cover
Contact Name
-
Contact Email
apghnjgai@gmail.com
Phone
-
Journal Mail Official
apghnjgai@gmail.com
Editorial Address
The Indonesian Society of Pediatric Gastroenterology, Hepatology, and Nutrition Jalan Letjen S Parman Kav 87, Jakarta, Indonesia
Location
Kota adm. jakarta pusat,
Dki jakarta
INDONESIA
Archives of Pediatric Gastroenterology, Hepatology, and Nutrition
ISSN : -     EISSN : 28305442     DOI : -
Core Subject : Health,
Archives of Pediatric Gastroenterology, Hepatology, and Nutrition (APGHN) is the official journal issued by the Indonesian Society of Pediatric Gastroenterology, Hepatology, and Nutrition (Perhimpunan Gastroenterologi, Hepatologi, dan Nutrisi Anak Indonesia). APGHN is issued four times in a year and published in English. Previously published in print form as Jurnal Gastrohepatologi Anak Indonesia (JGAI), APGHN is committed to promote scientific development in child’s health through high-quality publication and provides recent updates on pediatric gastroenterology, hepatology, and nutrition for health practitioners and scholars. APGHN accepts original articles, case reports, review articles, medical illustrations and clinical practice guidelines, all of which have been peer-reviewed carefully by our selected experts.
Articles 84 Documents
Infantile Liver Failure as the Initial Manifestation of SCYL1-Related CALFAN Syndrome: A Case Report and Literature Review Deepika Yadav; Nishant Wadhwa; Megha Sharma
Archives of Pediatric Gastroenterology, Hepatology, and Nutrition Vol. 5 No. 2 (2026): APGHN Vol. 5 No. 2 May 2026
Publisher : The Indonesian Society of Pediatric Gastroenterology, Hepatology, and Nutrition

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.58427/apghn.5.2.2026.86-97

Abstract

Background: CALFAN (Cholestasis, Acute Liver Failure, and Neurodegeneration) syndrome is a rare autosomal recessive disorder caused by biallelic pathogenic variants in SCYL1 (SCY1-like pseudo-kinase 1). It is classically associated with low or normal gamma-glutamyl transpeptidase (GGT) cholestasis, infection-triggered acute liver failure (ALF), and progressive neurodegeneration. Because neurological and skeletal manifestations may be absent during the first hepatic presentation, early diagnosis can be missed unless the hepatic phenotype is recognized. Case: We describe a 9-month-old female infant born to third-degree consanguineous parents who developed fever-triggered cholestatic jaundice and ALF. Structural biliary disease, viral hepatitis, and common metabolic disorders were excluded. Whole-exome sequencing revealed a homozygous pathogenic nonsense variant in SCYL1 (c.1567C>T; p.Arg523*), consistent with autosomal recessive CALFAN syndrome. No neurological, neuroimaging, or skeletal abnormalities were present at initial presentation. The clinical course was notable for persistent hyperbilirubinemia and a family history of sibling death from infantile liver failure. Discussion: This case adds to the SCYL1 spectrum by demonstrating isolated infantile ALF without neurological features at presentation, a severe hepatic phenotype with persistent cholestasis, and a novel homozygous null variant in a consanguineous family. Conclusion: SCYL1 deficiency should be considered in infants with fever-triggered ALF and low/normal-GGT cholestasis, even when neurological and skeletal signs are absent. Early genomic testing, systematic exclusion of low-GGT cholestasis mimics, longitudinal neurological surveillance, timely transplant referral, and recurrence-risk counselling are essential.
From Paper to Precision: A Systematic Review on Digital Technologies for Improving the Quality of Childhood Growth Monitoring Assyifa Gita Firdaus; Dhio Pratama Putra
Archives of Pediatric Gastroenterology, Hepatology, and Nutrition Vol. 5 No. 2 (2026): APGHN Vol. 5 No. 2 May 2026
Publisher : The Indonesian Society of Pediatric Gastroenterology, Hepatology, and Nutrition

