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References in periodicals archive ?
Normal intact PTH and low 24-hour urinary calcium excretion distinguishes patients with PHPT from those with less common familial hypocalciuric hypercalcemia.
Causes of hypercalcemia Primary hyperparathyroidism Malignancy * Hematologic cancers (non-Hodgkin's lymphoma, multiple myeloma, leukemia) * Squamous cell carcinomas (lung, esophagus, cervix, vulva, skin) * Adenocarcinomas (breast, kidneys, ovaries, bladder) * Parathyroid carcinoma Chronic renal failure Endocrine disorders (hyperthyroidism, pheochromocytoma, Addison's disease) Familial hypocalciuric hypercalcemia Immobilization Laboratory artifact resulting from altered albumin concentration or pH Medications (vitamin A toxicity [dietary fads, isotretinoin overdose], estrogens, antiestrogens, thiazides, lithium) Milk alkali syndrome Vitamin D toxicity (granulomatous disease [sarcoidosis, tuberculosis], vitamin D supplementation) Based on Hutton E, (1) and Carroll MF et al.
sensing receptor gene cause familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism.
Familial hypocalciuric hypercalcemia and other disorders with resistance to extracellular calcium.
Markedly reduced activity of mutant calcium-sensing receptor with an inserted Alu element from a kindred with familial hypocalciuric hypercalcemia and neonatal severe hyperparathyroidism.
Maximal urine-concentrating ability: familial hypocalciuric hypercalcemia versus typical primary hyperparathyroidism.
Mutations of the calcium-sensing receptor (CASR) in familial hypocalciuric hypercalcemia, neonatal severe hyperparathyroidism, and autosomal dominant hypocalcemia.
This G-protein-linked receptor is mutated in the disorders of familial hypocalciuric hypercalcemia (17), neonatal severe hyperparathyroidism, and autosomal dominant hypocalcemia (18,19).