Journal of the New Zealand Medical Association, 18-June-2004, Vol 117 No 1196
Osteomalacia: recovery of bone density
A 78-year-old Caucasian woman presented to Tokoroa Hospital with long-term severe back pain, proximal limb myopathy, and walking difficulty—associated with biochemical features of osteomalacia and radionucleide bone scan pseudofractures.
In the preceding 25 years, she had sustained four separate fractures of bone after minor trauma, indicating preceding postmenopausal osteoporosis. Serum calcium at 76 years was 2.41 mmol/L, and phosphate was 1.37 mmol/L.
At 78 years of age, her pre-treatment biochemical results were: serum calcium (corrected) = 1.98 mmol/L (n = 2.15–2.57), phosphate = 0.93 mmol/L (n = 0.9–1.55), alkaline phosphatase (ALP) = 457 u/L (n = 40–120 u/L), parathyroid hormone (PTH) = 66 pmol/L (n=1.2–6.2), creatinine = 0.08 mmol/L, 25 hydroxy vitamin D = 5.5 nmol/L (n>50), 1,25 dihydroxy vitamin D = 55 pmol/L (n= 40–155).
Pre-treatment dual energy absorption (DXA) test for bone mineral density (BMD): at lumbar spine L2–L4, mean BMD = 0.4676 g/cm2, T score = -3.69. Proximal radius/ulnar: BMD = 0.2627g/cm2, T score = -7.20.
Treatment was commenced with oral calcium 1.0 g/day; oral vitamin D 2, 50,000 u/day for 7 days and thereafter 800 u/day; plus oral alendronate 70 mg/week (single dose). Therapy was maintained for 24 months.
Table 1. Effect of treatment on bone mineral density (BMD) at lumbar spine (L2–L4)
Observations made throughout treatment:
Vitamin D deficiency is common in elderly people in Australasia.1 Lack of sunlight, poor vitamin D intake, and diminished ageing skin response to sunlight contribute.
Oral calcium and vitamin D2 is efficient in restoring vitamin D status,2 occurring within 4 weeks here, accompanied by inhibition of secondary hyperparathyroidism.
Prolonged therapy thereafter continued to increase lumbar BMD. Alendronate, a potent inhibitor of calcium-resorbing osteoclasts, contributed to some rise in BMD (about 9.6% over 3 years) resulting from osteoporosis.3
When monitoring long-term bone recovery BMD measurements are superior to ALP, which underestimates the duration of the skeletal recovery process. ALP fell to normal by 5 months. At 4 months, lumbar spine BMD had increased to 26.4%; at 10 months, BMD was 46.1%; and at 24 months, BMD was 61.8%.
Back pain disappeared completely at 4 weeks when vitamin D status had returned to normal. ALP rose at 2 weeks (to 540u/L), and at 4 weeks (to 499 u/L), indicating that ALP is sensitive indicator for early bone response. Lumbar spine BMD had probably risen (as judged by an increase in BMD at 2 months of 24.8%).
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