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Hypercalciuria in children with febrile convulsions
A Papadimitriou1, P Nicolaidou, A Garoufi
1Second Department of Pediatrics, P&A Kyriakou Children's Hospital, Athens, Greece. lix@ath.forthnet.gr
Insights
Idiopathic hypercalciuria, a condition of excess calcium in the urine, was found in 23.7% of children with febrile convulsions. This suggests a potential link between high urine calcium and the development of febrile seizures in children.
Area of Science:
- Pediatric Nephrology
- Neurology
- Clinical Biochemistry
Background:
- Febrile convulsions are common in childhood.
- The underlying causes of idiopathic hypercalciuria are not fully understood.
- Investigating potential links between metabolic disorders and neurological events is crucial.
Purpose of the Study:
- To determine if idiopathic hypercalciuria is associated with the development of febrile convulsions in children.
- To explore the relationship between urinary calcium levels and the occurrence of febrile seizures.
- To investigate potential metabolic factors contributing to febrile convulsions.
Main Methods:
- A case-control study involving 38 children with febrile convulsions and 45 healthy controls.
- Measurement of 24-hour urine calcium and phosphate excretion.
- Analysis of serum calcium, phosphate, alkaline phosphatase, and intact parathyroid hormone (PTH).
Main Results:
- Hypercalciuria was observed in 23.7% of children with febrile convulsions, compared to 6.7% in controls.
- Hypercalciuric children exhibited significantly higher urinary phosphate and serum intact PTH levels.
- Children with hypercalciuria experienced more frequent convulsive episodes.
Conclusions:
- The findings suggest that renal hypercalciuria may play a role in the pathogenesis of febrile convulsions.
- Elevated urinary calcium and associated metabolic changes could be contributing factors.
- Further research is warranted to elucidate the mechanisms linking hypercalciuria and febrile seizures.
Background:
The purpose of the present study was to investigate whether idiopathic hypercalciuria may be implicated in the pathogenesis of febrile convulsions.
Methods:
We studied 38 children (22 boys) with febrile convulsions (mean (+/- SD) age 3.25 +/- 1.09 years) and 45 healthy children (28 boys) of similar age who served as controls. Twenty-four hour urine calcium and phosphate, as well as serum calcium, phosphate, alkaline phosphatase and intact parathyroid hormone (PTH) concentrations were determined.
Results:
Hypercalciuria (urine Ca >4.0 mg/kg bodyweight per 24 h) was found in nine children with febrile convulsions (23.7%) and in three controls (6.7%). Hypercalciuric children excreted significantly more phosphate in their urine (37.0 +/- 11.6 mg/kg bodyweight per 24 h) than normocalciuric children (18.7 +/- 8.7 mg/kg bodyweight per 24 h) and controls (20.2 +/- 7.6 mg/kg bodyweight per 24 h). They also had higher serum intact PTH concentrations (49.87 +/- 15.36 pg/mL) than normocalciuric (35.39 +/- 15.67 pg/mL) and control children (28.21 +/- 14.00 pg/mL). According to the calcium-loading test, eight of nine children with hypercalciuria had the renal type of the disorder. Furthermore, hypercalciuric children had significantly more convulsive episodes (2.77 +/- 1.98) than normocalciuric children (1.86 +/- 1.24).
Conclusions:
Our results suggest that renal hypercalciuria may be implicated in the pathogenesis of febrile convulsions.