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NEONATAL HYPERCALCEMIA DUE TO MATERNAL HYPOCALCEMIA
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Dr Ira Shah
M.D, DNB, DCH(Gold Medalist), FCPS
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Case Report |
A one & a half months old male infant presented with 5 episodes of apnea followed by cyanosis since 1 day. There was no lethargy or refusal of feeds or fever. He was a preterm AGA with a birth weight of 1.8 kg. The postnatal period was uneventful. On examination, there was no significant finding. Mother was treated with calcium supplements for hypocalcemia during pregnancy. Laboratory investigations revealed a normal compete blood count and normal blood sugar and electrolytes. His blood culture was negative. Echocardiography was normal ruling out a heart disease. His ultrasound of the brain and EEG were also normal ruling out a CNS involvement. His S. calcium was 11.2 mg% suggestive of hypercalcemia with a normal phosphorus (3.0 mg%) and increased serum alkaline phosphatase [290 IU/L, Normal = 57-180 IU/L]. Thus a differential diagnosis of Neonatal hyperparathyroidism secondary to maternal hypocalcemia and familial hypercalciuric hypercalcemia was considered. His urine calcium/creatinine ratio was 0.4 and S. PTH levels were increased [107 pg/ml, Normal = 12-95 pg/ml]. Thus a diagnosis of Neonatal hyperparathyroidism secondary to maternal hypocalcemia was established.
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Discussion
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Hypercalcemia in neonates can be life threatening. It leads to polyuria leading to dehydration due to resistance to antidiuretic hormone. Patients may develop hypertension due to direct vasoconstrictive effect of calcium and increased renin-angiotensin activity. Due to hypercalcemia patients may develop lethargy, hypertonia and seizures. Long standing hypercalcemia may lead to metastatic calcification and/or nephrocalcinosis.
Etiology:
- Iatrogenic due to over treatment with calcium salts
- Primary hyperparathyroidism due to diffuse parathyroid hyperplasia
- Neonatal hyperparathyroidism secondary to maternal hypocalcemia
- Subcutaneous fat necrosis
- Bartter’s syndrome
- Breast milk induced rickets of prematurity
- Infantile hypophosphatasia
- William’s syndrome
- Familial benign hypocalciuric hypercalcemia.
Primary neonatal hyperparathyroidism: In addition to the above-mentioned features of hypercalcemia, affected children have severe bone deformities at birth due to generalized demineralization with multiple spontaneous fractures. These patients are hypophosphatemic with increased alkaline phosphate activity, hypercalciuria and increased phosphaturia. Serum PTH is very high.
Treatment : Subtotal parathyroidectomy.
Neonatal hyperparathyroidism secondary to maternal hypocalcemia: They have radiographic features of primary hyperparathyroidism but all usually not hypercalcemic. The disorder resolves spontaneously within a few weeks after the patient receives an adequate calcium and phosphorus supply through milk.
Resolution phase of subcutaneous fat necrosis : In this phase, transient hypercalcemia may develop lasting a few weeks and responds to a diet low in calcium and vitamin D. Severe cases need to be treated with glucocorticoids.
Bartter’s syndrome : Neonates present with episodes of fever, vomiting, diarrhea and failure to thrive. Excessive production of prostaglandin may be the cause as the disease is controlled by indomethacin.
Breast milk induced rickets of prematurity : Preterms exclusively fed human milk receive a relatively phosphate-deficient diet leading to hypophosphatemia and decreased bone formation. This causes increased production of calcitriol with increase in intestinal calcium absorption and hypercalcemia.
Infantile Hypophosphatasia : It is an autosomal recessive disorder where calcium is deposited inadequately in the bone due to deficient alkaline phosphatase activity leading to subsequent hypercalcemia with hypercalciuria and nephrocalcinosis and severe rickets. Urinary phosphoethanolamine is markedly increased.
Familial hypocalciuric hypercalcemia (Familial benign hypercalcemia): Patients are usually asymptomatic and hypercalcemia is a chance finding. PTH levels are inappropriately normal and serum magnesium levels are elevated mildly. Urinary calcium to creatinine clearance is usually decreased. It is an autosomal dominant disorder with 100% penetrance. It is due to increased proximal renal tubular reabsorption of calcium. Parathyroid gland size is normal in FHH.
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References
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- The Metabolic & Molecular Bases of Inherited Disease – Charles R. Scriver et al, 7 th ed. McGraw Hill Inc. pg.3103-3104.
Last Updated on 01-05-2004
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How to cite this url |
Shah I.Neonatal Hypercalcemia Due to Maternal Hypocalcemia .Pediatric Oncall [serial online] 2004 [cited 2004 May 1];1. Available from:
http://www.pediatriconcall.com/fordoctor/casereports/hypercalcemia.asp
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