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Letters to the Editor |
Department of Reproductive Medicine and Pediatrics "Santa Chiara" Hospital I-56125 Pisa, Italy
We thank Dr. Finkelstein and coworkers for their letter, giving us the opportunity to discuss some aspects of bone mineral density (BMD) in young men with histories of constitutional delay of puberty (CDP).
As indicated in the letter (above), there is evident discrepancy between our data (1) and those of Finkelstein et al. (2, 3). We found reduced lumbar BMD area but normal BMD volume in young men with CDP (1), while they reported that both lumbar BMD area (2, 3) and BMD volume (letter) were decreased. In agreement with our data, Moore et al. (4) showed reduced lumbar BMD area and normal BMD volume in young men with histories of CDP; they also found normal femoral neck BMD volume (4).
In their letter, Finkelstein et al. suggest that androgen therapies administered to some of our patients during puberty may have influenced BMD measurement in young adulthood. We think this hypothesis is incorrect. In fact, no significant difference, in both BMD area and BMD volume at lumbar spine (1, 4) and femoral neck (4), has been found between men who received androgens during puberty and those left untreated. Finkelstein et al. also suggest that our results might be the consequence of the mean age of the control group. On this matter, we used the same criteria proposed by Finkelstein et al. (2) in selecting the controls. In addition, all the controls had attained final height before the BMD measurement and were more than 17 yr old. Thus, they were approaching their peak lumbar BMD (5, 6). Indeed, comparing lumbar BMD values of adolescents and adult men, it has been shown that lumbar peak bone mass is achieved by the age 17 yr in males (6). Finkelstein et al. (3) also wrote "the peak bone density of the spine and the femoral neck is usually reached between the ages of 16–18 yr in boys" (3). Thus, it is unlikely that the cause of the discrepancy between Finkelstein’s (2, 3) and our data lies in the age of controls (19 yr). However, we are following up both patients and controls to elucidate this aspect.
Furthermore, keep in mind that both lumbar BMD area and BMD volume are surrogates of the true bone density (7). The calculation of BMD volume by the ancillary data of dual energy x-ray absorptiometry reflects only an estimation of true bone density (1, 7). To correct BMD area values, we used the mathematical Kroger’s formula (8) assuming the vertebral body as a cylinder. The data of Moore et al. (4) were also done with the formula of Kroger et al. (8). Finkelstein et al. calculated BMD volume (letter) by using the formula of Carter et al. (9), assuming the vertebral body as a cube. Because the lumbar spine vertebral body is neither a cylinder nor a cube (10), the discrepancy may be due, at least in part, to technical differences in estimating lumbar BMD volume. There may be differences in bone mass (weight of bone), which is caused by different bone sizes not entirely normalized by mathematical methods of correction, instead of true differences in bone density, which is fairly constant from birth to adulthood (11). Vertebral quantitative computed tomography analysis may give additional information on real BMD in patients with CDP, clarifying the inferences derived from the mathematical models used to estimate bone volume in these patients with altered growth pattern (12). Because this technique requires high radiation exposure, we have some concerns about its use in adolescents and young adults who are in good health except for their history of CDP and who have shown neither increased fracture rate (1) nor abnormalities in the serum levels of biochemical bone markers (1, 3).
CDP remains an intriguing diagnosis (13, 14). Under this diagnosis likely falls a mix of patients affected by various disorders associated with short stature and pubertal delay (e.g. partial gonadotropin deficiency, partial growth hormone deficiency, and a combination of CDP and familial short stature) (13, 14). Asymptomatic coeliac disease may also cause growth and pubertal delay (15). Because all these disorders can impair bone mass acquisition, selection of patients may affect BMD measurements. Geographical and life-style differences may be additional causes. As stated in our paper (1), longitudinal studies on carefully selected patients should be done to understand the behavior of BMD in CDP from preadolescence to young adulthood.
Finally, we apologize for the incorrect citation. At any rate, the statement of Finkelstein et al. (2) that "many adult men (with history of CDP) may have lower than average peak bone mineral density and thus may be at increased risk for osteoporotic fractures" has been used as a strong argument for therapeutic intervention in CDP, at least in Europe.
Footnotes
Address correspondence to: Dr. Silvano Bertelloni, Department of Reproductive Medicine and Pediatrics, University of Pisa, "Santa Chiara" Hospital, Via Roma, 67, Pisa, Italy I-56125.
Received May 25, 1999.
References
This article has been cited by other articles:
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  E. Seeman Sexual Dimorphism in Skeletal Size, Density, and Strength J. Clin. Endocrinol. Metab., October 1, 2001; 86(10): 4576 - 4584. [Full Text] [PDF]
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