Lactic Acidosis Due to Thiamine Deficiency in a Preterm Infant Associated with Inadequate Parenteral Nutrition.

BACKGROUND Premature low birth weight infants may require prolonged parenteral feeding, which can be associated with deficiencies of vitamins and micronutrients. Deficiency in thiamine (vitamin B1) can result in metabolic crisis and lactic acidosis. This report describes a premature male infant born at 30 weeks of gestation with thiamine deficiency and lactic acidosis associated with inadequate parenteral nutrition. CASE REPORT A preterm boy was born at 30 weeks+5 days, with a weight of 0.830 kilograms and Apgar scores of 8 and 9 at 1 and 5 minutes, respectively. Total parenteral nutrition started on day 1 of life. On day 21 of life, while he was on total parenteral nutrition, severe lactic acidosis with a high anion gap was noted. Sepsis work-up along with radiological studies were immediately done, and antibiotics were initiated to cover common suspected organisms. Repeated blood gas analysis showed further increases in lactate levels. A fluid bolus was administered, with no improvement, so sodium bicarbonate was started. Despite all interventions, the lactate level continued to increase up to 13.78 mmol/l. Thiamine deficiency was suspected next, and a dose of vitamin B1 was given intravenously. There was an immediate drop in lactate level, and the patient proceeded to a full recovery. CONCLUSIONS This report shows that lactic acidosis is a potentially life-threatening condition that can result from thiamine deficiency. When standard parenteral nutrition preparations are used for prolonged periods in premature neonates, continuous monitoring of vitamin levels, micronutrient levels, and biochemical parameters is required.

Unusual Presentation of Epstein-Barr Virus-Associated Cholestatic Hepatitis in an Infant.

Epstein-Barr virus (EBV) infections are prevalent in the pediatric population but are subclinical in the majority of cases. Elevated transaminases in the acute setting rarely increase beyond 5 times the normal upper limit. We present a girl aged 1 y with fever, vomiting, and diarrhea. Although initial physical examination was unremarkable, she developed jaundice, hepatomegaly, abdominal distension, and a maculopapular rash during admission. Laboratory investigations revealed marked increase in transaminases (alanine aminotransferase 7,664.5 IU/L, aspartate aminotransferase 12,266 IU/L), elevated γ-glutamyl transferase (224 IU/L), and hyperbilirubinemia (total 130.7 µmol/L, direct 104.9 µmol/L). Abdominal ultrasound reported hepatomegaly with mild ascites. Serology revealed that both Monospot test and EBV immunoglobulin G were positive. With supportive therapy, improvement was noted within a week of symptom onset. We hereby elucidate the importance of considering EBV as a cause of acute cholestatic hepatitis in a very young pediatric patient who develops a rapid elevation of liver enzymes.