Metabolic Bone Disease

Metabolic bone disease is a condition of bone demineralization leading to osteomalacia, osteopenia, or osteoporosis in patients receiving long-term PN. Metabolic bone disease, to some degree, may occur in as many as 40% to 100% of patients receiving long-term PN.3 Often patients are asymptomatic, although symptoms can include bone pain, back pain, and fractures. Patients often will have increased serum alkaline phosphatase concentrations, low to normal parathyroid hormone (PTH) concentrations, normal 25-hydroxy vitamin D, low 1,25 dihydroxyvitamin D concentra tions, hyper-calcemia or hypocalcemia, and hypercalcuria.41 Because patients may be asymptomatic, diagnosis can be incidental. Radiologic techniques commonly used in diagnosing bone disease include quantitative computed tomography (CT) and bone mineral density.41

Factors that can predispose patients to developing metabolic bone disease include deficiencies of phosphorus, calcium, and vitamin D; vitamin D and/or aluminum toxicity; amino acids and hyperosmolar dextrose infusions; chronic metabolic acidos-

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is; corticosteroid therapy; and lack of mobility. ' Calcium deficiency (due to decreased intake or increased urinary excretion) is one of the major causes of metabolic bone disease in patients receiving PN. Provide adequate calcium and phosphate with PN to improve bone mineralization and help to prevent metabolic bone disease. Administration of amino acids and chronic metabolic acidosis also appear to play an important role. Provide adequate amounts of acetate in PN admixtures to maintain acid-base balance.

Vitamin D toxicity has been suggested as a cause of metabolic bone disease. However, vitamin D deficiency results in bone loss, and data on vitamin D excess and metabolic bone disease remain controversial.

Aluminum toxicity appears to play a role in the development of metabolic bone

disease in patients on long-term PN, possibly by impairing calcium bone fixation, inhibiting the conversion of 25-hydroxyvitamin D to the active 1,25-dihydroxyvitamin D, and/or reducing PTH secretion.38,43 The FDA has been investigating the issue of aluminum contamination in parenteral products and issued a rule specifying acceptable aluminum concentrations in large-volume parenterals in the year 2000.4 The rule further stated that the package insert ("Precautions") for large-volume parenterals used in making PN should indicate that the product contains no more than 25 mcg/L of aluminum and defined a safe upper limit for par-enteral aluminum intake at less than 4 to 5 mcg/kg/day. This has required a great amount of effort by manufacturers to meet these limits and requires pharmacy policies for monitoring aluminum concentrations in PN admixtures. Pharmacies should use products with the lowest labeled aluminum content for the making of PN. Patients who are chronically dependent on PN should have their serum aluminum concentrations routinely monitored or whenever metabolic bone disease is suspected or diagnosed.

Encourage patients on long-term PN to engage in regular low-intensity exercise. Yearly bone density measurements also should be performed on patients on long-term PN and when metabolic bone disease is suspected.

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