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Body Weight and Bone Mineral Density in Hyperparathyroidism
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Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
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TO THE EDITOR:
We recently reported that body weight and fat mass are increased in postmenopausal women with mild, asymptomatic primary hyperparathyroidism [1]. We have now obtained lifetime weight histories from 38 of the hyperparathyroid women and 30 of the controls from our original study. The controls were similar in all respects to the larger group described in the original study. The body weight of the women who developed primary hyperparathyroidism was significantly higher than that of their eucalcemic peers at ages 40 and 60 years (P < 0.001 for both time points) but not at age 20 years (P = 0.18) (Table 1). A similar proportion of patients in each group reported an increase in body weight of more than 5 kg during the last 10 years.
Because primary hyperparathyroidism rarely occurs in women younger than age 40 years [2], these findings suggest that increased body weight precedes the onset of primary hyperparathyroidism in postmenopausal women. Body weight is an important determinant of bone mineral density [3], and the current findings suggest that as a result of their mild obesity earlier in life, postmenopausal women who develop primary hyperparathyroidism may have had higher than normal bone density before the onset of parathyroid disease. The association between primary hyperparathyroidism and increased body weight is unlikely to be the result of an anabolic effect of parathyroid hormone on adipose tissue. Although ascertainment bias may be responsible for this association, potential biological explanations include an effect of obesity on parathyroid gland function, perhaps mediated by long-standing secondary hyperparathyroidism [4] or by a shared genetic predisposition to both conditions.
Andrew Grey, MB, ChB
Ian Reid, MD
Auckland Hospital; Auckland; New Zealand
The Editors welcome submissions for possible publication in the Letters section. Authors of letters should:
•Include no more than 300 words of text, three authors, and five references
•Type with double-spacing
•Send three copies of the letter, an authors' form signed by all authors, and a cover letter describing any conflicts of interest related to the contents of the letter.
Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned.
Annals welcomes electronically submitted letters.
- Copyright ©2004 by the American College of Physicians
