: follow-up was not available in 24/244 (10%) children; among the 220 others 140/220 (64%) were cured and 80/220 (36%) remained infected. From these 80 children, HP strains could be isolated and cultured in 55 out of the 58 who underwent a second endoscopy. Resistance to at least one antibiotic was found in 34/55 (62%) HP strains. In 30/55 (54%) the antibiogram remained unchanged whereas in 4/55, the primary resistance was no more detected and, in 21/55 (38%), an acquired resistance against the last antibiotic used was found. Conclusions: 1) following treatment acquired secondary resistance of HP strains is a frequent mechanism that can account for failure of eradication 2) the emerging of a secondary resistance in 38% and the loss of resistance in 8% of HP strains, implies that children can probably be infected with multiple strains bearing different phenotypes.
As in other European countries, Belgian hospitals encounter difficulties in recruiting paediatricians. The task of a paediatrician in the hospital is more diversified than in other specialties. The Belgian Academy of Paediatrics performed a survey in 2007 in order to assess the demographic characteristics and the workload of the hospital paediatricians in Belgium. There is an ongoing feminization among hospital paediatricians. No gender difference could be observed in the time spent in the various types of paediatric medical activity in the hospital. Male paediatricians spend however more than two half-days in clinical activities outside the hospital. Ambulatory care remains important as well in regional as in university paediatric departments. Non-curative tasks form about one third of the working time. The number of days on-call per paediatrician is higher in regional vs university hospitals. The mean size of paediatric regional hospital teams in Flanders is smaller than in French-speaking Belgium (4 vs 8), resulting in a higher on-call activity per paediatrician. In 2007, about 100 vacancies were reported by the heads of the paediatrics department, in three out of four hospitals.
We compared the efficacies of prednisolone and dexamethasone for treatment of children with oesophageal burns due to ingestion of caustic substances. The criteria of efficacy used were a) stricture severity by 3 weeks post-ingestion, b) reduction in burn severity by 3 weeks post-ingestion and c) number of dilatations required over the first year post-ingestion.
The non-invasive 13C-urea breath test (13C-UBT) is validated as a reliable method for the detection and follow-up after treatment of Helicobacter pylori (HP) infection in children. It has been suggested that the increment of the delta value above the baseline (DBV) reflects the severity of the infection. We have simplified this test using a single sample at 20 min after ingestion of a dose of 2 mg/kg body-weight of 13C-urea and by lowering the cut-off of the DBV at 3.5 instead of 5 ‰ and shown that the DBV was influenced not only by the test-meal but also by the galenic presentation of the 13C-urea (J Pediatr Gastroenterol Nutr 1996, 22: 432). Interpretation of 13C-UBT becomes difficult in cases with borderline DBV, more frequent in young children. AIM: to determine whether borderline DBV could be avoided by increasing the amount of the 13C-urea substrate ingested. METHODS: in 11 children with confirmed HP gastritis (median age 5.4 years, range 3.0 to 9.4 years, median weight 20 kg, range 14 to 33 kg) the usual 13C-UBT was performed with the dose of 2 mg/kg of 13C-urea after a test-meal; the test was repeated a few days later with a higher standard dose of 100 mg of 13C-urea. Breath samples were collected at 0 and 20 min and assayed by mass spectrometry. RESULTS: with the 2 mg/kg dose, DBV were comprised between 4.2 and 27.5 ‰ (median 13.0 ‰), whereas with the 100 mg standard dose DBV were comprised between 8.0 and 42.5 ‰ (median 19.8 ‰) and previously borderline tests fell well in the positive range. CONCLUSIONS: 1) larger doses of 13C-urea are recommended in young children in order to increase DBV and improve the discriminating power of the test. 2) since 13C-UBT depends on many parameters and that variations of DBV occur depending on the nature of the test meal, on the galenic presentation and on the dose of 13C-urea, it is unwise to rely on this test to evaluate the load of the HP infection or to assess the severity of the gastritis.
98 Aim: verify whether eradication of the infection modifies the degree of glycemic control in IDDM reported to be more frequently infected by HP. Method: anti-HP IgG were assayed (ELISA Cobas Core Roche) in 296 IDDM, mean age 18 years (5 to 37 y) with a mean duration of diabetes of 10 years (1-17 y). Before treatment a proposed endoscopy was accepted in 86 duly informed HP-seropositive symptomatic IDDM in order to collect histologic and microbiologic data. The efficacy of treatment was checked with the 13C-urea breath test and an electrogastrography recording (EGG) was performed before and two months after treatment. The quality of glycemic control was assessed by HbA1c levels (100% optimal; mean of our global population is 115%). Results: HP-seropositivity was found in 98/296 (33%). In IDDM younger than 18 years (mean age 13 y; mean duration of diabetes 5 y), 56/173 (32%) are HP-seropositive and 35/56 (63%) belong to immigrant families. Current HP gastritis was confirmed by endoscopy in 62/86 (72%) IDDM. Resistant strains (R) were found in 13 cases (5 macrolide-R and 1 imidazole-R in IDDM younger than 18 years vs 2 macrolide-R and 5 imidazole-R in older patients). Chronic or active gastritis was found in all HP-pos patients except in one 27 y old with atrophic gastritis. EGG traces available in 37 HP-pos and 37 HP-neg IDDM show preprandial arrhythmia in 63% HP-pos and 37 % HP-neg patients (p<0.05) not influenced by glycemic levels similar in the two groups (167 sd 81 vs 181 sd 91). Other parameters such as post-prandial arrhythmia's and power ratio are within normal limits in both groups. The overall eradication rate of HP infection is 68%. The degree of control of diabetes, assessed by HbA1c was not modified by HP eradication: HbA1c values were 136% before, 137% two months after and 135% six months after successful treatment and 147% before, 147% two months after and 145% six months after unsuccessful treatment. Conclusions: 1) the prevalence of HP infection is higher in IDDM adolescents than in asymptomatic subjects of the same age (32 % vs 16 %) but 2) ethnic distribution is similar to that of infected children of our series; 3) the significant preprandial arrhythmia observed in infected patients is probably not due to 4) the control of the diabetes which is not influenced by the outcome of the treatment of HP infection; 5) HP serology is unreliable for the monitoring of current HP infection and this is even more prominent in this series of IDDM patients.
