Advantages of Fluoroscopy for Accidental Ingestion of Multiple Magnets.

Foreign body ingestion is one of the common problems among children. A three-year-old girl presented to the emergency department 2 h after ingesting three small disk-type neodymium magnets. She had no gastrointestinal symptoms. Abdominal radiography revealed a foreign body in the left upper quadrant, which was the three circular magnets. Fluoroscopy was performed. She was placed in the right lateral decubitus position for 3 min and slowly returned to the supine position. Abdominal fluoroscopy revealed a foreign body migrating near the middle of the spine. Similarly, when she was placed in the left lateral decubitus position for 3 min and slowly returned to the supine position, the foreign body migrated to the outermost part of her left upper quadrant. Thus, we anticipated that the magnets could be excreted spontaneously. The patient did not develop any gastrointestinal symptoms after returning home, and two days later, three overlapping magnets were finally found in her stool. During accidental ingestion of single or multiple desk-type neodymium magnets, endoscopic removal may not be necessary if they are mobile and clump together in the stomach. Regarding the ingestion of multiple desk-type neodymium magnets, fluoroscopy is useful to determine the extent of endoscopic intervention.

Hyperammonemia in a carbamoyl-phosphate synthetase 1 deficiency recipient after living-donor liver transplantation from a carrier donor: a case report.

Carbamoyl-phosphate synthetase 1 (CPS1) deficiency is an autosomal recessive congenital urea cycle disorder (UCD) characterized by hyperammonemia. The recipients of liver transplantation (LT) for UCD are often children, and the potential donors are often the parents. Hereditary congenital diseases involving UCD entail the possibility of both parents being genetically heterozygous. Herein, we describe the case of a 12-year-old girl with CPS1 deficiency receiving a liver transplant (soon after birth) from her father, who had a heterozygous CPS1 mutation. She was referred to our hospital with respiratory distress after contracting two infections (respiratory syncytial virus and human metapneumovirus) within a short period, both of which presented with hyperammonemia. Medication for hyperammonemia quickly lowered the ammonia levels. The hyperammonemia was thought to be caused by the heterozygous mutation in the donor liver; moreover, it is likely that the low enzyme activity in the patient's liver was increased due to the infections. This is the first study to report hyperammonemia in a CPS1 deficiency patient due to an infection after LT. Thus, patients with CPS1 deficiency should be aware of the development of hyperammonemia after LT.