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Bone Loss in Celiac Disease Is Related to Secondary Hyperparathyroidism
Author(s) -
Selby Peter L.,
Davies Michael,
Adams Judith E.,
Mawer E. Barbara
Publication year - 1999
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.1999.14.4.652
Subject(s) - medicine , bone density , endocrinology , malabsorption , forearm , parathyroid hormone , bone disease , secondary hyperparathyroidism , hyperparathyroidism , bone mineral , metabolic bone disease , femoral neck , osteopenia , osteoporosis , vitamin d and neurology , calcium , anatomy
Celiac disease is a major cause of intestinal malabsorption. Previous studies have demonstrated that celiac disease is associated with significant osteoporotic bone loss. These studies have suggested that successful treatment of the malabsorption is associated with amelioration of the bone loss. Such studies have failed to examine bone mass at peripheral skeletal sites which is more likely to be responsive to changes in parathyroid hormone (PTH) in response to calcium malabsorption. We have examined bone density in the lumbar spine, femoral neck, and distal forearm in 35 patients with celiac disease who had been established on gluten‐free diet. In addition, the concentrations of PTH and 1,25‐dihydroxyvitamin D (1,25(OH) 2 D) were measured. Bone density was below that expected for the subject's age and gender at all sites. This was most marked in the distal forearm where the bone density was 1.40 SD below expected ( p < 0.0001). In the forearm, there was a negative relationship between bone density and PTH concentration ( r = −0.49, p = 0.009). In the forearm and lumbar spine, there was a negative relationship between 1,25(OH) 2 D concentration and bone density. Bone mass was not related to the concentration of 25‐hydroxyvitamin D at any of the skeletal sites measured. Bone density is reduced in the peripheral skeleton in celiac disease and this deficit persists despite treatment with apparent normalization at axial skeletal sites. This reduction in bone mass is related to the presence of secondary hyperparathyroidism which should be sought in all patients with treated celiac disease.