St. Barnabas Osteoporosis and Metabolic Bone Disease Center, Arthritis and Rheumatic Disease Center Livingston, New Jersey 07039
Address correspondence to: Marjorie Luckey, M.D., St. Barnabas Osteoporosis and Metabolic Bone Disease Center, Arthritis and Rheumatic Disease Center, 200 South Orange Avenue, Livingston, New Jersey 07039. E-mail: mluckey{at}sbhcs.com.
To the editor:
Dr. Barzel refers in his letter to his recently published study in Gerontology (1) that also identified a high prevalence of "significant underlying conditions" in patients referred to their university-based osteoporosis center. The prevalence of newly identified abnormalities was similar in our study (32%; Ref. 2) and theirs (25%), with a slightly higher prevalence perhaps due to the identification of low urinary calcium excretion and calcium malabsorption, which were not addressed in their study.
Dr. Barzel points out in his letter that the prevalence of vitamin D deficiency in their study (17.9%) is significantly greater than the 4.6% prevalence reported by us, despite the fact that both populations are from the New York City area. It is important to note, however, that the diagnostic cut-off used to define vitamin D deficiency differed in the two studies (25 OH vitamin D concentration of <16 ng/ml in his study; <12.5 ng/ml in ours). If we reanalyze our data using the less than 16 ng/ml criterion, 10% of our subjects had vitamin D deficiency.
Several important population differences could explain the remaining discrepancy in the incidence of vitamin D deficiency between these two studies. Subjects with diseases or taking medications known to impair absorption or metabolism of vitamin D (such as inflammatory bowel disease, malabsorption, hepatic dysfunction, and anticonvulsant use) were specifically excluded from our study. Also excluded were all patients referred to us for known osteomalacia or for abnormal laboratory results suggestive of vitamin D deficiency, which undoubtedly lowered the incidence of vitamin D deficiency in our population. There were no patient exclusion criteria reported by Freitag and Barzel (1). In addition, the mean age of their population was 6.3 yr older, which may also have resulted in a higher prevalence of vitamin D deficiency.
Dr. Barzel suggests that measurement of 25(OH) vitamin D be included in the evaluation of patients with osteoporosis, a recommendation with which we strongly agree. The costs and benefits of potential screening strategies are highly dependent on the diagnostic criteria used to define a clinically significant disorder. When this study was originally designed, the generally accepted value for vitamin D deficiency was a 25(OH) vitamin D level of less than 12.5 ng/liter (30 nmol/liter), based on its association with rickets and osteomalacia. Parfitt (3), however, has pointed out that mild to moderate degrees of vitamin D insufficiency produce osteoporosis, not osteomalacia. There is now evidence that vitamin D sufficiency requires levels ranging from approximately 3350 ng/ml (80120 nmol/liter), with lower levels associated with reduced calcium absorption, higher concentrations of PTH, and increased rates of bone resorption (4, 5, 6, 7, 8). On the basis of these studies, it is generally accepted that 25(OH) vitamin D values below 20 ng/ml indicate significant vitamin D deficiency. whereas values between 20 and 32 ng/ml (4880 nmol/liter) can be associated with metabolic consequences such as suboptimal calcium absorption and increased PTH secretion.
If we apply these newer diagnostic criteria to our data, 21% of our 173 subjects were vitamin D deficient, whereas an additional 34% had vitamin D insufficiency. At this diagnostic yield, the cost-effectiveness of 25(OH) vitamin D measurements is very high. In addition, there are important therapeutic implications to diagnosing vitamin D deficiency because currently recommended vitamin D supplementation may not produce adequate vitamin D levels in patients with vitamin D sufficiency (9, 10). Thus, 25(OH) vitamin D measurements should be included in the evaluation of osteoporotic patients to identify a correctable secondary cause of bone loss and to help to optimize therapy.
Received December 11, 2002.
References
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