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Metabolic Bone Disease in Viral Cirrhosis: A Prospective Study

DOI: 10.1155/2013/276563

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Abstract:

Background/Aim. Metabolic Bone disorders are well-recognized extrahepatic complications of cirrhosis. The aim was to report their prevalence and the associated factors to their development in patients with viral cirrhosis. Patients and Methods. All consecutive patients with viral cirrhosis were prospectively enrolled. Parathyroid hormone, 25-hydroxyvitamin D, liver function, and phosphocalcic tests were measured in all patients. Bone mineral density was measured at the lumbar spine and total hip by dual-energy X-ray absorptiometry. Data were analyzed using SPSS software. Results. Forty-six cirrhotic patients were included with hepatitis C (87%) and hepatitis B (13%). The Child-Pugh score was grade A in 87% of cases and grade B in 13%. Thirty-seven patients had decreased bone mineral density with osteopenia in 24 patients and osteoporosis in 13 patients. Decreased 25-hydroxyvitamin D was found in 95.6% of cases. Bone disorders were significantly more frequent in old patients with low body mass index, long duration of liver disease, and low 25-hydroxyvitamin D level. None of these factors was an independent factor associated with bone disorders. Conclusion. Our study revealed a high prevalence of metabolic bone disorders among viral cirrhotic patients. Consequently, bone mineral density assessment should be performed systematically in all cirrhotic patients. 1. Introduction The association between metabolic bone abnormalities and chronic liver disease is now well recognized. Often known as hepatic osteodystrophy, these disorders are a common complication of liver cirrhosis with a reported prevalence of 12% to 86% [1–4]. Osteoporosis is the well-known major complication of hepatic osteodystrophy. Its prevalence varies considerably and ranges from 20% to 50% [5]. It is related to the severity of cirrhosis and affects 38% of patients awaiting liver transplantation [6, 7]. Osteoporosis is characterized by low bone mass and microarchitectural deterioration of bone tissue leading to bone fragility and increased fracture risk, a source of morbidity and mortality in patients already weakened by their chronic liver disease. The pathogenesis of bone demineralization in cirrhosis remains incompletely understood. It is most often multifactorial and many factors affecting directly or indirectly bone turnover have been implicated: insulin growth factor-I, interleukin-1, tumor necrosis factor-α, and osteoprotegerin, which promote osteoclastic bone resorption in addition to the receptor activator of NF kappa beta (RANK) and the receptor activator of NF kappa beta ligand

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