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Detection and confirmation C-cell hyperplasia (the precursor of medullary carcinoma of thyroid) as well as a tumor marker for diagnosis and management of medullary carcinoma of the thyroid gland. Preoperative serum calcitonin is reported to roughly correlate with tumor weight or extent of disease; therefore, postoperative levels also have prognostic application. The doubling time of serum levels correlates with a recurrence.1 Multiple endocrine neoplasia (MEN) type II includes medullary carcinoma of the thyroid, hyperparathyroidism, and pheochromocytoma (Sipple syndrome). MEN type IIB includes medullary carcinoma of the thyroid, pheochromocytoma, mucosal neuromas, marfanoid habitus, and intestinal ganglioneuromatosis.2 An important use of calcitonin assay is in follow-up of patients with medullary carcinoma and work-up of their families to detect early, subclinical cases. Indications for calcitonin assay include family history of unspecified type of thyroid cancer, calcified thyroid mass, thyroid tumor associated with hypercalcemia and/or pheochromocytoma, amyloid-containing metastatic carcinoma with unknown primary site and the presence of mucosal neuromas.3
In a number of patients with medullary carcinoma of the thyroid (especially those with familial medullary carcinoma of thyroid) the baseline calcitonin may be normal; however, an abnormally large calcitonin response may follow provocative infusion of calcium and/or pentagastrin4 (usually 3 to 20 times baseline). Most subjects with microscopic medullary carcinoma and all with C-cell hyperplasia have normal basal calcitonin levels; provocative testing is needed (see the online Endocrine Appendix: Calcium-Pentagastrin Stimulation). Occasional spurious high results are encountered. Hemolysis can cause spurious high levels. Calcitonin in patients' sera lacks immunoreactive uniformity. Calcitonin is not a screening test.
High concentrations of calcitonin occur not only in patients with malignant parafollicular or C-cell tumors (medullary thyroid carcinoma), but also in many patients with carcinomas of the lung; in some individuals with carcinoma of breast, carcinoids, islet cell tumors, apudomas, in patients with pancreatitis, thyroiditis and in renal failure. Hypergastrinemia may account for calcitonin elevations in the Zollinger-Ellison syndrome and in pernicious anemia. Medullary carcinoma arises from thyroid C cells (parafollicular cells). C-cell hyperplasia is a preneoplastic state in patients with MEN. Provocative tests that may be used for diagnosis of medullary thyroid carcinoma are pentagastrin and calcium infusion.3 A combined calcium pentagastrin test is described in the see the online Endocrine Appendix: Calcium-Pentagastrin Stimulation.2,3 These tests are much more useful than random plasma levels of calcitonin for the diagnosis of MCT. Early diagnosis of medullary carcinoma of thyroid is needed; total thyroidectomy is curative if the tumor is treated early. Medullary carcinomas of the thyroid gland have a variable histologic picture. Correlation between serum calcitonin levels and immunoperoxidase staining of the neoplastic thyroid tissue for calcitonin may assist in confirming the diagnosis in difficult cases. The direct manifestation of high calcitonin levels is secretory diarrhea in 30% of patients with medullary thyroid carcinoma.
1. Miyauchi A, Matsuzuka F, Kuma K, et al. Evaluation of surgical results and prediction of prognosis in patients with medullary thyroid carcinoma by analysis of serum calcitonin levels. World J Surg. 1988; 12(5):610-615. PubMed 3245215
2. Mendelsohn G, Baylin SB. Medullary thyroid carcinoma: Diagnostic and clinical features. Lab Management. 1983; 21-31.
3. Gagel RF. Calcitonin in thyroid carcinoma and other disease. Lab Management. 1982; 35-48.
4. Guilloteau D, Perdrisot R, Calmettes C, et al. Diagnosis of medullary carcinoma of the thyroid (MCT) by calcitonin assay using monoclonal antibodies: Criteria for the pentagastrin stimulation test in hereditary MCT. J Clin Endocrinol Metab. 1990; 71(4):1064-1067. PubMed 2401708
Austin LA, Heath H III. Calcitonin: Physiology and pathophysiology. N Engl J Med. 1981; 304(5):269-278 (review). PubMed 7003392
Boultwood J, Wynford-Thomas D, Richards GP, et al. In situ analysis of calcitonin and CGRP expression in medullary thyroid carcinoma. Clin Endocrinol (Oxf). 1990; 33(3):381-390. PubMed 2253409
Ghillani PP, Motte P, Troalen F, et al. Identification and measurement of calcitonin precursors in serum of patients with malignant diseases. Cancer Res. 1989; 49(23):6845-6851. PubMed 2555054
Rougier P, Calmettes C, LaPlanche A, et al. The values of calcitonin and carcinoembryonic antigen in the treatment and management of nonfamilial medullary thyroid carcinoma. Cancer. 1983; 51(5):855-862. PubMed 6821852
