Bone disease in burn patients

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Abstract
Burn patients are at risk for bone disease due to aluminum (AI) exposure from use of antacids and albumin, partial immobilization, and increased production of endogenous glucocorticoids. Moreover, severely burned children are growth impaired up to 3 years after the burn. To determine the extent of bone disease, we studied nine men and three women, ages 18–41 years, with greater than 50% body surface area burn. Seven patients underwent iliac crest bone biopsy following double tetracycline labeling, one additional patient expired after a single label, and three others had postmortem specimens obtained for quantitative AI only. Serial serum and urine samples were obtained weekly until biopsy or death. All biopsied patients had reduced bone formation and osteoid area, surface, and width, with mineral apposition rate, osteoblast surface, and osteoclast number with normal eroded surfaces compared to age‐ and sex‐matched normal ambulatory volunteers. Burn patients also had reduced bone formation, mineral apposition rate, osteoid area, and surface compared to age‐matched volunteers at short‐term bed rest. Serum levels of osteocalcin were low. Most patients had mild hypercalcemia but only a third had hypercalciuria. All patients had elevated AI in blood or urine; urine AI correlated inversely with serum osteocalcin. In 60% significant bone AI was detectable by stain or quantitation. Our data are compatible with burn patients having markedly reduced bone turnover. AI loading, partial immobilization, endogenous corticosteroids, and cytokine production may be among the etiologic factors.
Funding Information
  • National Institutes of Health (AR30692)