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Letter to the Editor |
Montefiore Medical Center and Albert Einstein College of Medicine Bronx, New York 10467
Address correspondence to: Uriel S. Barzel, M.D., Montefiore Medical Center, Montefiore Medical Group, Department of Medicine, 3400 Bainridge Avenue, Bronx, New York 10467-2490. E-mail: ubarzel{at}montefiore.org.
To the editor:
Based on a retrospective charts review, Tannenbaum et al. (1) propose groups of tests to identify secondary contributors to osteoporosis in otherwise healthy women. Having essentially the same objective in mind, we examined prospectively 272 patients who were referred to this University Hospital for evaluation of osteoporosis (2). Our patients’ age was 71.8 ± 11.9 yr (mean ± SD). Ninety-six percent of them were women. We carefully reviewed the medical history of each patient, paying special attention to history of thyroid disease, anticonvulsant therapy, glucocorticoid therapy, heparin therapy, kidney stones, and fractures. Each patient was subjected to an in-depth laboratory evaluation designed to identify the following conditions: osteomalacia, hyperparathyroidism, hypercalciuria, hyperthyroidism, hyperadrenocorticism, prolactinoma, anemia, and liver disease.
Our findings were that 17.9% of the patients had vitamin D deficiency, defined by us as 25-hydroxyvitamin D (25OHD) blood level less than 16 ng/ml. In this group, intact PTH blood level was 78.1 ± 16.4 pg/ml, compared with a level of 45.0 ± 35.0 pg/ml (P = 0.001) in the patient group with no underlying disease (75.4% of the total group). The elevation of PTH indicates that the low 25OHD was physiologically significant. Despite the limitation of 24-h urine collection (2, 3), we found that 6.3% of the patients had hypercalciuria, defined as urinary calcium excretion greater than 250 mg/24 h, ranging from 260–390 mg/24 h. The hypercalciuric patients were not significantly different from those without underlying disease in terms of age, T-score of the spine or the femur, serum calcium, 25OHD, or PTH. Two of our patients (0.7%) were found to have hyperparathyroidism. One patient on heparin therapy had had actively progressive osteoporosis with multiple fractures. Thyroid disease was not a significant contributor to the osteoporosis, and occult prolactinoma, occult hyperadrenocorticism, anemia, and liver disease were not found in our cohort.
We agree with Tannenbaum et al. that there is no way of identifying hypercalciuric patients other than by an adequate 24-h urine collection. The main difference between our prospective study and the retrospective study of Tannenbaum et al. is in the number of patients with low 25OHD. Having excluded patients with osteomalacia from their study, they identified only 4.6% of their subjects as having low 25OHD. This is much lower than the prevalence of vitamin D deficiency observed by us (17.9%) and that reported from the Midwest (4) and Boston (5, 6).
The conclusions of our study were therefore slightly different from those of Tannenbaum et al. We concluded that, at the minimum, patients with low bone density should have simultaneous determinations of blood calcium, 25OHD level, and 24-h urinary calcium excretion. [We have previously described the importance of thyroid function screening in the elderly (7).]
There is a tendency among primary physicians to assume that all patients with low bone density have osteoporosis and to treat them with antiresorptives or with selective estrogen receptor modulators, without subjecting them to any additional diagnostic workup. Our observation is that this is clearly inappropriate in approximately 25% of patients.
In summary, it should be recognized that densitometry identifies subjects with low bone density but does not provide the diagnostic information needed for the optimal treatment of each individual patient. Determinations of blood calcium, 25OHD level, and 24-h urinary calcium excretion are, in our opinion, the minimum workup required in such cases.
Received October 24, 2002.
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