Ba. Duresmith et al., CALCIUM DEFICIENCY IN FLUORIDE-TREATED OSTEOPOROTIC PATIENTS DESPITE CALCIUM SUPPLEMENTATION, The Journal of clinical endocrinology and metabolism, 81(1), 1996, pp. 269-275
To test the hypothesis that the osteogenic response to fluoride can in
crease the skeletal requirement for calcium, resulting in a general st
ate of calcium deficiency and secondary hyperparathyroidism, we assess
ed calcium deficiency, spinal bone density by quantitative computed to
mography, and serum PTH in three groups of osteoporotic subjects. Two
of the three groups had been treated with fluoride and calcium (at lea
st 1500 mg/day) for 32 +/- 19 months. Group I consisted of 16 fluoride
-treated subjects who had shown rapid increases in spinal bone density
(+3.8 +/- 2.6 mg/cm(3) month), group II consisted of 10 fluoride-trea
ted subjects who had shown decreases or only slow increases in spinal
bone density (-0.05 +/- 0.6 mg/cm(3) month), and group III consisted o
f 10 age-matched untreated osteoporotic controls. Calcium deficiency w
as assessed by measurement of calcium retention after calcium infusion
. The results of our studies showed that 1) 94% of the subjects in Gro
up I were calcium deficient compared with only 30% in groups II and II
I (P < 0.01 for each); 2) the subjects in group I retained more calciu
m (79%) than the subjects in group II (60%, P < 0.001) or the subjects
in group III (64%, P < 0.005); 3) calcium retention was proportional
to serum PTH (r = 0.37, n = 36, P < 0.03); and 4) calcium retention wa
s proportional to the (previous) fluoride-dependent increase in quanti
tative computed tomography spinal bone density (in groups I and II, r
= 0.48, n = 26, P < 0.02). To test the hypothesis that the calcium def
iciency and the secondary hyperparathyroidism that were associated wit
h the positive response to fluoride would respond to concomitant calci
triol treatment, a subgroup of 7 calcium-deficient subjects were selec
ted from group I and treated with calcitriol (plus fluoride and calciu
m) for an average of 7 months. The calcitriol therapy reduced the calc
ium deficit in all 7 subjects, decreasing calcium retention from 80% t
o 62% (P < 0.02), and decreasing PTH from 50 to 28 pg/mL (P < 0.02). T
ogether, these data indicate that fluoride-treated osteoporotic subjec
ts may develop calcium deficiency in proportion to the effect of fluor
ide to increase bone formation, and this calcium deficit is responsive
to calcitriol therapy.