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Objectives: The aims of the study was to expand the pediatric experience on hepatitis-B virus (HBV) reactivation, a known complication in patients with hematologic malignancies or on immunosuppression., Methods: Retrospective appraisal of HBV therapy/prophylaxis in immunocompromised children, studied from April 2006 to March 2020., Results: Eighteen HBV-positive patients, 5 girls, median age 11.1 (4.1--17.9) years were included. Seventeen of 18 were immunosuppressed at HBV-infection diagnosis. Seventeen were at high risk of reactivation, 1 at moderate risk. Five of 18 had acute hepatitis B as first infection or reactivation, 6 had HBeAg-positive infection, 1 an HBeAg-negative infection and 6 HBsAg-negative infection. Median follow-up was 2.7 (0.7--12.5) years. No HBV-related mortality was observed. Prophylaxis had to be repeated in 1. Lamivudine was used in 6/12 viremic patients and HBV-DNA negativization obtained in 2/6 (33%). Tenofovir-DF was used in 2/12 and entecavir in 4/12: 100% attained HBV-DNA negativization. Therapy had to be switched from tenofovir-DF to entecavir in 1 patient because of renal impairment. Virological breakthroughs were observed in 1 lamivudine-treated patient, leading to a hepatitis flare; 1 patient on entecavir had a hepatitis flare at immunoreconstitution. Mortality was 33% in the HBsAg-positive group. Seven prophylactic treatments were administered to 6 patients with HBsAg-negative infection: tenofovir-DF in 2 HBV-DNA-positive, lamivudine in 5 HBV-DNA-negative, without reverse HBsAg seroconversion, morbidity or mortality., Conclusions: There is a residual risk of acute hepatitis B in immunocompromised children, mortality rate was substantial, potentially related to the delays in commencing chemotherapy caused by liver dysfunction. Tenofovir-DF or entecavir are the drugs of choice for HBV treatment in immunocompromised children., (Copyright © 2020 by European Society for Pediatric Gastroenterology, Hepatology, and Nutrition and North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition.)

Serum pepsinogen I (PG I) levels were determined by radioimmunoassay in 23 children with peptic ulcer disease (PUD) before and after treatment with ranitidine and in 44 children who were being investigated for recurrent abdominal pain. Upper gastrointestinal endoscopy was performed in all. No lesions were detected in controls, while 18 patients showed a duodenal ulcer, 4 had an antral ulcer, and 1 had both. An 8-week course of ranitidine healed PUD in 93.5% of them, while long-term (1-5 years) endoscopic follow-up showed a 41.9% ulcer relapse rate after stopping treatment. Gastric acid secretion after pentagastrin stimulation [maximal acid output (MAO)] was tested in all controls and in 22 PUD patients: While controls had normal MAO values for their age, 65% of patients had a secretion above the normal range. No significant correlation was detected between serum PG I and MAO either in controls or in patients. Mean serum PG I concentrations were not significantly higher in the whole patient group than in controls, but PUD patients who relapsed after discontinuing ranitidine treatment had shown on admission significantly higher PG I levels when compared both with those who did not relapse and with controls. All patients who relapsed, but only 42.8% of those who did not, had a serum PG I concentration above the normal upper limit for a pediatric population (56.7 ng/ml). None of the PUD patients who had serum PG I levels under this limit relapsed. Our results suggest that pretreatment serum PG I levels in children with PUD may predict fairly accurately which will not relapse after attaining ulcer healing by a short-term ranitidine course.