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J Hepatol. 2001 Feb;34(2):292-8.

A controlled trial of calcitonin therapy for the prevention of post-liver transplantation atraumatic fractures in patients with primary biliary cirrhosis and primary sclerosing cholangitis.

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  • 1Division of Gastroenterology, Mayo Medical Center, Rochester, MN 55905, USA.



Accelerated bone loss occurs early after liver transplantation (OLT) and, in cholestatic patients with pre-existing osteopenia, causes spontaneous fracturing. This study aimed to investigate the efficacy of calcitonin, a powerful inhibitor of bone resorption, in preventing or reducing the accelerated rate of bone loss and fracturing which occurs in patients with primary biliary cirrhosis and primary sclerosing cholangitis early after OLT.


Sixty-three patients undergoing OLT for primary biliary cirrhosis (n = 26) and primary sclerosing cholarigitis (n = 37) were randomized to receive: (a), 100 IU/day of salmon calcitonin subcutaneously for the first 6 months posttransplant; or (b), no therapy. At pretransplant, and at 4 and 12 months after OLT, patients were investigated clinically, biochemically, by bone mineral density of the lumbar spine, and by radiographs of the thoracolumbar spine, chest and site of any bone pain.


The bone mineral density of the lumbar spine fell equally at 4 months in both groups, from 0.85 to 0.81 g/cm2 in calcitonin-treated patients (n = 29) and from 0.88 to 0.82 g/cm2 in controls (n = 34); at 12 months, both groups had stabilized to 0.83 g/cm2. Fracturing was the same in both groups.


Calcitonin therapy for the first 6 months after OLT is unable to prevent or reduce accelerated bone loss or spontaneous fractures which occur in the first posttransplant year.

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