Hypercalcemia may occur in approximately 15% of children with the Williams-Beuren syndrome. The episodes of hypercalcemic crisis usually respond well to initial hyperhydration, loop diuretics and calcitonin, bisphosphonates, or subsequent dialysis. However, many patients suffer from recurrent or persistent hypercalcemia after the resolution of the hypercalcemic crisis. Although hypercalcemia in the Williams-Beuren syndrome is generally considered transient, it may last for several months, result in significant morbidity, and compromise physical growth. There are no guidelines for the management of persistent or recurrent hypercalcemia in patients with the Williams-Beuren syndrome. In this report, we describe our experience of conducting oral corticosteroid therapy in a child with the Williams-Beuren syndrome who continued to have hypercalcemia after the resolution of the hypercalcemic crisis.
Furosemide is one of the most common drug used to treat anasarca in childhood nephrotic syndrome. It has minimal side effects on short-term usage, but prolonged use can result in polyuria, hypokalemia and metabolic alkalosis. This pseudo-bartter complication can be treated by discontinuation of the drug with adequate potassium replacement. We report a child who was given furosemide for 20 days elsewhere to treat the edema due to nephrotic syndrome and then presented to us with bartter-like syndrome. Furosemide was discontinued and potassium replacement was initiated. However, the child continued to have polyuria leading to repeated episodes of hypotensive shock. In view of severe symptoms, she was given a short course of oral indomethacin for 6 days, to which she responded. This case highlights the fact that indomethacin can provide symptomatic improvement in furosemide induced pseudo-bartter.
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