[Treatment of malignancy-associated hypercalcemia].
Malignancy-associated hypercalcemia (MAH) is caused by tumor over-production of parathyroid hormone-related protein (PTHrP), or by locally enhanced bone resorption in metastatic lesions of solid cancers. Medical treatment of MAH includes hydration by saline infusion, loop diuretics to promote urinary calcium excretion and anti-resorptives such as calcitonin and bisphosphonates. Particularly, bisphosphonates are the current mainstay for MAH treatment : they not only inhibit osteoclastic bone resorption to ameliorate hypercalcemia but can also alleviate bone pain and can even prevent cancer cell expansion in bone metastatic lesions.
Endo
Itsuro
I
University of Tokushima, Graduate School Institute of Health Biosciences, Department of Medicine and Bioregulatory Sciences.
Inoue
Daisuke
D
D001859:Bone Neoplasms / Q000188:drug therapy / Q000556:secondary; D001862:Bone Resorption; D002116:Calcitonin / Q000627:therapeutic use; D004164:Diphosphonates / Q000627:therapeutic use; D015195:Drug Design; D004359:Drug Therapy, Combination; D005440:Fluid Therapy; D006023:Glycoproteins / Q000627:therapeutic use; D006801:Humans; D006934:Hypercalcemia / Q000209:etiology* / Q000628:therapy*; D009369:Neoplasms / Q000150:complications*; D053244:Osteoprotegerin; D044162:Parathyroid Hormone-Related Protein; D018160:Receptors, Cytoplasmic and Nuclear / Q000627:therapeutic use; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D012965:Sodium Chloride / Q000008:administration & dosage; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000627:therapeutic use
D004164:Diphosphonates; D006023:Glycoproteins; D053244:Osteoprotegerin; D044162:Parathyroid Hormone-Related Protein; D018160:Receptors, Cytoplasmic and Nuclear; D018124:Receptors, Tumor Necrosis Factor; D049994:Sodium Potassium Chloride Symporter Inhibitors; C506030:TNFRSF11B protein, human; D012965:Sodium Chloride; D002116:Calcitonin