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To investigate the clinical characteristics, diagnosis, and treatment of asparaginase-associated pancreatitis (AAP) in children to assess the risk factors of AAP and improve its clinical prognosis. We performed a retrospective analysis of 24 patients with AAP who suffered from acute lymphoblastic leukemia (ALL) and received asparaginase chemotherapy, and who were admitted to the Children's Hospital of Zhejiang University School of Medicine from January 2009 to January 2019. We analyzed the general situation, drug application, clinical manifestations, laboratory tests, imaging findings, treatment, and prognosis. In 796 patients with ALL who received asparaginase chemotherapy, the incidence of AAP was 3% (24/796). Among these patients, 11 (45.8%) developed AAP during the first application of asparaginase during the induction of remission, six cases developed AAP during the second application of asparaginase, and seven cases developed AAP during the third and above application. The median time from the diagnosis of AAP in 24 patients to the last asparaginase treatment was 8 days (1–18 days), among whom, the main clinical symptoms were abdominal pain, vomiting, nausea, bloating, and fever, which accounted for 95.8%, 37.5%, 33.3%, 20.8%, 4.0%, and 42.7%, respectively. Additionally, seven patients had peritoneal effusion. At initial diagnosis, 62.5% of the patients (15/24) had an increase in blood amylase levels to more than three times the upper limit of normal. The abdominal ultrasound results of 91.7% (22/24) of the patients were consistent with the imaging changes observed in pancreatitis. All 24 patients immediately stopped asparaginase treatment and received symptomatic supportive treatment, including fluid resuscitation, fasting, nutritional support, antibiotics, pancreatin inhibitors, and treatment of complications, as needed. Twenty-three patients were relieved after treatment, and one died. Following the resolution of symptoms in 14 patients with AAP, asparaginase chemotherapy was reintroduced, and 3 patients relapsed with AAP, all of which were mild. Symptoms were relieved 72 h after stopping asparagine chemotherapy. According to the data from this single-center study, the incidence of AAP in patients with ALL was 3%, most of which occurred during the first or second exposure to asparaginase. Abdominal pain was the most common clinical manifestation. The diagnosis of AAP should be based on clinical manifestations, laboratory tests, and imaging findings. The prognosis of AAP is good, and whether asparaginase treatment can be reintroduced requires an evaluation of the benefits of asparaginase treatment and the risk of recurrence of pancreatitis. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori (H. pylori) infection is the main cause of chronic gastritis and duodenal ulcer in children. Little is known about the effect of H. pylori on gastric microbiota in children with duodenal ulcer. This study is aimed at the characteristics of gastric microbiota in children with duodenal ulcer on H. pylori infection. Methods: We studied 23 children diagnosed with duodenal ulcer by gastric endoscopy because of the gastrointestinal symptoms, 15 children were diagnosed with H. pylori infection, while 8 children were without H. pylori infection. Endoscopic mucosal biopsy samples were obtained for DNA extraction. Microbiomes were analyzed by 16S rRNA profiling and microbial functions were predicted using the software Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt). Results: Bacterial richness and diversity of gastric microbiota in duodenal ulcer with H. pylori -positive were lower than those negative. The gastric microbiota in H. pylori -positive group significantly reduced proportions of six phyla and fifteen genera; only Helicobacter taxa were more abundant in H. pylori- positive group. Co-expression network analysis showed a more complex network of interactions in the H. pylori- positive group than that in the H. pylori- negative group. For the predicted functions, lower abundance in the pathways of carbohydrate metabolism, signal transduction, amino acid metabolism, and lipid metabolism were found in H. pylori- positive group than the H. pylori- negative group. H. pylori colonization reduces a microbial community with genotoxic potential in the gastric mucosa of children with duodenal ulcer. Conclusions: The presence of H. pylori significantly influences gastric microbiota and results in a lower abundance of multiple taxonomic levels in children with duodenal ulcer. Children with duodenal ulcer exhibit a dysbiotic microbial community with genotoxic potential, which is distinct from that of children with H. pylori infection. Clinical Trial Registration: [http://www.chictr.org.cn], identifier [ChiCTR1800015190]. [ABSTRACT FROM AUTHOR]

