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Bone Loss and Reduced Osteoblast Function in Primary Biliary Cirrhosis

STEPHEN F. HODGSON, M.D.; E. ROLLAND DICKSON, M.D.; HEINZ W. WAHNER, M.D.; KENNETH A. JOHNSON, M.D.; KENNETH G. MANN, Ph.D.; and B. LAWRENCE RIGGS, M.D.
[+] Article and Author Information

Grant support: In part by a grant from the R. K. Mellon Foundation and by grants RR-585 and AM-27065 from the Public Health Service.

▸Requests for reprints should be addressed to Stephen F. Hodgson, M.D.; Mayo Clinic, 200 First Street S.W.; Rochester, MN 55905.


Rochester, Minnesota


©1985 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1985;103(6_Part_1):855-860. doi:10.7326/0003-4819-103-6-855
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The association of bone loss with primary biliary cirrhosis is poorly understood. In 15 premenopausal female patients, only 2 of whom had fractures, mean bone mineral density was reduced at the lumbar spine but not at the midradius or distal radius. Bone loss was not statistically related to the duration or severity of liver disease. Urinary hydroxyproline excretion, an index for bone resorption, was not different from that of 15 age-matched normal women, but the serum concentration of bone Gla-protein (osteocalcin), a specific marker for bone turnover, was decreased (p < 0.001). Bone histomorphometric examination in 13 patients showed no osteomalacia but a reduced bone formation rate despite normal values for fractional osteoblast-osteoid interface. The substantial early loss of trabecular bone is mediated by a severe reduction in osteoblast function, which may be caused by retained toxic substances associated with cholestasis.

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