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Prophylactic Thyroidectomy in Multiple Endocrine Neoplasia Type 2A
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     To the Editor: In their report on the effects of early prophylactic thyroidectomy in patients with multiple endocrine neoplasia type 2A (MEN-2A) (Sept. 15 issue),1 Skinner et al. identified a group of patients with postoperative calcitonin levels that increased in response to calcium–pentagastrin stimulation but remained within the normal range. The finding was regarded as presumptive evidence of persistent or recurrent medullary thyroid carcinoma. An alternative possibility that has not been ruled out is that there was production of calcitonin by extrathyroidal cells, particularly cells in the parathyroid glands or lung. Immunohistochemical detection of calcitonin in hyperplastic parathyroid tissue has been reported in two studies,2,3 one of which also involved the localization of calcitonin messenger RNA to the immunoreactive cells with the use of in situ hybridization.2 Immunoreactive calcitonin has also been reported in neonatal lung tissue.4 Both immunohistochemical analysis and in situ hybridization are methods fraught with potential artifacts, and the authors' findings require replication by more specific techniques. Such confirmation would require modification of the postoperative assessment of pediatric patients who undergo thyroidectomy. It would also raise a number of interesting questions, including why extrathyroidal calcitonin-producing cells are not sites of origin for new primary medullary carcinomas in patients with MEN-2A.

    Arthur S. Tischler, M.D.

    Tufts–New England Medical Center

    Boston, MA 02111

    atischler@tufts-nemc.org

    Ashraf Khan, M.D.

    University of Massachusetts Memorial Medical Center

    Worcester, MA 01655

    Ronald A. DeLellis, M.D.

    Lifespan Academic Medical Center

    Providence, RI 02903

    References

    Skinner MA, Moley JA, Dilley WG, Owzar K, Debenedetti MK, Wells SA Jr. Prophylactic thyroidectomy in multiple endocrine neoplasia type 2A. N Engl J Med 2005;353:1105-1113.

    Schmid KW, Morgan JM, Baumert M, Fischer-Colbrie R, Bocker W, Jasani B. Calcitonin and calcitonin gene-related peptide mRNA detection in a population of hyperplastic parathyroid cells also expressing chromogranin B. Lab Invest 1995;73:90-95.

    Khan A, Tischler AS, Patwardhan NA, DeLellis RA. Calcitonin immunoreactivity in neoplastic and hyperplastic parathyroid glands: an immunohistochemical study. Endocr Pathol 2003;14:249-255.

    Becker KL, Monaghan KG, Silva OL. Immunocytochemical localization of calcitonin in Kulchitsky cells of human lung. Arch Pathol Lab Med 1980;104:196-198.

    The author replies: Dr. Tischler and colleagues and others whom they cite detected calcitonin with the use of immunohistochemical techniques in neonatal lung tissue or in hyperplastic or adenomatous parathyroid tissues (but not in normal parathyroid tissue). They propose that such extrathyroidal sources of calcitonin may account for the elevated plasma levels of this hormone that were detected postoperatively in some children in our study.

    Although plausible, their proposal raises some concerns. Each of the three cited studies involved the use of immunohistochemical analysis of formalin-fixed and paraffin-embedded tissues. However, there were no functional studies to show that hyperfunctioning parathyroid cells or neonatal lung tissues actively secreted calcitonin into the bloodstream. Without such data, it is difficult to prove or disprove their hypothesis. We agree with the statement of Tischler et al. that immunohistochemical analysis and in situ hybridization are fraught with potential artifacts and require replication by more specific techniques. We would hope that data confirming that extrathyroidal sources of calcitonin either do or do not cause elevated blood levels of the hormone will be forthcoming in future studies.

    Samuel A. Wells, Jr., M.D.

    Duke University Medical Center

    Durham, NC 27710

    wells029@mc.duke.edu