Background: Helicobacter pylori infection is the main cause of chronic gastritis in children. Little is known about the effect of Helicobacter pylori on microbiota and immunity. This study was aimed at characterizing stomach microbiota and immune-regulatory properties of children with Helicobacter pylori colonization. Methods: We studied 122 children who had undergone gastric endoscopy due to gastrointestinal symptoms, 57 were diagnosed with Helicobacter pylori infection. Endoscopic mucosal biopsy samples were obtained for DNA and RNA extraction. Microbiomes were analyzed by 16S rRNA profiling, with the differentially expressed genes analyzed using RNA sequencing. The RNA-sequencing results of selected genes were validated by qRT-PCR. Results: Bacterial diversity of Helicobacter pylori -positive gastric specimens were lower than those of negative, and both groups were clearly separated according to beta diversity. Helicobacter pylori -positive group significantly reduced proportions of six phyla and eight genera; only Helicobacter taxa were more abundant in Helicobacter pylori- negative group. Gastric tissues RNA sequencing showed increased expression of multiple immune response genes in Helicobacter pylori -infection. Helicobacter pylori -infected children with restructured gastric microbiota had higher levels of FOXP3, IL-10, TGF-β1 and IL-17A expressions, which were consistent with increased CD4+T cell and macrophagocyte, compared with non-infected children. Conclusions: Presence of Helicobacter pylori significantly influences gastric microbiota and results in lower abundance of multiple taxonomic levels in children. Meanwhile, it affects gastric immune environment and promotes the occurrence of gastritis. Clinical Trial Registration: [ http://www.chictr.org.cn ], identifier [ChiCTR1800015190] [ABSTRACT FROM AUTHOR]

Abstract Background Bile reflux is one of the primary factors involved in the pathogenesis of gastric mucosal lesions in patients with chronic gastritis; however, little is known about the exact histological features of bile reflux and its contributions to gastric mucosal lesions in this disease, especially in children with primary bile reflux gastritis (BRG). The aim of this study was to investigate the classic histological changes of the gastric mucosa in children with primary BRG. Methods The Bilitec 2000 was used for 24 h monitoring of gastric bile in 59 children with upper gastrointestinal symptoms. The histological characteristics of the gastric mucosa were examined and scored. Results Thirteen of the 59 patients had a helicobacter pylori infection and were excluded; therefore, 46 cases were included in this study. The positive rate of pathological duodenogastric reflux was significantly higher in patients with foveolar hyperplasia than those without foveolar hyperplasia; however, the rate was significantly lower in patients with vascular congestion than those without vascular congestion. The longest reflux time and the total percentage time of bile reflux were significantly lower in patients with vascular congestion than those without vascular congestion. A total of 9 types of histological changes were analyzed using a binary logistic regression. Foveolar hyperplasia and vascular congestion in the superficial layer became significant variables in the last step of the stepwise regression. Conclusions Foveolar hyperplasia was associated with the severity of bile reflux, suggesting that it is a histological feature of primary BRG in children, while vascular congestion may be a protective factor.

Background and Aims: Helicobacter pylori (HP) culture for diagnosing HP infection is time‐consuming and technologically complex. This study evaluated the clinical significance of gastric mucosal gene chip technology in the rapid diagnosis of HP infection and detection of drug resistance in children. Methods: Patients (between the age of 2.5 and 16.0 years old) manifesting gastrointestinal symptoms were enrolled in this study. HP culture of gastric mucosa and drug sensitivity test were performed. A gene chip of gastric mucosa was used to detect the presence of HP infection, some single nucleotide polymorphisms in HP drug resistance genes, or associated gene mutation. DNA sequencing was investigated and compared with the gene chip test results. Results: Out of 267 cases, HP culture was positive in 169 cases and negative in 98 cases. HP detection by the gene chip method was positive in 208 cases and negative in 59 cases. The sensitivity, specificity, and accuracy of the gene chip technology for diagnosing HP infection were 96.1, 85.0, and 93.6%, respectively. HP resistance gene locus using the gene chip showed the main mutation locus of clarithromycin to be 2143A/G, levofloxacin at locus GyrA 91 and GyrA 87, and amoxicillin at PBP1 556ser. Concordance rates between gene chip and DNA sequencing for VacA‐S/M, 16S rRNA, 23S rRNA, and GyrA were greater than 95%, and that of PBP1 was greater than 82%. Conclusion: Gastric mucosal gene chip technology can be used for rapid diagnosis and drug resistance detection of HP infection in children. [ABSTRACT FROM AUTHOR]

Background and Aim: Upper gastrointestinal bleeding is a rare and potentially life‐threatening condition in children. Herein, clinical features and risk factors in children with upper gastrointestinal bleeding were analyzed, and a clinical scoring system was constructed to assess severity. Methods: This retrospective cohort study involved 224 children hospitalized with upper gastrointestinal bleeding between January 2012 and April 2018. Demographic data, clinical information, and laboratory test results on admission were statistically examined. Results: Out of 224 upper gastrointestinal bleeding cases, 76 were diagnosed as severe and 148 as mild cases according to the rate of blood loss and severity. Severe group was significantly different from mild group in 23 items including age, number of patients aged more than 7 years, and so forth (P < 0.01 or P < 0.05). Positive detection rate of bleeding etiology was gradually decreased (P < 0.01) in relation to delay in timing of endoscopy. Analysis of logistic regression evinced five independent risk factors for severe cases to be associated with poor consciousness, hemoglobin < 80 g/L, hemoglobin drop of > 20 g/L, hematochezia, and anemic appearance (P < 0.01 or P < 0.05). Using these five parameters, a number of scoring models were tested. The most predictive resulted in a scoring system constructed with a total of 16 and a cutoff for intervention of 8. Conclusions: Amalgamation of risk factors with the scoring system plays an important role in assessing upper gastrointestinal bleeding severity in children. [ABSTRACT FROM AUTHOR]

