We performed a retrospective study of 237 patients attending a specialty os
teoporosis practice. Secondary causes for reduced bone mineral density (BMD
) were evaluated in 196 postmenopausal women and 41 premenopausal women; me
an age was 56 +/- 13.8 years (mean +/- SD). BMD was measured by dual-energy
X-ray absorptiometry (DXA) (QDR 1000W/2000 Hologic). Levels of intact para
thyroid hormone (iPTH), calcidiol [25(OH)D], thyroid-stimulating hormone, a
nd 24-hour urinary calcium were measured, and serum and urine protein (SPEP
and UPEP) electrophoresis were performed. Overall, 16% of our patients had
25(OH)D levels <15 ng/ml, the lowest acceptable vitamin D level without a
concomitant rise in iPTK levels. Among the osteoporotic patients (T score <
-2.5 SD), 17% had 25(OH)D levels <15 ng/ml and 7% <10 ng/ml. Among the oste
openic patients (-2.5 < T < -1.0 SD), 11% had 25(OH)D levels <15 ng/ml. Sev
enteen percent of patients with Z score less than or equal to-1.0 SD (low r
ange normal value) had 25(OH)D levels <15 ng/ml. Low 25(OH)D levels were in
versely related to high iPTH values (r = 0.30, P < 0.0001). Hypercalciuria
was present in 15% of our patients, elevations of PTH levels (>65 pg/ml, up
per normal limit of assay) were present in 11.5%, and hyperthyroidism in 4%
. A 25(OH)D level of <25 ng/ml in women (n = 86) with no known secondary ca
uses of low BMD was associated with an iPTH level above 49 pg/ml. The measu
rement of 25(OH)D levels is recommended in the evaluation of secondary caus
es for reduced BMD. Supplementation with vitamin D appears needed to keep 2
5(OH)D above 25 ng/ml, the level required to prevent increments in iPTH lev
els.