Epidemiology and pathophysiology of <Emphasis Type="Italic">Helicobacter pylori</Emphasis> infection in children

Helicobacter pylori is one of the commonest bacterial pathogens in human. The organism is associated with development of peptic ulcer diseases, lymphoproliferative disorders and gastric cancer. Residence in a developing country, poor socioeconomic conditions and genetic predisposition are regarded as risk factors. Prevalence of infection is higher in developing countries and re-infection is higher among under five children. It is transmitted mainly through feco-oral route in developing countries and gastro-oral route in developed nations. Transmission of close-contact infection depends on the degree of mixing and age-distribution between susceptible and infected individuals. Host and bacterial factors with interaction of environment contribute pathogenicity. H. pylori cytotoxin-associated geneA (cagA), vacuolating toxinA (vacA) and adherence factors to gastric epithelium have been linked to enhanced pathogenicity of the bacterium. Host genetic polymorphism of cytokines, related legends, receptors and enzymes influence H. pylori infection.     

<Emphasis Type="Italic">Helicobacter pylori</Emphasis> and micronutrients

Helicobacter pylori (HP) infection causes morbidity in several systems, especially in the gastrointestinal tract. The prevalence of disease is inversely related to social-economic and developmental status. It is more common in the developing than in developed countries. In the countries where social-economic status is low, not only HP infection, but also malnutrition and growth failure have a higher prevalence. According to these data, the relationship of nutrition and HP infection is still a question. Does HP infection affect nutritional status? On the contrary, does nutritional status affect HP infection? If so, how? This review was prepared after searching thoroughly almost all of the publications about relationship between HP infections and micronutrients, especially publications pertaining to childhood, from 1990 to 2009 in PubMed. Some valuable adult and experimental publications were also reviewed. These studies related H.pylori to iron, vitamin B₁₂, vitamin C, vitamin A, vitamin E, folate, and selenium. Published studies reveal some evidence that HP has a negative effect on iron, vitamin B₁₂ and vitamin C metabolism, but its influence on others is not clear.     

Lack of evidence for <Emphasis Type="Italic">Helicobacter pylori</Emphasis> to prevent children growth efficiently

We have read with great interest an article by Kocaoglu et al published in May issue of the World Journal of Pediatrics.[1] A total of 243 children aged between 8-18 years were examined based on growth determinants and existence of Helicobacter pylori (H.pylori) colonization in Turkey.The conclusion of this research is that H.pylori colonization affected children growth;and the longer duration of infection,the worse effect on growth.     

Acquired angioedema and<Emphasis Type="Italic"> Helicobacter pylori</Emphasis> infection in a child

We describe a 10-year-old boy with acquired Helicobacter pylori infection and simultaneous angioedema which is a rare but life-threatening condition. Our patient was hospitalised with generalised angioedema and severe circulatory shock due to extreme loss of fluids and proteins into interstitial tissues (weight gain 10 kg within 2 days, extreme haemoconcentration – haemoglobin 206 g/l, haematocrit 0.570, leucocytosis 18,300 /µl, high lactate 13.8 mmol/l) and simultaneous failure of the complement system (C3 <0.16 g/l, C4 <0.13 g/l, CH50 45 U/ml, i.e. 50% of normal value, C1 inhibitor 0.21 g/l at the lower limit). All possible known causes of angioedema were excluded (infection, allergy, auto-immune disease, NSAIDs, lymphoproliferative disease) except for the simultaneous H. pylori infection which was proven serologically and histologically. Eradication therapy led to a complete remission of the H. pylori infection. An absence of angioedema and the restoration of the complement system was later observed. To the best of our knowledge, no similar case report of a child has yet been published. Conclusion: Helicobacter pylori infection should be considered in the development of angioedema in childhood.     

<Emphasis Type="Italic">Helicobacter pylori</Emphasis> culture and antimicrobial resistance in Iran

Objective Helicobacter pylori is considered as an important etiologic factor in pathogenesis of peptic ulcer disease, chronic gastritis and gastric cancer. To eradicate this micro-organism, numerous regimens containing various antimicrobial agents have been suggested. However, H pylori antimicrobial resistance is a leading factor to treatment failure and recurrence of the disease. The aim of the study was to evaluate the prevalence of H pylori resistance to metronidazole, clarithromycin, tetracycline, amoxicillin, erythromycin and furazolidone in authors pediatric patients. Methods Antral biopsy of all pediatric patients with negative history of receiving anti-H pylori regimen and endoscopic findings of nodular gastritis or peptic ulcer without previous history of NSAID consumption, burning and trauma were performed for H pylori histology, urease test and culture. All positive cultures were tested for antimicrobial susceptibility. Results Twenty four patients (14 male and 10 female) between 3.5 and 14 years of age were culture positive. 54.16% of the isolates were resistant to metronidazole, 8.33% to amoxicillin, 4.16% to erythromycin and 4.16% to clarithromycin. None of authors patients were resistant to tetracycline and furazolidone. Conclusion H. pylori antimicrobial resistance could be a major contributor to failure of H pylori eradication. Continuous prospective surveillance of H. Pylori is essential. Moreover, culture and antimicrobial susceptibility test is recommended for resistant cases after the first failure to therapy.     

Refractory iron-deficiency anaemia due to silent<Emphasis Type="Italic"> Helicobacter pylori</Emphasis> gastritis in children

We describe the cases of three children with chronic active Helicobacter pylori gastritis and iron-deficiency anaemia without evidence of oesophagogastrointestinal bleeding. In all cases, long-standing iron supplementation became effective only after eradication of Helicobacter pylori. CONCLUSION: Iron-deficiency anaemia may be due to clinically inapparent H. pylori gastritis.     

<Emphasis Type="Italic">NPHS2</Emphasis> mutations

Objective  To uncover the frequency and the spectrum of NPHS2 mutations in Egyptian children with non familial steroid-resistant nephrotic syndrome (SRNS). Methods  Sixteen patients were screened by PCR-single-strand conformation polymorphism analysis of NPHS2 gene followed by direct sequencing. Results   NPHS2 mutations were evident in four patients (25%) who were bearing four novel mutations including two frame shift mutations (R238fs and P45fs) and two missense mutations (I136L and F216Y). There were no phenotypic or histological characteristics of patients bearing NPHS2 mutations, apart from the earlier onset of the disease, compared to those who were not bearing mutations. Conclusion   NPHS2 mutations are prevalent in Egyptian children with non-familial SRNS and this may in part explain the less favorable prognosis reported in these patients.