Bone disease in prolonged parenteral nutrition: osteopenia without mineralization defect.
A metabolic bone disease characterized by a mineralization defect, low plasma 1,25(OH)2D, and hypercalciuria has been described in patients receiving prolonged total parenteral nutrition (TPN). Because the practice of TPN differs from center to center, we investigated 13 home TPN patients to determine whether they had similar or different bone abnormalities. They had received TPN for a mean period of 51 +/- 38 mo. Bone pain occurred in six patients and two had multiple vertebral and rib fractures (with trauma in one patient). Bone pain was mild to moderate and not incapacitating. Bone histomorphometry showed reduced bone volume, reduced osteoid with normal resorption and calcification rates. These abnormalities were associated with hypercalciuria, but the plasma levels of 1,25(OH)2D were normal. Abnormalities in bone metabolism in this group of patients suggest a fundamental decrease in bone matrix-formation rather than a mineralization defect as the underlying mechanism.
D000328:Adult; D000368:Aged; D001846:Bone Development; D001851:Bone Diseases, Metabolic / Q000209:etiology* / Q000378:metabolism; D001857:Bone Matrix / Q000503:physiopathology; D001842:Bone and Bones / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D004100:Dihydroxycholecalciferols / Q000097:blood; D005260:Female; D006699:Home Care Services; D006801:Humans; D008297:Male; D008875:Middle Aged; D008903:Minerals / Q000378:metabolism*; D010018:Osteomalacia / Q000209:etiology; D010281:Parathyroid Hormone / Q000097:blood; D010289:Parenteral Nutrition, Total / Q000009:adverse effects*; D010758:Phosphorus / Q000097:blood; D013997:Time Factors
D004100:Dihydroxycholecalciferols; D008903:Minerals; D010281:Parathyroid Hormone; D010758:Phosphorus; D002118:Calcium