The clinical impact of metabolic bone disease in coeliac disease.

Bone mineral density was measured by dual energy x ray absorptiometry (DEXA) at the lumbar spine and femoral neck in 15 adults who had metabolic bone disease in association with coeliac disease (mean age at diagnosis 53.5 years, range 37 to 66). Results were expressed as a T score (the number of standard deviations by which patient's bone density differed from the sex matched young adult mean). Three patients had no skeletal symptoms and normal routine calcium biochemistry but severely reduced axial bone mineral density on DEXA. Eleven patients had symptomatic skeletal fractures, including fractures of proximal femur (3), vertebrae (4), and radius (6). Three patients had osteomalacia confirmed on bone biopsy, two of whom had characteristic biochemistry. Secondary and tertiary hyperparathyroidism were seen. Seventy five further patients (60 female) with coeliac disease (mean age 52.0 years, median duration of gluten-free diet 3.4 years) and 75 paired healthy age and sex matched controls were questioned on past fracture history. Patients with coeliac disease underwent detailed studies of calcium biochemistry, dietary intake, and bone mineral density. Sixteen had a past history of fractures (chi(2) = 10.7, p = 0.0004, v controls), which were of typical osteoporotic type. Ten patients had fracture before diagnosis of coeliac disease and six after diagnosis. Patients who had a fracture were older (56.3 v 50.3 years, p < 0.02, Wilcoxon rank sum test) than those with no fracture. There was no significant difference in bone mineral density (z score -0.31 v -0. 77), serum calcium (2.30 v 2.26 mmol/l), 25-hydroxyvitamin D (19.7 v 23.7 nmol/l), parathyroid hormone (2.6 v 3.1 pmol/l), or dietary calcium intake (1021.0 v 1033.0 mg/day) in patients with fracture compared with those without fracture. Metabolic bone disease is common in coeliac disease and is associated with premature osteoporotic fractures.

Effect of a gluten free diet on osteopenia in adults with newly diagnosed coeliac disease.

BACKGROUND/AIMS: Calcium and vitamin D malabsorption in coeliac disease predispose to skeletal demineralisation. This study aimed to determine bone mineral density in patients studied in the first year after diagnosis of coeliac disease, and to detect changes in bone mineral density over the subsequent year. METHODS: Lumbar spine and femoral neck bone mineral density was measured in 21 adults with coeliac disease, diagnosed and started on a gluten free diet during the preceding year, with dual energy x ray absorptiometry and repeated after 12 months. RESULTS: Bone mineral density was significantly lower in patients than in paired controls (matched for age and sex), at lumbar spine (0.819 g/cm2 compared with 1.021 g/cm2, p < 0.001 Wilcoxon signed rank test) and femoral neck (0.663 g/cm2 compared with 0.794 g/cm2, p < 0.001). Repeat measurement after 12 months demonstrated that patients had a significant gain in bone mineral density at lumbar spine (16.6%/year), and femoral neck (15.5%/year, p < 0.002, Wilcoxon signed rank test at both sites), whereas no significant change in bone mineral density was detected in controls. CONCLUSIONS: Treatment of coeliac disease with a gluten free diet is associated with a significant increase in bone mineral density, although patients still had lower bone mineral density than controls.

Osteoporosis in treated adult coeliac disease.

Forty five women and 10 men with coeliac disease diagnosed in adult life, who were already on a gluten free diet, had serial bone mineral density measurements at the lumbar spine and femoral neck over 12 months. Osteoporosis, defined as a bone mineral density (BMD) < or = 2 SD below the normal peak bone mass was found in 50% of male and 47% of female coeliac patients. Patients with a BMD < or = 2 SD below age and sex matched normal subjects, had a significantly lower body mass index (21.3 kg.m-2 compared with 25.2 kg.m-2, p < 0.02 Wilcoxon rank sum test) and lower average daily calcium intake (860 mg/day compared with 1054 mg/day, p < 0.05 Wilcoxon rank sum test) than patients with normal bone mineral density. In postmenopausal women with coeliac disease there was a strong correlation between the age at menopause and BMD at both the lumbar spine (r = 0.681, p < 0.01, Spearman's rank correlation) and femoral neck (r = 0.632, p < 0.01). No overall loss of bone was shown over the 12 months of follow up, and relative to the reference population there was a significant improvement in BMD at the lumbar spine in women (p < 0.025, paired t test) and at the femoral neck in men (p < 0.05, paired t test). There was a significant negative correlation between the annual percentage change in BMD at the lumbar spine and the duration of gluten free diet (r = -0.429, p<0.01, Spearman's rank correlation), with the largest gain in BMD in patients with most recently diagnosed coeliac disease. Osteoporosis was shown in 47% of patients with treated adult coeliac disease. Recognised risk factors for osteoporosis in the general population including low body mass index, dietary calcium intake, and early menopause are particularly important in coeliac disease. Treatment of coeliac disease with a gluten free diet probably protects against further bone loss, and in the early stages is associated with a gain in bone mineral density.