Hypocalcemic Tetany in a 13-Year-Old Girl with Wilson's Disease / 대한소아소화기영양학회지

Wilson's disease is an autosomal recessive disorder marked by disruptions in copper metabolism which leads to accumulation of copper in the liver, brain, cornea, and other tissues. Manifestations of this disease are more likely to be hepatic during early childhood and neurologic in adolescent. In addition, abnormalities that develop during disease progression may result in other manifestations such as hematologic, endocrine, or renal findings. Here we report a 13-year-old girl who presented with hypocalcemic tetany shortly after being diagnosed with Wilson's disease. Despite aggressive calcium, magnesium, and vitamin D replacement therapy, the hypocalcemia and hypomagnesemia did not promptly respond. Mineral levels in the blood took longer than 3 weeks to normalize. We speculate that a parathyroid insufficiency and disrupted vitamin D metabolism caused by copper accumulation and hepatic dysfunction resulted in hypocalcemic tetany.

A Case of Severe Hyperphosphatemia and Hypocalcemic Tetany after Sodium Phosphate Administration in a Patient with Normal Renal Function / 대한신장학회잡지

Oral sodium phosphate (NaP) is increasingly used to prepare patients for gastrointestinal procedures such as colonoscopy. Severe hyperphosphatemia may complicate bowel-cleansing preparation using oral NaP. The risk of hyperphosphatemia is known to increase with excessive and/or repeated doses, increased intestinal absorption, or impaired renal excretion of phosphate. Hyperphosphatemia may produce acute renal failure, but the mechanism is not yet clear. Some authors suggest that renal injury is caused by intrarenal calcium-phosphate deposition, but others suggest that direct tubular toxicity or a disturbance in renal hemodynamics may induce renal injury. A 74-year-old woman was admitted with generalized weakness after taking NaP for colonoscopy. She had no underlying diseases such as renal disease. She was hypotensive and had carpopedal spasm with hypocalcemia, severe hyperphosphatemia, metabolic acidosis, and non-oliguric acute renal failure. She was treated with aggressive hydration, calcium replacement and aluminum-containing antacid, but hyperphosphatemia was aggravated (35.6 mg/ dL). Hemodialysis was done and phophate concentration was lowered to 5.5 mg/dL. It is suggested that caution should be taken when using phosphate- containing laxatives especially for elderly patients even if they have no underlying diseases.