Background: Helicobacter pylori infection is known to alter growth-related hormones and cause growth faltering in young children. It is still unknown if maternal H. pylori infection has an impact on the levels of cord blood growth-related hormones and can predict intrauterine growth restriction and poor physical and neurodevelopmental outcomes in children. This study aimed to examine the associations between maternal H. pylori infection and pregnancy-related adverse events, fetal growth and early childhood development. Methods: The prospective cohort study recruited singleton pregnant women without major medical illnesses from January 2014 to January 2015. Seropositivity for H. pylori was defined by >12 U/ml of anti- H. pylori IgG in the maternal serum. Demographic data and pregnancy-related medical issues of the cohort were documented. Cord blood levels of insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), insulin, and ghrelin were determined using ELISA test. The growth of eligible neonates was monitored annually for up to 3 years, and cognitive development was assessed using the comprehensive developmental inventory for infants and toddlers (CDIIT) test 3 years after birth. Results: Of the 106 enrolled women, 25 (23.6%) were H. pylori -seropositive. Maternal H. pylori seropositivity was correlated with a higher risk of developing gestational hypertension (GH) (12% vs. 1.2%, p =0.04) and lower cord blood levels of IGF-1 (<35 ng/ml, 70.0% vs. 40.7%, p =0.02) and IGFBP-3 (<1120 ng/ml, 100.0% vs. 76.3%, p =0.02) compared with the seronegative women. No significant impact on birth weight, childhood growth and cognitive development was found to correlate with maternal H. pylori seropositivity during pregnancy. Conclusions: Maternal H. pylori infection during pregnancy was more likely to develop GH, but not correlated with fetal and childhood growth and development. In addition to close monitoring of hypertension, H. pylori eradication can be considered for such H. pylori -infected mothers.

This study aimed to elucidate the characteristics and the risk factors for asparaginase-associated pancreatitis (AAP) in pediatric acute lymphoblastic leukemia (ALL) under the Taiwan Pediatric Oncology Group (TPOG)-ALL regimen.

Background: This study aimed to elucidate the characteristics and the risk factors for Asparaginase-associated pancreatitis (AAP) in children with acute lymphoblastic leukemia (ALL) under Taiwan Pediatric Oncology Group (TPOG)-ALL regimen. Methods: The retrospective hospital-based cohort study was conducted by reviewing the chart records of total 191 pediatric ALL patients aged 1-18 years treated with TPOG-ALL (2002 and 2013) protocols at the National Cheng Kung University Hospital, Tainan, Taiwan, from 2002 to 2019. The disease incidence, clinical presentations, laboratory data, complications, and outcomes of AAP were investigated. Results: The incidence of AAP among 191 ALL children was 4.7%. The incidence was significantly higher in children treated with the TPOG-ALL-2013 (n=62) than TPOG-ALL-2002 (n=129) protocol (11.3% vs. 1.6%, p= 0.006). Multivariate analysis identified using TPOG-ALL-2013 protocol was an independent risk factor for AAP. All of the 9 AAP cases had associated complications, such as systemic inflammatory response syndrome, thrombocytopenia, coagulopathy, liver dysfunction, hypoalbuminemia, jaundice, ascites, pleural effusion, hyperglycemia and hypertriglyceridemia. Pancreatic necrosis or pseudocysts developed in 7 (78%) patients. Notably, 1 (11%) AAP cases developed diabetes mellitus and 4 (44%) had chronic pancreatitis during a 1-year observational period. None were mortality. Conclusions: The incidence of AAP was 4.7% in ALL patients treated with TPOG-ALL protocol. Although a higher cumulative dose of Asparaginase in TPOG-ALL-2013 may attribute to the pancreatic toxicity, unidentified factors such as genetic predisposition still need further study.

Background Helicobacter pylori infection is known to alter growth-related hormones and affect growth in young children. However, i t is still unknown whether maternal H. pylori infection has an impact on the levels of cord blood growth-related hormones and whether this can predict intrauterine growth restriction and poor physical and neurodevelopmental outcomes in children. This study aimed to examine associations between maternal H. pylori infection and pregnancy-related adverse events, fetal growth and early childhood development. Methods In this prospective cohort study, we recruited singleton pregnant women without major medical illnesses from January 2014 to January 2015. Seropositivity for H. pylori was defined as >12 U/ml of anti- H. pylori IgG in maternal serum. Demographic data and pregnancy-related medical issues of the cohort were documented. Cord blood levels of insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), insulin, and ghrelin were determined using ELISA. The growth of the included neonates was monitored annually for up to 3 years, and cognitive development was assessed using the comprehensive developmental inventory for infants and toddlers (CDIIT) test 3 years after birth. Results Of the 106 enrolled women, 25 (23.6%) were H. pylori -seropositive. Maternal H. pylori seropositivity was correlated with a higher risk of developing gestational hypertension (GH) (12% vs. 1.2%, p =0.04) and lower cord blood levels of IGF-1 (<35 ng/ml, 70.0% vs. 40.7%, p =0.02) and IGFBP-3 (<1120 ng/ml, 100.0% vs. 76.3%, p =0.02) compared with the seronegative women. No significant impacts on birth weight, childhood growth and cognitive development were found to be correlated with maternal H. pylori seropositivity during pregnancy. Conclusions Maternal H. pylori infection during pregnancy was more likely to lead to the development of GH, but was not correlated with fetal and childhood growth and development. In addition to close monitoring of hypertension, H. pylori eradication can be considered for mothers with H. pylori infection .

Background Helicobacter pylori infection is known to alter growth-related hormones and affect growth in young children. However, it is still unknown whether maternal H. pylori infection has an impact on the levels of cord blood growth-related hormones and whether this can predict intrauterine growth restriction and poor physical and neurodevelopmental outcomes in children. This study aimed to examine associations between maternal H. pylori infection and pregnancy-related adverse events, fetal growth and early childhood development. Methods In this prospective cohort study, we recruited singleton pregnant women without major medical illnesses from January 2014 to January 2015. Seropositivity for H. pylori was defined as >12 U/ml of anti-H. pylori IgG in maternal serum. Demographic data and pregnancy-related medical issues of the cohort were documented. Cord blood levels of insulin-like growth factor-1 (IGF-1), insulin-like growth factor binding protein-3 (IGFBP-3), insulin, and ghrelin were determined using ELISA. The growth of the included neonates was monitored annually for up to 3 years, and cognitive development was assessed using the comprehensive developmental inventory for infants and toddlers (CDIIT) test 3 years after birth. Results Of the 106 enrolled women, 25 (23.6%) were H. pylori-seropositive. Maternal H. pylori seropositivity was correlated with a higher risk of developing gestational hypertension (GH) (12% vs. 1.2%, p=0.04) and lower cord blood levels of IGF-1 (<35 ng/ml, 70.0% vs. 40.7%, p=0.02) and IGFBP-3 (<1120 ng/ml, 100.0% vs. 76.3%, p=0.02) compared with the seronegative women. No significant impacts on birth weight, childhood growth and cognitive development were found to be correlated with maternal H. pylori seropositivity during pregnancy. Conclusions Maternal H. pylori infection during pregnancy was more likely to lead to thedevelopment of GH, but was not correlated with fetal and childhood growth and development. In addition to close monitoring of hypertension, H. pylori eradication can be considered for mothers withH. pyloriinfection.