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Letters to the Editor |
Laboratoire d’Explorations Fonctionnelles, Hôpital Necker-Enfants malades Catherine Cormier, Service de Rhumathologie A, Hôpital Cochin, Assistance Publique-Hôpitaux de Paris, 75015 Paris, France
Address correspondence to: Jean-Claude Souberbielle, Laboratoire d’Explorations Fonctionnelles, Hôpital Necker-Enfants malades, 149 rue de Sèvres, 75015 Paris, France.
To the editor:
We would like to thank Drs. Glendenning and Vasikaran for their interest and comments concerning our paper, which appeared in the July 2001 issue of JCEM (1). The basis of our reasoning was that 1) given the high frequency of vitamin D insufficiency in an apparently healthy elderly population, a condition that remains ignored if 25 hydroxy vitamin D (25OHD) is not measured, and 2) given that vitamin D insufficiency induces secondary hyperparathyroidism (2), only subjects without vitamin D insufficiency (which means that 25OHD must have been measured beforehand) should be recruited to participate in a reference population to establish reference values for serum PTH. By doing that, we found in apparently healthy elderly subjects, that the upper limit (97th percentile) for serum PTH in those without vitamin D insufficiency was approximately 70% of the PTH concentration commonly considered as the upper normal limit, which suggests an overestimation of normal PTH values when vitamin D status is not taken into account. Although we have not tested subjects aged less than 60 yr, we agree with our Australian colleagues that vitamin D status should also be considered in younger subjects. However, whether the same cutoff for serum 25OHD should be used in old and younger subjects deserves additional studies.
Like us, Drs. Glendenning and Vasikaran found that their calculated PTH range was lowered (to a similar extent than in our study) when they excluded individuals with low serum 25OHD from their reference group. However, their 25OHD cutoff (50 nM or 20 ng/ml), similar to what was already reported by others (3), was somewhat higher than ours (30 nM or 12 ng/liter), and this raises an important issue regarding the definition of vitamin D insufficiency, which, for different reasons, depends on the 25OHD assay used. Indeed, one cause for the discrepancy between our respective cutoff values may be that they used the DiaSorin RIA (radiocompetitive immunoassay after a simple extraction by acetonitrile), whereas we used our in-house radiocompetition assay (after a more complex extraction step). To go further with this hypothesis, we recently compared our assay with the DiaSorin RIA on 40 serum samples. The two assays were well correlated (r2 = 0.85), but the DiaSorin kit gave values that were 1.29 times higher than with our in-house assay (mean ± SE: 42.2 ± 4.2 nM vs. 54.5 ± 4.7 nM for our assay and the DiaSorin kit, respectively). Because both assays recognize equally vitamin D2 and D3, this difference should not be related to a specificity problem as pointed out for other 25OHD assays (4), but is rather likely due to differences in calibration and/or in the extraction/purification procedures, underlining the need for a careful interlaboratory cross-calibration as already proposed (5). Nevertheless, when expressed as "DiaSorin equivalent," our 25OHD cutoff value becomes approximately 39 nM, which is closer to, but still different from, our Australian colleagues’ cutoff value. How the definition of vitamin D insufficiency (i.e. the 25OHD concentration below which PTH statistically rises in a population) can be so different in two populations, while the same 25OHD assay is used, remains unclear but argues for the need for further work in this field to propose a consensus.
Received September 20, 2001.
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