Hypercalcemia with calcium supplementation

Calcium is contraindicated in patients with hypercalcemia or ventricular fibrillation and in patients taking digitalis. Calcium is used cautiously in patients with cardiac disease. Hypercalcemia may occur when calcium is administered with the thiazide diuretics. When calcium is administered with atenolol there is a decrease in Hie effect of atenolol, possibly resulting in decreased beta blockade. There is an increased risk of digitalis toxicity when digitalis preparations are administered with calcium. The clinical effect of verapamil may be decreased when the drug is administered with calcium. Concurrent ingestion of spinach or cereal may decrease file absorption of calcium supplements. 

PhosLo End-stage renal failure patients may develop hypercalcemia when given calcium with meals. Do not give other calcium supplements concurrently with PhosLo. Monitor serum calcium levels twice weekly during the early dose adjustment period. Do not allow serum calcium times phosphate product to exceed 66. 

There was hypercalcemia in 12% of 119 patients taking PTH1 g4 100 micrograms/day with daily calcium and vitamin D and in 14% of 59 taking additional alendronate. After stopping the calcium supplements only two women needed a dosage reduction of parathormone (14,17). 

The principal therapeutic concern is to restore normocalcemia and normophosphatemia. Under most circumstances, vitamin D (25,000-100,000 units three times per week) and dietary calcium supplements suffice. More rapid increments in serum calcium can be achieved with calcitriol, though it is not clear that this metabolite offers a substantial advantage over vitamin D itself for long-term therapy. Many patients treated with vitamin D develop episodes of hypercalcemia. This complication is more rapidly reversible with cessation of therapy using calcitriol rather than vitamin D. This would be of importance to the patient in whom such hypercalcemic crises are common. Dihydrotachysterol and 25(OH)D have not received much study as therapy for hypoparathyroidism, though both should be effective. Whether they offer advantages over vitamin D sufficient to justify their added expense remains to be seen. 

Although it might seem reasonable to treat osteoporosis with vitamin D, it must be realized that the primary funebon of vitamin D is to maintain plasma calcium levels, not to promote bone formation. An end-effect of vitamin D supplementa-hon is an increase in bone resorpbon and increased excretion of calcium in the urine. Calcium supplements should not be used indiscriminately Two types of persons should not receive calcium supplements persons with hypercalcemia and persons with kidney stones or a family history of kidney stones. These two issues are discussed in the following pages. 

However, calcium supplementation in combination with even therapeutic doses of hormonally active vitamin D compounds bears a high risk of acute hypercalcemia, which may be lethal if not immediately treated. 

Hyperparathyroidism is associated with hypercalcemia and, if symptoms are significant, is best managed by surgery. Vitamin D (and calcium) supplements are commonly used in postmenopausal patients. Vitamin D may counter the decreased intestinal absorption of calcium that occurs in menopause. The answer is (B). 

Mineral balance Severe hypercalcemia (4.95 mmol/l) was reported in a patient with a history of gastric banding for morbid obesity, hypertension, dyslipidemia, and hypothyroidism taking calcium supplements and hydrochlorothiazide [lO ]. The... 

Hypoparathyroidism has long been recognized as a disease which is difficult to manage with large doses of vitamin D and calcium supplements. Because the full effects of vitamin D are slow in both onset and reversal, considerable time may elapse before the action of a particular dose is established or the harmful effects of inadvertent overdose are relieved. 7 0.25—1.0 pg daily dose of la,25-dihydroxyvitamin D3 corrects the hypocalcemia of parathyroid insufficiency, and hypercalcemia resulting from overdose decreases quickly upon withdrawal of therapy. 

Dietary supplement (RDA) PO 1200 mg/day. Maximum 2.5 g/day. Hyperphosphatemia PO (calcium acetate) 2 tablets 3 times a day with meals. May increase gradually to bring serum phosphate level to less than 6 m dl as long as hypercalcemia does not develop. 

In healthy individuals - that is, with normal kidney function and with no history of nephrolithiasis - supplementation with up to 2-3 g calcium per day appears to be associated with only a minimal risk of hypercalcemia and kidney stone formation (Ringe... 

Following initiation of anti hypertensive therapy with thiazide diuretics, transient hypercalcemia has been seen in over one-third of patients (87). Two percent of patients receiving long-term thiazide diuretics administration had persistent hypercalcemia (68). In the elderly (especially women), combined administration of thiazides with vitamin 0 supplements (for osteoporosis) can have synergistic effects on the elevation of serum calcium levels resulting in severe hypercalcemia (69). Similarly, if the patient is predisposed to hypercalcemia (IHPT, 2HPT or immobilization), thiazides can precipitate significant and sustained hypercalcemia (68,70). 

Long-term consumption of approximately 1500-2000 mg calcium per day is safe for most individuals, although there will be some reduction in the efficiency of iron absorption. However, higher intakes from supplements (62.5 mmol or 2.5 g per day) can result in milk-alkali syndrome (MAS), with symptoms of hypercalcemia, renal insufficiency, metabolic alkalosis, and severe alterations in metabolism. Based on risk of developing MAS, the upper Hmit for calcium intake is 2500 mg per day for adults and children. 

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