Background and aim: Systemic inflammatory response syndrome (SIRS) has to do with how the body reacts to injury. Herein, we analyzed the clinical features of acute pancreatitis (AP) in children with SIRS complication and investigated the role of SIRS score combined with C-reactive protein (CRP) level in assessing AP severity in children. Methods: This retrospective cohort study involved 111 children hospitalized with AP at the Children's Hospital of Zhejiang University School of Medicine between January 2012 and August 2017. Presence of SIRS, demographic data, clinical information and laboratory test results on admission were statistically examined. Results: Out of the 111 AP cases, 45 were diagnosed with SIRS. Differences in CRP, interleukin-6 (IL-6), age, temperature, heart rate (HR), white blood cell (WBC), neutrophil count (NC), body mass index (BMI), duration of onset of disease symptoms as well as cases requiring intensive care unit (ICU) treatment were significantly higher in patients with SIRS than those without SIRS (p < .01 or p < .05). Logistic regression analyses evinced two independent risk factors for SIRS to be coexisted diseases (odds ratio (OR) = 4.871, p = .02) and fever (OR = 3.56, p = .007). SIRS was an independent predictor for AP severity (OR = 10.820, p = .005). The optimal cut-off value of CRP was 27.5 mg/L for severe AP classification according to receiver operating characteristic (ROC) (area under curve was 0.733). Conclusion: Amalgamation of SIRS criterion with CRP level potentially plays an important role in assessing AP severity in children. [ABSTRACT FROM AUTHOR]

Abstract: Background: The decreasing eradication rate of Helicobacter pylori is mainly because of the progressive increase in its resistance to antibiotics. Studies on antimicrobial susceptibility of H. pylori in children are limited. This study aimed to investigate the resistance rates and patterns of H. pylori strains isolated from children. Materials and Methods: Gastric mucosa biopsy samples obtained from children who had undergone upper gastrointestinal endoscopy were cultured for H. pylori, and susceptibility to six antibiotics (clarithromycin, amoxicillin, gentamicin, furazolidone, metronidazole, and levofloxacin) was tested from 2012‐2014. Results: A total of 545 H. pylori strains were isolated from 1390 children recruited. The total resistance rates of H. pylori to clarithromycin, metronidazole, and levofloxacin were 20.6%, 68.8%, and 9.0%, respectively. No resistance to amoxicillin, gentamicin, and furazolidone was detected. 56.1% strains were single resistance, 19.6% were resistant to more than one antibiotic, 16.7% for double resistance, and 2.9% for triple resistance in 413 strains against any antibiotic. And the H. pylori resistance rate increased significantly from 2012‐2014. There was no significant difference in the resistance rates to clarithromycin, metronidazole, and levofloxacin between different gender, age groups, and patients with peptic ulcer diseases or nonulcer diseases. Conclusions: Antibiotic resistance was indicated in H. pylori strains isolated from children in Hangzhou, and it increased significantly during the 3 years. Our data strongly support current guidelines, which recommend antibiotic susceptibility tests prior to eradication therapy. [ABSTRACT FROM AUTHOR]

Nodular gastritis (NG) represents a frequently observed clinical presentation of Helicobacter pylori (H. pylori) infection in pediatric patients. This investigation aimed to explore the microbiota and histological features of the gastric mucosa in children with H. pylori colonized NG. The current investigation examined a sample of 120 children who underwent gastroscopy due to symptoms of gastrointestinal distress, which showed that 64 were patients with H. pylori infection. Endoscopic procedures were conducted to acquire mucosal biopsies for the purpose of DNA extraction and histopathological analysis. The 16S rRNA profiling was utilized to examine the gastric mucosal microbiota. In conjunction with endoscopic evaluation, 26 of 64 patients were diagnosed with NG. The NG group had significantly higher inflammation scores and activity scores on histological assessment than the non-NG group. The NG group exhibited a significant reduction in the richness levels of the five genera. In terms of the predicted functions, the pathways of synthesis and degradation of ketone bodies and phagosome in the NG group were less abundant compared with the non-NG group, while the Wnt signaling pathway was significantly enriched. NG does not increase a microbial community that possesses genotoxic potential within the gastric mucosa. In conclusion, NG group exhibited significant severe inflammation and reduced abundance levels of several bacterial genera compared to the non-NG group. However, individuals with NG did not have a dysregulated microbial community with genotoxic potential. • Nodular gastritis (NG) group had significantly higher inflammation scores and activity scores on histological assessment than the non-NG group. • There was a degree of difference between the two groups in terms of population abundance levels, co-network analysis and functional prediction. • NG does not increase a microbial community that possesses genotoxic potential within the gastric mucosa, suggesting that children with nodular gastritis do not have an increased risk of mucosal carcinogenesis. [ABSTRACT FROM AUTHOR]