This article is from the Interpretation Of Lab Test Profiles, by Ed Uthman firstname.lastname@example.org with numerous contributions by others.
Hypercalcemia is seen in malignant neoplasms (with or without
bone involvement), primary and tertiary hyperparathyroidism,
sarcoidosis, vitamin D intoxication, milk-alkali syndrome,
Paget's disease of bone (with immobilization), thyrotoxicosis,
acromegaly, and diuretic phase of renal acute tubular necrosis.
For a given total calcium level, acidosis increases the
physiologically active ionized form of calcium. Prolonged
tourniquet pressure during venipuncture may spuriously increase
total calcium. Drugs producing hypercalcemia include alkaline
antacids, DES, diuretics (chronic administration), estrogens
(incl. oral contraceptives), and progesterone.
Hypocalcemia must be interpreted in relation to serum albumin
concentration (Some laboratories report a "corrected calcium" or
"adjusted calcium" which relate the calcium assay to a normal
albumin. The normal albumin, and hence the calculation, varies
from laboratory to laboratory). True decrease in the
physiologically active ionized form of Ca++ occurs in many
situations, including hypoparathyroidism, vitamin D deficiency,
chronic renal failure, Mg++ deficiency, prolonged anticonvulsant
therapy, acute pancreatitis, massive transfusion, alcoholism,
etc. Drugs producing hypocalcemiainclude most diuretics,
estrogens, fluorides, glucose, insulin, excessive laxatives,
magnesium salts, methicillin, and phosphates.