A number of gastrointestinal and hepatic diseases cause disordered calcium and phosphate homeostasis, which ultimately leads to bone disease. As bariatric surgery becomes more common, this problem is likely to increase. The bones in such patients show a combination of osteoporosis and osteomalacia. Osteitis fibrosa does not occur, in contrast to renal osteodystrophy. The important common feature in this group of diseases appears to be malabsorption of calcium and vitamin D. Liver disease may, in addition, reduce the production of 25(OH)D from vitamin D, although its importance in patients other than those with terminal liver failure remains in dispute. The major explanation for the low 25(OH)D levels in patients with liver disease is the reduction in D-binding protein production, the major carrier of vitamin D metabolites in the blood. Free 25(OH)D is generally normal in patients with liver disease. The malabsorption of vitamin D is probably not limited to exogenous vitamin D as the liver secretes into bile a substantial number of vitamin D metabolites and conjugates that are normally reabsorbed in (presumably) the distal jejunum and ileum. Interference with this process could deplete the body of endogenous vitamin D metabolites in addition to limiting absorption of dietary vitamin D.
In mild forms of malabsorption, high doses of vitamin D (25,000–50,000 IU one to three times per week) should suffice to raise serum levels of 25(OH)D into the normal range. Many patients with severe disease do not respond to vitamin D. Clinical experience with the other metabolites is limited, but both calcitriol and calcifediol have been used successfully in doses similar to those recommended for treatment of renal osteodystrophy. Theoretically, calcifediol should be the drug of choice under these conditions, because no impairment of the renal metabolism of 25(OH)D to 1,25(OH)2D and 24,25(OH)2D exists in these patients. However, calcifediol is only approved in the United States for use in chronic kidney disease and secondary hyperparathyroidism. Both calcitriol and 24,25(OH)2D may be of importance in reversing the bone disease. Intramuscular injections of vitamin D would be an alternative form of therapy, but there are currently no FDA-approved intramuscular preparations available in the United States. The skin remains a good source of vitamin D production, although care is needed to prevent UVB overexposure (ie, by avoiding sunburn) to reduce the risk of photoaging and skin cancer.
As in the other diseases discussed, treatment of intestinal osteodystrophy with vitamin D and its metabolites should be accompanied by appropriate dietary calcium supplementation and monitoring of serum calcium and phosphate levels.