Endocrine Abstracts

Bone densitometry (DEXA) is the best method available today for diagnosing low bone density. However, DEXA is not able to differentiate osteoporosis from osteomalacia. The definitive diagnosis of osteomalacia is made by bone biopsy – rarely used in medical practice – which shows excess unmineralized bone. Tests of blood and urine may also be helpful: concentration of serum and urinary calcium and phosphorus, 25-hydroxyvitamin D and parathyroid hormone blood levels and bone turnover markers. We present the case of a patient with important bone loss of multiple causes, osteomalacia being the most important of them.

Case report: Forty-three years woman, with precocious menopause at age 29 years and protein-losing exudative enteropathy at age 31 years presented with important bone loss (lumbar T score=−4.8 and Z score=−3.8). She was under quasi-continuous cortisone therapy (Prednisone 10–15 mg/day). Laboratory results included: low normal/slightly decreased serum calcium and phosphorus, extremely low 25-hydroxyvitamin D level and secondary hyperparathyroidism. After one year of oral treatment with bisphosphonates, high doses of calcium (2000–3000 mg/day) and cholecalciferol (2000 UI/day), lumbar T score was −3.1, Z score=−2.2 and 25-hydroxyvitamin D level was still low. We switched oral to parenteral cholecalciferol therapy, also in high doses: 400.000 then 600.000 UI/month. The results were spectacular: normalization of plasma 25-hydroxyvitamin D level and of lumbar T score: −0.1.

Although early installed estrogen deficiency and chronic corticotherapy are determinants of bone loss, in this case the main cause was vitamin D deficiency secondary to it’s malabsorption in inflammatory bowel disease.

Conclusion: We emphasize the importance of assessing vitamin D status in all patients with osteoporosis diagnosed by DEXA. Adequate doses of vitamin D supplementation are indispensable for therapeutic succes.