OSTEODYSTROPHY IN PATIENTS WITH CHRONIC HEPATITIS AND LIVER-CIRRHOSIS

Bone mineral density (BMD) of the lumber vertebrae and factors related to bone metabolism were determined in patients with chronic viral hep atitis and patients with liver cirrhosis to clarify correlations betwe en hepatic dysfunction, considered to be one of the causes of hepatic osteodystrophy, and decrease in bone mass. BMD of the second to fourth lumbar vertebrae was determined with a Lunar (Madison, WI, USA) DPX, a dual-energy X-ray absorptiometry diagnostic system. BMD was signific antly lowest in patients with liver cirrhosis, followed by patients wi th chronic hepatitis, and healthy subjects, in this order. There was a significantly positive but weak correlation between albumin and BMD. Levels of 25(OH)D and 1,25(OH)(2)D were significantly lower in patient s with liver cirrhosis than in those with chronic hepatitis. BMD and v itamin D were decreased in all patients whose cholinesterase (ChE) was below 0.3 Delta pH. Urinary pyridinoline(Upyr) was significantly high er in the patients with liver cirrhosis, in whom bone mass was decreas ed, than in the patients with chronic hepatitis, whereas serum osteoca lcin levels were distributed in the upper normal range in patients wit h chronic hepatitis and those with liver cirrhosis. There was a positi ve correlation between 25(OH)D and serum osteocalcin levels in patient s with liver cirrhosis. These results indicate that osteogenesis is de creased and suggest that the decrease in BMD which occurs in viral liv er cirrhosis, probably related to decreased, bone formation and slight promotion of bone resorption, reflects deranged hepatic function. Thi s is the first report of Upyr and urinary deoxypyridinoline (UDpyr) de termination in patients with liver cirrhosis and patients with chronic hepatitis. The negative correlation of Upyr and UDpyr with ChE is a n ovel finding.