Hepatic Osteodystrophy

The mechanism of metabolic bone disease in patients with liver disease is multifactorial. The liver is a source of factors involved in bone remodeling and these factors are reduced in chronic liver disease. Patients with liver disease have impaired osteoblast proliferation and thus decreased bone formation. The liver is a source of insulin-like growth factor (IGF)-1, which is important in bone remodeling. Animal data suggest that the decrease in IGF-1 in cirrhosis results in decreased bone formation. In humans, however, the correlation between IGF-1 and osteopenia is less clear. OPG is also produced by the liver, and reductions in this may result in increased osteoclast activity. In general cholestatic liver diseases are associated with lower BMD than noncholestatic liver diseases. In particular patients with PBC appear to have decreased BMD but this may also occur because patients are generally older, postmenopausal women. There are also data to suggest that patients with PBC or autoimmune hepatitis are at an increased risk of celiac disease, both of which may contribute to low BMD. Liver transplantation, although beneficial for treatment of the underlying liver disease, appears to worsen BMD especially within the 2 years following the orthotopic liver transplantation (OLT). These data likely reflect the use of glucocorticoids and calcineurin inhibitors following OLT (discussed later in this chapter).

Repeat bone mineral density annually

FIGURE 55-2. Diagnostic algorithm for metabolic bone disease. Ca++ = calcium; DXA = dual-energy x-ray absorptiometry; OLT = orthotopic liver transplantation; PBC = primary biliary cirrhosis; PTH = parathyroid hormone.

Repeat bone mineral density annually

FIGURE 55-2. Diagnostic algorithm for metabolic bone disease. Ca++ = calcium; DXA = dual-energy x-ray absorptiometry; OLT = orthotopic liver transplantation; PBC = primary biliary cirrhosis; PTH = parathyroid hormone.

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Constipation Prescription

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