Efficacy of treatment of HP gastritis with several associations of antibiotics is largely documented in the literature; however the sensibility of the germ is rarely reported. Like any other microbial agent, HP can develop a pattern of resistance to the drugs used to eradicate it. Since similar antibiotics are widely used in paediatrics for the treatment of common respiratory infections and for HP gastritis, a selection of HP resistant strains is due to occur. AIM: Study of antibiotic resistance of HP strains in our population. METHODS: The fundus and antral gastric biopsies of 1160 children and adolescents were studied for detection of HP infection (urease rapid test, culture and histology). HP gastritis was diagnosed in 259 of them. An antibiogram to amoxicillin, bismuth salts, imidazoles (I) and macrolides (M) is available in the HP strains collected from 243 children. RESULTS: There was no resistance to amoxicillin and bismuth salts. Resistance to macrolides (M) and imidazole (I), listed in the table, was often present at the initial endoscopy. In 1995, failure of HP eradication in one child (in spite of good compliance) was probably due to secondary macrolides-resistance of that HP strain. Table CONCLUSION: As resistance of HP strains is increasing, treatment of HP gastritis in paediatrics ought to be conducted following antibiogram indications.
Gastric mucosal atrophy is a rare finding in children and it is seldom seen even in association with Helicobacter pylori infection (1). Atrophic gastritis predisposing to gastric tumours is observed in 20% of patients with autoimmune type 1 insulin-dependent diabetes mellitus (IDDM) patients with parietal cell antibodies (2). Evidence for type 1 diabetes being an autoimmune process is based on the presence of "diabetes autoantibodies" (3). The role of CD4+CD25+ regulatory T cells in protecting against a variety of autoimmune diseases is admitted (4). Autoimmune gastritis is a disease caused by a CD4+T cell response to the gastric H+/K+-ATPase encoded by Atp4a and Atp4b H+/K+-ATPase. In recent experimental work on mice, it is proposed that prevention of autoimmune gastritis requires extrathymic T cell deletion and suppression by regulatory T cells (5). We report the case of a boy with early IDDM who developed an extensive exfoliative gastritis progressing toward mucosal atrophy with intestinal and malpighian metaplasia. An attenuated form of immune dysregulation, polyendocrinopathy, enteropathy, X-linked syndrome (IPEX) was eventually confirmed by FoxP3 mutation. CASE REPORT The patient is the firstborn of nonidentical twin boys who was diagnosed with IDDM at the age of 22 months. Following ingestion of a "hoax" candy at the age of 8 months, he presented a profusely bleeding gastritis, sloughing of a severely damaged mucosa with exfoliating hemorrhagic pangastritis, ulcerated mucosa, severe gland distortion, and submucosal eosinophilic infiltration contrasting with normal oesophagus and duodenum. Extensive work-up using cultures, polymerase chain reaction, and serology in blood, stools, and gastric biopsies excluded infection by Helicobacter pylori, other bacteria, viruses, parasites, and fungi. Antibodies against parietal cells, intrinsic factor, salivary glands, reticulin, endomysium, extractable nuclear antigen, antinuclear antigen, smooth and striated muscle, colon, skin, β cells, thyroglobulin, glomerular basal membrane, and adrenal glands were negative. Adrenal and thyroid functions as well as gastric hydrochloric acid production were normal. The complement system, leucocytes, lymphocytes, and subclasses CD4, CD8 and acquired immunity against vaccinations were normally expressed. Concentrations of total γ-globulins IgG, IgA, IgM, and IgE were within normal ranges but with low levels of IgG2. Circulating immune complexes were not detected. On gastric biopsies, cytokine dosage showed production of interferon-γ and tumor necrosis factor-α but IL-2, IL-4, IL-5, and IL-10 were negative. Despite treatment with omeprazole and parenteral nutrition, the gastritis progressed towards an atrophic mucosa with eosinophilic infiltration of antral and fundic submucosae, lymphoid nodules, and clusters of intestinal metaplasia extending from fundus to antrum while oesophagus, duodenum, and colon remained normal. Partial endoscopic and histologic remission was observed after 4 months of immunosuppressive treatment with prednisolone. However, a prepyloric ulceration evolved into pyloric stenosis despite successful control of acid secretion with omeprazole. The patient remained under the 10th centile for height and weight and developed vitamin B12 deficiency. Temporary partial remission was obtained after a second course of parenteral nutrition, vitamin B12 supplements, and treatment with ciclosporine and high-pulse doses of prednisolone while the gastric fundus was invaded by an oesophageal-like mucosa with ciliated cells (Fig. 1). Intestinal metaplasia of the gastric mucosa represents a well-known precancerous lesion and, therefore, the