Background and Objectives: Drug-induced esophageal ulcer is caused by focal drug stimulation. It may occur in adults and children. Limited research is available in pediatric patients with drug-induced esophageal ulcer; therefore, we designed this study to determine the characteristics of this disease in this population. Materials and Methods: Thirty-two pediatric patients diagnosed with drug-induced esophageal ulcers from a hospital database of upper gastrointestinal tract endoscopies were included. After treatment, patients were followed for 2 months after upper gastrointestinal endoscopy. Results: Female patients were predominant (56.2%/43.8%). The mean age of patients was 15.6 years (median, 16 years; interquartile range, 2 years). Doxycycline was administered in most cases (56.3%); other drugs were dicloxacillin, amoxicillin, clindamycin, L-arginine, and nonsteroidal anti-inflammatory drugs. Doxycycline was associated with kissing ulcers. Esophageal ulcers induced by nonsteroidal anti-inflammatory drugs were more often associated with gastric or duodenal ulcers. The most common location was the middle-third of the esophagus (78.1%). Patients were treated with proton pump inhibitors, sucralfate, or H2-blockers. The mean duration for which symptoms lasted was 9.2 days. No esophageal stricture was found in 24 patients who were followed for 2 months after upper gastrointestinal endoscopy. Conclusions: The authors suggest informing patients to take medicine with enough water (approximately 100 mL) and enough time (15–30 min) before recumbency, especially high-risk drugs, such as doxycycline or nonsteroidal anti-inflammatory drugs.

Ingestion of alkaline substances should not be disregarded because a small amount can cause chemical burns in the esophagus, with esophageal stricture being the most common late complication. We enrolled children with alkaline corrosive damage receiving treatment at China Medical University Children's Hospital's emergency department between 2008 and 2018. Patients were divided into groups A (ingested causative agents other than alkaline oil), and B (ingested alkaline oil). Altogether, 40 (27 [67.5%] male and 13 [32.5%] female) patients aged 7 months-7 years were enrolled. The most commonly ingested agent was alkaline oil (13 cases, 32.5%), followed by oven and drainage cleaners (8 cases, 20%), bleach (6 cases, 15%), laundry and dish cleaners (4 cases, 10%), sodium hydroxide (4 cases, 10%), sodium carbonate (2 cases, 5%), sodium phosphate (2 cases, 5%), and sodium citrate (1 case, 2.5%). High proportions of children had esophagitis (40/40, 100%), erosive gastritis (7/40, 17.5%), and gastric ulcer (6/40, 15%). The incidence of esophageal stricture was 38.4% (5/13) and 7.4% (2/27) in groups B and A, respectively. In group B, 4 children developed growth stunting or malnutrition during the first decade after onset, with reduced immunity and feelings of inferiority. Alkaline ingestion usually results in esophageal injury that is difficult to cure. Corrosive esophageal strictures cause swallowing difficulties and growth stunting in children. Young children who ingested alkaline oil have more complications. Given that alkaline corrosive injuries are often accidental, prevention of corrosive agent ingestion is crucial.

Background: Neonatal intrahepatic cholestasis caused by citrin deficiency (NICCD) is a rare autosomal recessive disease. The incidence of citrin deficiency is estimated between 1/10,000 and 1/20,000 in Taiwan. Case report: This report describes a case of a 42 day old female infant who suffered from prolonged jaundice, poor weight gain, and anemia. The initial total/direct bilirubin levels were 8.1/3.11 mg/dL. Liver biopsy was performed at 47 days old. The pathology revealed lobules marked with macrovesicular and microvesicular fatty metamorphosis. The serum amino acid profile showed elevated levels of threonine, methionine, citrulline, and arginine. Newborn screening disclosed normal results, but the genetic study revealed SLC25A13 mutation 851–854 del and 615 + 5G > A. The genetic study of her parents showed that the father carried the SLC25A13 mutation 851–854 del and the mother carried the SLC25A13 mutation 615 + 5G > A. Treatment with ursodeoxycholic acid decreased the bilirubin levels to a normal range at the age of 5 months. Conclusion: This report illustrates that hepatic steatosis is a feature of NICCD. For every young infant patient who develops cholestasis, the pediatrician must consider NICCD as a differential diagnosis even if newborn screening shows normal findings.

Colonic polyps are a common cause of persistent bloody stools in pediatric patients. Such polyps are easily diagnosed by a barium study of the lower gastrointestinal tract or by colonoscopy. Polypectomies utilizing electric ligators are generally performed on pediatric patients, and such patients can be easily operated on. However, giant colonic polyps have been reported in pediatric patients. In the past, a laparotomy or laparoscopy would have been performed in some pediatric patients diagnosed with a giant colonic polyp; however, the large size, location, or position of the polyp would sometimes be too large or the location or position of the polyp would make successful operation difficult. In general, larger stumps with large feeding arteries are associated with larger colonic polyps. Therefore, if such a polyp is removed via electric polypectomy alone, there may be a higher risk of post-polypectomy bleeding from its stump. We report a case of a 14-year-old male patient who presented with a 2-month history of bloody stools. A giant juvenile colonic polyp was detected by colonoscopy in the transverse colon. Finally, we successfully removed the giant polyp by using endoloop-assisted polypectomy.