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Clinical features of mercury poisoning are nonspecific, and a detailed history is very valuable. The silvery, shiny appearance of mercury makes it very exciting and attractive for children. The overall half-life of elemental mercury in the body averages approximately 2 months. Chelation therapy with dimercaptosuccinic acid is the treatment of choice if the urine or blood level of mercury is high or the symptoms are profound. Here, we describe a 14-year-old boy with fever, respiratory distress, and body rash. Investigation leading to a diagnosis of mercury poisoning was made only after his mother presented with the similar symptoms a few days later.

Fructose-1,6-diphosphatase (FDPase) enzyme deficiency is a rare inherited metabolic disease. Affected patients usually present with metabolic crisis including hypoglycemia, acidosis, ketonuria, and hyperuricemia. A previously healthy 8-month-old male infant presented with fever, vomiting, and hypoactivity. He had tachycardia, tachypnea, and a tendency to sleep. The patient had signs of severe dehydration and shock. Laboratory findings revealed significant lactic acidosis, hyperuricemia, hyperglycemia, elevated liver enzyme level, and hyperlipidemia. The urine analysis had evidence of glycosuria and ketonuria. Hyperuricemia, lactic acidemia, and hyperglycemia persisted despite insulin infusion, adequate hydration, and perfusion. Consequently, peritoneal dialysis was started. About 12 hours after dialysis, his metabolic derangements were normalized, and clinical status was improved dramatically. His metabolic disease workup was compatible with FDPase deficiency. Here, we described a metabolic attack of FDPase deficiency presented with hyperglycemia mimicking diabetic ketoacidosis.