Risk of Gastric Cancer in Children with Helicobacter pylori Infection Children;endoscopy;gastric cancer;H. pylori;metaplasia;prevention; Background: Helicobacter pylori (H. pylori) is the most common chronic infectious agent in the stomach. Most importantly, it may lead to atrophy, metaplasia and cancer. The aim of this study was to investigate the incidence of H. pylori infection and to detect early mucosal changes that may lead to malignant degeneration in children. Materials and Methods: Children who underwent upper gastrointestinal endoscopy were included. Familial history of gastric cancer was noted. Endoscopic examinations were performed by a single pediatric gastroenterologist. A minimum of three biopsy samples were collected during endoscopy. The patients were accepted as H. pylori infected if results of biopsies and rapid urease test were both positive. Biopsies were evaluated for the presence and degree of chronic inflammation, the activity and severity of gastritis, glandular atrophy and intestinal metaplasia. Results: A total of 750 children (388 boys, 362 girls) were evaluated in our study, with a mean age of 10.1 years. A total of 390 patients (52%) were found to be infected with H. pylori. Among the H. pylori infected patients, 289 (74%) were diagnosed to have chronic superficial gastritis, 24 (6.2%) had gastric atrophy. Most strikingly, intestinal metaplasia was observed in 11 children, all were in the H. pylori positive group. There was no difference in the mean of age, gender and socioeconomic class between H. pylori infected and non-infected groups. The frequency of gastric cancer in family members (4 in number) was higher in patients with H. pylori infection. No gastric cancer case was reported from the parents of non-infected children. The worst biopsy parameters (atropy and metaplasia) were improved after H. pylori eradication on control endoscopy. Conclusions: The current study shows a higher prevalence of familial history of gastric cancer in H. pylori infected children. Intestinal metaplasia was also higher in the infected children. Eradication of H. pylori infection for this risk group may prevent subsequent development of gastric cancer.

Chemotherapy-induced immunosuppression can lead to hepatitis B virus (HBV) reactivation in cancer patients. Both HBV carriers and individuals with serological signs of previously resolved HBV exposure are under the risk of severe hepatitis and liver failure during and after chemotherapy. The objective of this largest retrospective study was to analyze the consequences of HBV status in children receiving chemotherapy. A total of 479 patients (273 boys and 206 girls) aged 1–211 months diagnosed with acute hematologic malignancies and solid tumors were included in the study. Serological markers for HBV before and after chemotherapy and clinical data of the patients were evaluated retrospectively. Two hundred thirty-four of the participants were found to have protective antibody titers to HBV at admission. Five children were carrying HBV before chemotherapy. They received antiviral therapy during treatment and no reactivation was detected. Antibody against hepatitis B surface antigen (antiHBs) remained positive in 194 patients after chemotherapy. However, 17.09% (40/234) lost antiHBs positivity. In this group, three patients (1.28%) who initially had positive antiHBs and antihepatitis B core antibody experienced HBV reactivation and lost their protective antiHBs at the end of the therapy. Median antiHBs titer significantly decreased after chemotherapy (213.14 [range: 24–888] vs. 180.85 [range: 0–850]) (p = 0.0094). The current relatively large trial demonstrated that protective antibody titers remarkably altered after chemotherapy, and at least 17% of the pediatric oncology cases lost antiHBs positivity. Therefore, vaccine prevention and close monitoring of serology should be considered during chemotherapy.

Background. Systemic oxidative stress may cause detrimental consequences for the liver, leading to hepatic fibrogenesis. Objectives. To investigate histopathological changes in liver tissues due to the increased systemic oxidative stress associated with rat extracorporeal shock wave lithotripsy (SWL) model and to document the consequences of N-acetylcysteine (NAC) administration. Material and methods. In this experimental SWL model, 18 Wistar albino rats were randomly assigned into 3 groups. The control group (group I) had no intervention. Group II underwent SWL treatment with intraperitonea I saline injection. Group III also had SWL with intra peritoneal NAC and was divided into short-term (group III-14 days) and long-term (group III-28 days) subgroup. Hepatectomy was performed for histopathological examinations. Histopathological alterations were evaluated with light microscopy. Immunohistological staining for p53 and myeloperoxidase was also performed. Results. Blood samples revealed a significant increase in plasma oxidative stress index (OSI) after plasma total antioxidant status (TAS) and total oxidant status (TOS) had been measured. It was shown that this increased systemic oxidative stress adversely affected liver tissues. Predominantly, sinusoidal dilatation was remarkably observed in rats with significantly high 051 values (p = 0.043). Similarly, periportal necrosis significantly increased in rats with high OSI values (p = 0.033). p53 positivity was also remarkable in rats with systemic oxidative stress (p = 0.049). N-acetylcysteine administration provided a significant decrease in OSI. N-acetylcysteine also improved all these alterations, including p53 staining. Particularly, sinusoidal dilatation was significantly protected in the long-term NAC group (group III-28 days). Conclusions. We demonstrated that SWL-induced systemic oxidative stress causes histological alterations in liver tissues. Increased p53 and myeloperoxidase staining as markers of oxidative damage were also detected. N-acetylcysteine may protect from these histological and ultra-structural alterations related to oxidative stress.