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.58427/apghn.5.2.2026.74-85

Abstract

Background: Childhood growth monitoring is essential for detecting malnutrition and growth disorders. However, traditional paper-based methods are prone to errors, incompleteness, and fragmentation. Digital technologies have emerged as potential tools to enhance efficiency of growth monitoring. This systematic review aims to synthesize evidence on the benefits and challenges of implementing digital technologies for growth monitoring in children. Methods: A systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. A comprehensive literature search was conducted across multiple databases. Eligible studies evaluated digital interventions such as mobile health applications with automated anthropometric calculations, computer-based growth monitoring integrated into the electronic health record, and chatbot-based reporting systems. Data were extracted on study design, population, technology features, and outcomes related to data and implementation. Result: Seven studies were analyzed, representing over 50,000 child growth assessments and involving approximately 400 frontline health workers. Digital technologies improved the completeness, accuracy, and timeliness of data collection. Automation reduced human error, supporting more consistent interpretation of nutritional status, earlier detection and reporting of inadequate growth, along with improved nutritional outcomes. These technologies were highly accepted by frontline health workers for their ability to simplify complex tasks. However, most challenges arose from constraints in digital infrastructure and uneven technology implementation across healthcare facilities. Conclusion: Digital technologies can transform growth monitoring from a manual, error-prone process into a precise and scalable system for early detection of malnutrition. Addressing challenges is essential for successful implementation and scale-up in health systems.
Prediction of Development of Neonatal Jaundice by Cord Blood Bilirubin and Albumin Babita Rani; Leesha Kaushik; Preeti Raikwar; Renu Garg; Vijayata Sangwan; Sanjay Kumar Jha; Anita Punia; Deepika Kataria
Archives of Pediatric Gastroenterology, Hepatology, and Nutrition Vol. 5 No. 2 (2026): APGHN Vol. 5 No. 2 May 2026
Publisher : The Indonesian Society of Pediatric Gastroenterology, Hepatology, and Nutrition

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.58427/apghn.5.2.2026.62-73

Abstract

Background: Neonatal jaundice is a common cause of early postnatal readmission and contributes to both financial and socio-economic burden. In resource-constrained nations, where the patient-to-resource-constrained-bed ratio is very high, early prediction of hyperbilirubinaemia will help in early discharge, prevent re-hospitalization, and reduce the duration of hospital stay. This study aims to estimate the cord blood bilirubin (CBB) and albumin (CBA) levels for future prediction of neonatal jaundice among deliveries at Bhagat Phool Singh Government Medical College for Women (BPS GMC (W)). Methods: A prospective study was conducted among 384 randomly selected neonates delivered at BPS GMC (W). Socio-demographic data were recorded, and cord blood samples were collected at birth for bilirubin and albumin estimation. Neonates were followed for 10 days to assess the development of clinical jaundice. Result: Incidence of neonatal jaundice was 21.4% with 10 days of follow-up. 94.8% neonates developed jaundice with CBB level ≥ 2mg/dL, proving it statistically significant. Additionally, 62.7% of neonates with serum albumin < 3 g/dL developed jaundice. Cord blood Bilirubin-to-Albumin ratio proved a good indicator, as area under the curve is 0.933 with sensitivity and specificity of 68.30% and 99.0% respectively at a cut-off level of 0.61. Conclusion: Cord blood bilirubin and bilirubin-to-albumin ratio may help identify neonates at higher risk of subsequent jaundice and may assist in prioritizing follow-up in resource-limited settings. A bilirubin-to-albumin ratio ≥ 0.61 was found to be a highly specific predictor.
Gut Endocrine Regulation of Pediatric Growth and Weight: Integrating Intestinal Hormones, Inflammation, and the GH–IGF-1 Axis in Health and Disease Ashraf T. Soliman; Fawzia Alyafei; Nada Alaaraj; Shayma Mohamed; Noor Hamed; Sohair Elsiddig
Archives of Pediatric Gastroenterology, Hepatology, and Nutrition Vol. 5 No. 2 (2026): APGHN Vol. 5 No. 2 May 2026
Publisher : The Indonesian Society of Pediatric Gastroenterology, Hepatology, and Nutrition

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.58427/apghn.5.2.2026.106-120

Abstract

Background: The intestine is increasingly recognized as an endocrine organ through enteroendocrine cells, gut-derived peptides, mucosal trophic factors, and microbiota–host signaling. In children, these pathways influence appetite, nutrient handling, body composition, and growth, including the growth hormone–insulin-like growth factor-1 (GH–IGF-1) axis. This review summarizes how intestinal endocrine function affects linear growth, weight gain, and GH–IGF-1 regulation in children with celiac disease, inflammatory bowel disease, environmental enteric dysfunction, and obesity. Discussion: Evidence supports a convergent model linking gut function to growth via gut hormone signaling (GLP-1, PYY, CCK, GLP-2, ghrelin), inflammation-driven GH resistance, and microbiota-mediated IGF-1 modulation. Celiac disease can cause growth failure reversible with a gluten-free diet; Crohn's disease impairs growth through inflammation and malabsorption; environmental enteric dysfunction drives population-level stunting; and in obesity, altered incretin responses highlight the intestine as a therapeutic target. Gut-endocrine pathways remain underutilized in pediatric practice. IGF-1 is frequently interpreted without accounting for mucosal inflammation or malabsorption, and cross-specialty fragmentation limits holistic growth assessment. Emerging therapies including GLP-2 analogues and incretin-based agents offer promise, though pediatric data remain limited. Standardizing gut-endocrine biomarkers and integrating intestinal health into growth frameworks are key research priorities. Conclusion: The intestine is a clinically important endocrine organ in pediatric growth medicine. Integrating gut-endocrine biology into endocrine assessment improves the interpretation of IGF-1 and growth patterns and guides management across undernutrition, chronic intestinal disease, and obesity.