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Letter to the Editor |
Department of Endocrinology and Metabolism, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205-7199
Address correspondence to: Dr. A. Michael Parfitt, Department of Endocrinology and Metabolism, 4301 West Markham, Little Rock, Arkansas 72205-7199. E-mail: parfittalwynm{at}uams.edu.
To the editor:
Yao et al. (1) present interesting data on parathyroid weight but make a statistical error and do not fully explore the implications of their results. As is evident from their data and from many other reports (2), parathyroid weight is not normally but is log normally distributed, so that the correct summary statistics are not arithmetic mean and additive SD, but are geometric mean and multiplicative SD (2). Fortunately, this error does not affect the conclusion that nonadenomatous glands removed at surgery weigh more than presumably normal glands removed at autopsy.
The authors’ main purpose was to provide surgeons with a more accurate basis for deciding how many glands to remove; from this standpoint, the reasons for the difference in weight are not important, but they still merit discussion. Since the supposedly normal glands were removed because of uncertainty about their normality, they are not representative of the general run of nonadenomatous glands, of which there would have been 87 in the operated patients. Nevertheless, 15 of 87 glands weighing more than 60 mg (17%) is a higher proportion than in most autopsy series. Most patients receive iv fluid during surgery, whereas autopsies are not usually performed until many hours after death, during which the cadaver is likely to lose some water. If the difference in weight was due only to a difference in hydration, the total number of parathyroid chief cells, which can be estimated using the Cavalieri principle (2), will be same. But if nonadenomatous glands have more cells than normal glands, this must be accounted for by any comprehensive theory of parathyroid adenoma pathogenesis.
Many years ago, Paloyan et al. (3) proposed that hyperparathyroidism was a generalized rather than a localized disease and recommended radical subtotal parathyroidectomy as the treatment of choice. This practice has deservedly been abandoned, but a subtle growth abnormality in one or more glands, not needing surgical recognition, would account for the persistent elevation of PTH secretion after adenoma removal (4). Such a growth abnormality need not be present in every gland. Parathyroid adenomas originate in a single cell that slowly proliferates (5). Plasma PTH will not rise above the reference range for some time, and plasma calcium may still be normal, a situation recently designated as incipient hyperparathyroidism (6). It could take many years for the clone of abnormal cells to become large enough to cause unambiguous hypercalcemia, and depending on the rate of growth and the growth target of the abnormal cells (2), this stage may never be reached during the patient’s life. To find (or rule out) a small microadenoma could require serial sections of the entire gland at intervals of no more than 100 µm. The incidence of double adenoma in primary hyperparathyroidism (including all the subclinical cases) is probably much higher than the 1% mentioned by the authors. I propose this as a plausible explanation for the unexpected prevalence of moderately enlarged glands, a proposal that Yao et al. have the material to confirm or refute.
Received September 20, 2004.
References
This article has been cited by other articles:
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  S. I. Roth, F. R. Singer, K. Yao, and A. E. Giuliano Authors' Response: Weight of Normal Parathyroid Glands in Patients with Parathyroid Adenomas J. Clin. Endocrinol. Metab., January 1, 2005; 90(1): 596 - 596. [Full Text] [PDF]
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