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Manifestations of chronic selenium deficiency in a child receiving total parenteral nutrition
Insights
This study shows that prolonged total parenteral nutrition can lead to selenium deficiency in children, causing muscle pain and nail changes. Selenium supplementation effectively reversed these adverse effects, highlighting its importance in pediatric nutrition.
Area of Science:
- Biochemistry
- Pediatric Nutrition
- Clinical Medicine
Background:
- Total parenteral nutrition (TPN) is a life-sustaining intervention for children with gastrointestinal failure.
- Long-term TPN can disrupt nutrient absorption and metabolism, potentially leading to deficiencies.
- Monitoring micronutrient status is crucial in patients on long-term TPN.
Observation:
- A pediatric patient on long-term TPN developed myalgia, elevated muscle enzymes (AST, ALT, CK), and leukonychia.
- Cardiac evaluation showed elevated creatine kinase-MB isoenzyme without evidence of myocardial damage.
- Retrospective analysis revealed critically low serum and urine selenium levels during TPN.
Findings:
- Intravenous selenium supplementation (42 mcg/day) was initiated 33.5 months after TPN commencement.
- Following supplementation, serum selenium and whole blood glutathione peroxidase activity normalized.
- Muscle enzyme activities and nail abnormalities significantly improved after selenium therapy.
Implications:
- This case highlights selenium deficiency as a potential complication of long-term TPN in children.
- Prompt diagnosis and selenium repletion are essential for resolving clinical manifestations.
- This underscores the importance of assessing selenium status in pediatric TPN patients.
Abstract:
A child receiving total parenteral nutrition for about 1 1/2 yr developed intermittent leg muscle pain and tenderness and elevation in serum activities of glutamic oxaloacetic transaminase, glutamic pyruvic transaminase, and creatine kinase. Approximately 6 months later he developed white fingernail beds. Detailed cardiological evaluation revealed no evidence of cardiac muscle cell damage despite markedly elevated serum activities of the MB isoenzyme of creatine kinase. Retrospective analyses of serum and 24 hr urine samples collected during this period demonstrated very low serum Se concentration (0.003 to 0.007 micrograms/g) and urine excretion (0.0 to 8.9 micrograms/day) Se. Intravenous Se supplementation (42 micrograms/day elemental Se as H2SeO3) and a prospective study of biochemical Se status were begun 33.5 months after initiation of total parenteral nutrition. Serum Se concentration and whole blood glutathione peroxidase activity and Se concentration were respectively 0.020 mu/g, 3.5 EU/g Hb, and 0.018 microgram/g, 1 month after intravenous Se therapy was started. These very low values increased after further Se therapy. Serum enzyme activities markedly improved and the fingernail bed abnormalities resolved after therapy.