Symptom Finder - Hypercalcemia
HYPERCALCEMIA
Hypercalcemia may result from disorders of calcium storage, intake, regulation, and transport.
Storage: Storage of calcium is in the bone. It follows that diseases that invade the bone will cause excessive release of calcium. Thus, metastatic carcinoma will cause an elevation of calcium in the blood.
Paget disease, by increasing the osteoclastic activity in the bone, may cause an elevated calcium level.
Intake: Increased intake of calcium usually does not cause hypercalcemia, but when associated with the milk–alkali syndrome or hypervitaminosis D, it may.
Regulation: Excessive secretion of parathyroid hormone (PTH) by the parathyroid gland or ectopic PTH secretion by a neoplasm elsewhere will cause hypercalcemia. Look for type 1 and type 11 multiple endocrine neoplasm syndrome in patients with parathyroid adenomas.
Transport: Half the calcium in the blood is transported by protein. It follows that the conditions with increased plasma protein (such as multiple myeloma and Boeck sarcoid) may be associated with hypercalcemia.
Approach to the Diagnosis
A history of neoplasm or clinical evidence of bone disease should alert one to the possibility of metastatic neoplasm. Symptoms of polyuria, polydipsia, weakness, pathologic fracture, and weight loss should suggest hyperparathyroidism. Hypercalcemia may also present with pancreatitis.
Serial calcium, phosphorus, and alkaline phosphatase levels and serum PTH assay and skeletal survey should pin down the diagnosis of hyperparathyroidism and metastatic neoplasm. A bone scan will also be helpful in identifying metastasis. A cortisone suppression test will help differentiate hyperparathyroidism from metastasis. The serum calcium will not be lowered by cortisone in hyperparathyroidism. A 24-hour urine calcium will be useful in differentiating familial hypocalciuria from hyperparathyroidism because the urine calcium will be high in the latter.
Other Useful Tests
1. CBC (myelophthisic anemia)
2. Sedimentation rate (neoplasm)
3. Chemistry profile (hyperparathyroidism)
4. Free thyroxine (T4) (hyperthyroidism)
5. Serum 25-hydroxy-calciferol (25-COH) vitamin D (hypervitaminosis D)
6. Protein electrophoresis (sarcoidosis, multiple myeloma)
7. MRI of the neck (parathyroid adenoma)
8. Endocrinology consult
Hypercalcemia may result from disorders of calcium storage, intake, regulation, and transport.
Storage: Storage of calcium is in the bone. It follows that diseases that invade the bone will cause excessive release of calcium. Thus, metastatic carcinoma will cause an elevation of calcium in the blood.
Paget disease, by increasing the osteoclastic activity in the bone, may cause an elevated calcium level.
Intake: Increased intake of calcium usually does not cause hypercalcemia, but when associated with the milk–alkali syndrome or hypervitaminosis D, it may.
Regulation: Excessive secretion of parathyroid hormone (PTH) by the parathyroid gland or ectopic PTH secretion by a neoplasm elsewhere will cause hypercalcemia. Look for type 1 and type 11 multiple endocrine neoplasm syndrome in patients with parathyroid adenomas.
Transport: Half the calcium in the blood is transported by protein. It follows that the conditions with increased plasma protein (such as multiple myeloma and Boeck sarcoid) may be associated with hypercalcemia.
Approach to the Diagnosis
A history of neoplasm or clinical evidence of bone disease should alert one to the possibility of metastatic neoplasm. Symptoms of polyuria, polydipsia, weakness, pathologic fracture, and weight loss should suggest hyperparathyroidism. Hypercalcemia may also present with pancreatitis.
Serial calcium, phosphorus, and alkaline phosphatase levels and serum PTH assay and skeletal survey should pin down the diagnosis of hyperparathyroidism and metastatic neoplasm. A bone scan will also be helpful in identifying metastasis. A cortisone suppression test will help differentiate hyperparathyroidism from metastasis. The serum calcium will not be lowered by cortisone in hyperparathyroidism. A 24-hour urine calcium will be useful in differentiating familial hypocalciuria from hyperparathyroidism because the urine calcium will be high in the latter.
Other Useful Tests
1. CBC (myelophthisic anemia)
2. Sedimentation rate (neoplasm)
3. Chemistry profile (hyperparathyroidism)
4. Free thyroxine (T4) (hyperthyroidism)
5. Serum 25-hydroxy-calciferol (25-COH) vitamin D (hypervitaminosis D)
6. Protein electrophoresis (sarcoidosis, multiple myeloma)
7. MRI of the neck (parathyroid adenoma)
8. Endocrinology consult
