Aim: This study was carried out to determine the prevalence and predictors of Helicobacter pylori (H. pylori) infection among symptomatic children and the effect on growth. Methods: A cross-sectional study was conducted in the Outpatient Clinics of the Gastroenterology Unit of the Pediatric Hospital, Cairo University. A total of 630 children complaining of any symptoms or signs suspicious of H. pylori infection were enrolled. Weight and height were measured for each child, and the standard deviation scores (Z-scores) for weightfor-age (WAZ), weight-for-height (WHZ), and height-forage (HAZ) were calculated. H. pylori was diagnosed using a stool antigen test. Results: The overall prevalence of infection was 64.6%. Socio-demographic variables significantly associated with H. pylori were residence in Upper Egypt (P = 0.013) and rural areas (P = 0.004), illiteracy of mothers (P = 0.017), household crowding index ≥ 3 (P = 0.011), absence of pure water supply (P = 0.005), and eating from street vendors (P < 0.001). Values of WAZ [median, interquartile range (IQR) in infected = − 1.3(− 2.7 to − 0.4) and non-infected = − 0.7(− 2.1 to − 0.1), P < 0.001], HAZ (P = 0.036), and WHZ (P = 0.005) were significantly lower in children infected with H. pylori. After performing a backward logistic regression analysis, eating from street vendors (OR = 1.879, 95% CI 1.346-2.625, P < 0.001), absence of pure water supply (OR = 1.725, 95% CI 1.162-2.561, P = 0.007), and overcrowding (OR = 1.547, 95% CI 1.100-2.177, P = 0.012) remained the significant predictors of H. pylori infection. Conclusion: A high prevalence of H. pylori infection among symptomatic children was detected. The extra-digestive effects of H. pylori were revealed in the form of affection of growth parameters and reduced levels of serum hemoglobin, iron, and ferritin.

Treatment with all-oral DAAs (SOF/LED) for 12 weeks was well tolerated in Egyptian children and adolescents infected with genotype 4 HCV, with 100% SVR12 and negligible side effects.

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Biallelic mutations in the SLC30A10 gene cause an inborn error of Mn metabolism characterized by hypermanganesemia, polycythemia, early-onset dystonia, and liver cirrhosis (HMDPC). To date, only 14 families from various ethnic groups have been reported. Here, we describe 10 patients from 7 unrelated Egyptian families with HMDPC. Markedly elevated blood Mn levels, the characteristic basal ganglia hyperintensity on T1-weighted images, and variable degrees of extrapyramidal manifestations with or without liver disease were cardinal features in all patients. Eight patients presented with striking early diseased onset (≤2 years). Unexpectedly, early hepatic involvement before the neurological regression was noted in 3 patients. Mutational analysis of SLC30A10 gene revealed 6 novel homozygous mutations (c.77T > C (p.Leu26Pro), c.90C > G (p.Tyr30*), c.119A > C (p.Asp40Ala), c.122_124delCCT (p.Ser41del), c.780_782delCAT (p.Iso260del) and c.957 + 1G > C). Treatment using 2,3 dimercaptosuccinic acid as a manganese chelating agent showed satisfactory results with improvement of biochemical markers, hepatic manifestations and relative amelioration of the neurological symptoms. Our findings present a large cohort of patients with HMDPC from same ethnic group. The majority of our patients showed severe and early presentation with clear phenotypic variability among sibship. Moreover, we extend the phenotypic and mutational spectrum and emphasize the importance of early diagnosis and treatment of this potentially fatal disorder.

Cure rate was double in the MMC group. MMC application significantly improved symptoms and reduced both the number and frequency of dilatations to alleviate dysphagia in patients with refractory caustic esophageal strictures and hence reduced the cost of treatment.

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BACKGROUND The caustic ingestion continues to be a major problem worldwide especially in developing countries. The long-term complications include stricture and increased life time risk of oesophageal carcinoma. Patients suffered from corrosive induced oesophageal strictures have more than a 1000-fold risk of developing carcinoma of the oesophagus. AIM To determine the possibility of oesophageal mucosal dysplasia after prolonged dilatation in post corrosive stricture. METHODS This observational study was conducted at the Paediatric Endoscopy Unit in Cairo University Children’s Hospital. It included children of both sexes older than 2 years of age who had an established diagnosis of post-corrosive oesophageal stricture and repeated endoscopic dilatation sessions for more than 6 mo. All patients were biopsied at the stricture site after 6 mo of endoscopic dilatation. A histopathological examination of an oesophageal mucosal biopsy was performed for the detection of chronic oesophagitis, inflammatory cellular infiltration and dysplasia. RESULTS The mean age of the enrolled children was 5.9 ± 2.6 years; 90% of the patients had ingested an alkaline corrosive substance (potash). The total number of endoscopic dilatation sessions were ranging from 16 to 100 with mean number of sessions was 37.2 ± 14.9. Histopathological examination of the specimens showed that 85% of patients had evidence of chronic oesophagitis (group A) in the form of basal cell hyperplasia, hyperkeratosis and subepithelial fibrosis. Thirteen percent of the patients had evidence of reactive atypia (group B) in the form of severe neutrophilic intraepithelial inflammatory cellular infiltration, and 2 patients (2%) had mild squamous dysplasia (group C); we rebiopsied these two patients 6 mo after the initial pathological assessment, guided by chromoendoscopy by Lugol's iodine. CONCLUSION The histopathology of oesophageal mucosal biopsies in post-corrosive patients demonstrates evidence of chronic oesophagitis, intraepithelial inflammatory cellular infiltration and dysplasia. Dysplasia is one of the complications of post-corrosive oesophageal stricture.

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