Prevention of Early Loss of Bone Mineral Density After Liver Transplantation by Prostaglandin E1

• Published in: Transplantation proceedings 2007-03, Vol.39 (2), p.540-543
• Main Authors: Hommann, M, Kämmerer, D, Lehmann, G, Kornberg, A, Küpper, B, Daffner, W, Wolf, G, Settmacher, U
• Format: Article
• Language: English
• Subjects: Alprostadil - therapeutic use; Biological and medical sciences; Bone Density - drug effects; Female; Femur; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Humans; Liver Transplantation - physiology; Lumbar Vertebrae; Male; Medical sciences; Middle Aged; Osteoporosis - prevention & control; Platelet Aggregation Inhibitors - therapeutic use; Postoperative Complications - prevention & control; Prevention and actions; Public health. Hygiene; Public health. Hygiene-occupational medicine; Surgery; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases; Tissue, organ and graft immunology
• ISSN: 0041-1345; 1873-2623
• DOI: 10.1016/j.transproceed.2006.12.016

Abstract Introduction As a result of preexisting chronic liver disease and immunosuppression, the majority of liver transplant patients develop bone mineral density (BMD) loss in the first 3 to 6 months posttransplantation, leading to an increased fracture risk. Using basic prophylaxis and treatment by administration of vitamin D, calcium, and bisphosphonates, BMD loss may be controlled in the long term. In contrast, there is no established medical concept for prevention of early posttransplant BMD loss. Material and Methods The aim of this trial was to evaluate the effect of prostaglandin E1 on BMD after liver transplantation. Between 1998 and 2004, 29 patients were enrolled in this study. BMD measurement was performed at lumbar spine and femoral neck using dual energy x-ray absorptometry pretransplant, and 3, 6, 12, and 24 months posttransplant. All patients received calcium and vitamin D as basic prophylaxis. In 13 patients, prostaglandin E1 (PGE) was additionally administered for 12 days posttransplant. Results BMD loss was significantly lower at 3 and 6 months posttransplant in the PGE group (lumbar spine, P < .03; femoral neck, P < .009). Development of BMD loss was comparable between both groups during further follow-up. In the PGE group there was a significantly lower fracture rate compared with the controls ( P < .02). Conclusion The application of PGE 1 proved to be beneficial in compensating the early posttransplant BMD loss and in subsequently reducing fracture rate. These positive effects of PGE 1 could be demonstrated in both the femoral neck and lumbar spine.