efficacy of the immunosuppressive treatment was regularly checked by gastric biopsies to detect early dysplasia. Although the stomach was the only part of the digestive tract involved, a gastrectomy was long postponed because it would complicate the diabetic control of this adolescent. Finally, at the age of 15 years, because of persistent failure to thrive, poor quality of life, and potential precancerous changes of the gastric mucosa, he underwent a total gastrectomy. At the age of 16 years, he presented with steatorrhea with abnormal sweat test and low level of faecal elastase-1 together with echographic images of pancreatic atrophy, compatible with cystic fibrosis. However, the patient was heterozygous for the ΔF508del and complete sequencing of the cystic fibrosis transmembrane regulator gene did not reveal a second mutation. After a long-lasting respiratory infection he developed bronchiectasis together with hypo-γ-globulinemia currently compensated by repeated γ-globulin injections. At the age of 19 years, the diagnosis of immune dysregulation in conjunction with an endocrinopathy was reviewed in the light of new descriptions of atypical cases of IPEX. Molecular analysis confirmed an IPEX syndrome in this patient presenting a mutation of the FoxP3 gene R347H inherited from his mother. The twin brother has developed normally and is in good health (Dr L. Perroni, Laboratory of Human Genetics, Ospedali Galliera, Genova).FIG. 1: Fundic malpighian metaplasia and ciliar cells.DISCUSSION The protracted evolution of the patient is puzzling. First, his IDDM was not classical type 1 autoimmune diabetes, because he had no autoantibodies (6). Second, no extrinsic factors that could provoke the gastritis were found. An autoimmune gastritis was suspected because of the predisposition of insulin-dependent patients to autoimmune diseases and because of the partial clinical and histological response to aggressive immunosuppressive therapy although no parietal cell antibodies were detected. Nonspecific cytotoxic activity was suggested by the increased levels of γ-intestinal trefoil factor and tumor necrosis factor-α in the gastric mucosa. The patient's gastritis followed a special and severe evolution towards atrophy and dysplasia including unusual ciliated dysplasia. Such ciliated dysplasia has not only been described in gastric adenocarcinoma but also in elderly patients from the Pacific basin presenting gastric intestinal metaplasia (7) and in a model of mice lacking the H+/K+-ATPase α-subunit (8). Third, at the time of the gastritis, the serum IgG levels were normal and he expressed adequate responses to the previous vaccinations similar to a report of another IPEX case (9). When the patient developed a hypo-γ-globulinemia, a common variable immunodeficiency was considered the relevant explanation for the long evolution of his immune disease. A syndrome including IDDM, diarrhoea, haemolytic anaemia, eczematous rashes, exaggerated responses to viral diseases and pathologic evidence of autodestruction of endocrine glands was reported as early as 1982, but our patient did not correspond to the description of the clinical characteristics established from data collected in 8 of the 17 male infants of the same family who died early (10). Recently the gene FoxP3 coding for IPEX was identified (11). It maps to Xp11.23-Xq13.3, a region close to the Wiskott-Aldrich syndrome protein gene (12). Its genetic equivalence with the mutation observed in the scurfy mouse was observed. When Scurfin, the FoxP3 gene product, is absent or inactive, T cells proliferate, resulting in early-onset autoimmune disease (13). In patients with IPEX, FoxP3 mutations result in heterogeneous biological abnormalities, leading not necessarily to a lack of differentiation of CD4+ CD25+ high T regulatory cells but rather to a dysfunction in these cells and in effector T cells (14). Several mutations within this gene have been described in patients with IPEX (15) with atypical presentations and prolonged survival in boys ages 7 to 24 years, such as isolated pemphigus (16), psoriasis and alopecia (17), and isolated enteropathies (18). Another type of IPEX syndrome has also been reported without mutation of the FoxP3 gene in the sister of an affected boy: an autosomal locus can, therefore, be suspected (15). The evolution of our patient, now age 22 years, is atypical because of his unusual gastritis, long survival and late onset of pulmonary symptoms, and pancreatic insufficiency as well as sweat test compatible with cystic fibrosis, despite the absence of the usual cystic fibrosis transmembrane regulator mutations. Conclusions This unusual presentation with delayed diagnosis of IPEX offers more questions than answers, as do many other cases of the IPEX syndrome with clinical, genetic, and biological heterogeneities. The mechanism of the gastropathy leading to severe intestinal and malpighian metaplasia is another unusual poorly understood feature.
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