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Late infantile tetany and secondary hyperparathyroidism in infants fed humanized cow milk formula. Longitudinal
Insights
Cow milk formula can cause hypocalcemic tetany in newborns due to high phosphorus levels. This can lead to secondary hyperparathyroidism, affecting calcium and magnesium balance.
Area of Science:
- Neonatal Nutrition
- Pediatric Endocrinology
- Biochemistry
Background:
- Infants fed cow milk-based formula can develop hypocalcemic tetany.
- This condition is characterized by low serum calcium levels and is often seen in the first weeks of life.
Purpose of the Study:
- To investigate the biochemical and hormonal changes in infants experiencing hypocalcemic tetany.
- To compare these changes with those in breast-fed and non-tetanic formula-fed infants.
Main Methods:
- Case study of five term infants with hypocalcemic tetany fed cow milk formula.
- Biochemical (serum calcium, phosphorus, magnesium) and hormonal (parathyroid hormone) measurements.
- Comparison with exclusively breast-fed and non-tetanic formula-fed infants.
Main Results:
- Tetanic infants showed initial low calcium, high phosphorus, and normal magnesium with elevated parathyroid hormone.
- After calcium supplementation, serum calcium and magnesium normalized, but parathyroid hormone remained elevated.
- Formula-fed infants had higher parathyroid hormone levels compared to breast-fed infants.
Conclusions:
- High phosphorus load in cow milk formula may induce hypocalcemic tetany.
- Continued phosphorus intake can lead to secondary hyperparathyroidism, impacting mineral homeostasis.
- Formula composition warrants consideration in neonatal feeding practices.
Abstract:
Five full-term infants with birth weights appropriate for gestational age presented with hypocalcemic tetany at 5 to 9 days of age. All infants had been fed Similac 20, a cow milk formula. Initial mean serum calcium (Ca), phosphorus (P), and magnesium (Mg) levels of the tetanic infants were 6.8, 9.5, and 1.6 mg/dL, respectively. The mean serum parathyroid hormone (PTH) level was elevated at 79 mu LEq/mL (adult normal values, less than or equal to 57 mu LEq/mL). Following restoration of normocalcemia with Ca supplements, feeding was reinstituted with Similac 20 in two infants and Similac PM 60/40 in three infants. Serum biochemical and hormonal values were compared with those of 18 exclusively breast-fed infants followed up from three weeks to six months and 14 Similac 20-fed full-term infants followed up from one week to six months. In tetanic infants, serum Ca concentrations became elevated (10.4 +/- 0.05 mg/dL; mean +/- SEM) by six weeks (vs 9.2 +/- 0.3 mg/dL in breast-fed infants) (P less than .001) and serum Mg concentrations (2.26 +/- 0.01 mg/dL) by four weeks (vs 1.92 +/- 0.07 mg/dL in breast-fed infants) (P less than .01). Mean serum P concentrations declined progressively. Mean serum PTH concentrations were elevated and ranged from 74 to 143 mu LEq/mL at two to 16 weeks (vs mean 28 to 35 mu LEq/mL in breast-fed infants (P less than .0001). In 14 formula-fed-nontetanic full-term infants, serum PTH concentrations were intermediate between formula-fed-tetanic and breast-fed infants, mean serum Ca concentrations ranged from 10.2 to 10.4 mg/dL, and mean serum P concentrations declined from 8.3 to 7.1 mg/dL. We speculate that acute hypocalcemic tetany in the study infants was induced by the relatively high P load in cow milk formulas (vs human milk); with the continued P load, secondary hyperparathyroidism continued, maintaining P, Ca, and Mg homeostasis.