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All Journal Archives of Pediatric Gastroenterology, Hepatology, and Nutrition
Sarthak Chakrabarti
Department of Paediatrics, All India Institute of Medical Sciences, Rishikesh, Uttarakhand, India
Medicine & Pharmacology

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Treatment of Severe Unconjugated Hyperbilirubinemia with Phenobarbitone in Two First-Degree Siblings with Crigler-Najjar Syndrome (CNS) Type 2: A Success Story Sachin Kumar; Siddhavatam Rahul Karthik; Gandharav Pahuja; Sarthak Chakrabarti; Prateek Kumar Panda; Indar Kumar Sharawat
Archives of Pediatric Gastroenterology, Hepatology, and Nutrition Vol. 4 No. 4 (2025): APGHN Vol. 4 No. 4 November 2025
Publisher : The Indonesian Society of Pediatric Gastroenterology, Hepatology, and Nutrition

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.58427/apghn.4.4.2025.201-207

Abstract

Background: Crigler–Najjar syndrome (CNS) type 2 is a rare autosomal recessive disorder of bilirubin conjugation caused by mutations in the UGT1A1 gene. It presents in infancy with unconjugated hyperbilirubinemia that does not respond to phototherapy but improves with phenobarbitone, which enhances residual enzyme activity. Although phenobarbitone remains the cornerstone of treatment, familial recurrence of CNS type 2 is rarely reported in pediatric literature. Case: We report two siblings born to consanguineous parents who presented with progressive jaundice during early infancy. The first child, a 2-month-old boy, had multiple hospitalisations for phototherapy without benefit. Laboratory evaluation revealed total bilirubin of 31 mg/dL with normal liver function and no evidence of hemolysis. Genetic testing confirmed a homozygous UGT1A1 (c.1456T>G; p.Tyr486Asp) mutation. He was treated with phenobarbitone (5–8 mg/kg/day) and calcium phosphate, achieving a bilirubin level <10 mg/dL within 4 weeks. Three years later, his younger sister developed similar unconjugated jaundice from day 4 of life and harboured the same mutation; she responded well to phenobarbitone alone. Both siblings remain well on long-term follow-up. Discussion: This case highlights the genetic basis and favorable response of CNS type 2 to phenobarbitone, which induces hepatic UGT1A1 expression. Familial clustering of CNS 2, though reported in few global studies, is seldom documented from India. Conclusion: Early genetic diagnosis, timely institution of phenobarbitone, and family counselling are critical for successful management of CNS type 2. These cases reaffirm the long-term safety and efficacy of phenobarbitone in familial presentations of this rare disorder.
Eosinophilic Gastritis as an Intriguing Case of Gastric Outlet Obstruction in a Female Toddler: A Case Report Amanjot Kaur; Kanojiya Atul Ghanshyam; Sarthak Chakrabarti; Ashok Singh; Yash Shrivastava; Nowneet Kumar Bhat
Archives of Pediatric Gastroenterology, Hepatology, and Nutrition Vol. 5 No. 3 (2026): APGHN Vol. 5 No. 3 August 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.5.3.2026.157-166

Abstract

Background Eosinophilic gastritis (EoG) is an uncommon form of eosinophilic gastrointestinal disease (EGID) characterized by dense eosinophilic infiltration of the gastric wall, most often involving the antrum and fundus. Although EoG can mimic other causes of gastric outlet obstruction (GOO), including infantile hypertrophic pyloric stenosis (IHPS), such presentations are rare. Diagnosis requires histological confirmation, and management typically involves dietary modification with elimination diets, corticosteroids, and proton pump inhibitors. Case: We report the case of a 3-year-old girl presenting with recurrent non-bilious, non-bloody projectile vomiting and abdominal pain over 15 days, with a 3 kg weight loss. Imaging revealed pyloric canal hypertrophy not meeting IHPS criteria, and upper gastrointestinal endoscopy showed an erythematous, edematous antrum with pinpoint pylorus. Pyloric biopsy demonstrated dense eosinophilic infiltration (>30 eosinophils/HPF in 5 fields), confirming EoG. The child was treated with oral prednisolone (2 mg/kg/day) and lansoprazole (1 mg/kg/dose twice a day), resulting in marked clinical improvement and weight gain within two weeks Discussion: EoG represents a spectrum of EGIDs, with clinical manifestations depending on the gastric layer involved. It may occur with or without peripheral eosinophilia and is frequently associated with atopic conditions. Diagnosis rests on gastrointestinal symptoms, tissue eosinophilia, and exclusion of secondary causes. Corticosteroids remain the cornerstone of treatment, though dietary elimination and PPIs also contribute to remission. Conclusion: EoG should be considered in children presenting with unexplained GOO. Early endoscopic biopsy and corticosteroid-based therapy can lead to rapid symptom resolution and prevent long-term morbidity.
Co-Authors Amanjot Kaur Ashok Singh Gandharav Pahuja Indar Kumar Sharawat Kanojiya Atul Ghanshyam Nowneet Kumar Bhat Prateek Kumar Panda Sachin Kumar Siddhavatam Rahul Karthik Yash Shrivastava