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Hypercalcitoninemia is not Pathognomonic of Medullary Thyroid Carcinoma
Open accessAbstract
Hypercalcitoninemia has frequently been reported as a marker for medullary thyroid carcinoma. Currently, calcitonin measurements are mostly useful in the evaluation of tumor size and progression, and as an index of biochemical improvement of medullary thyroid carcinomas. Although measurement of calcitonin is a highly sensitive method for the detection of medullary thyroid carcinoma, it presents a low specificity for this tumor. Several physiologic and pathologic conditions other than medullary thyroid carcinoma have been associated with increased levels of calcitonin. Several cases of thyroid nodules associated with increased values of calcitonin are not medullary thyroid carcinomas, but rather are related to other conditions, such as hypercalcemias, hypergastrinemias, neuroendocrine tumors, renal insufficiency, papillary and follicular thyroid carcinomas, and goiter. Furthermore, prolonged treatment with omeprazole (>2-4 months), beta-blockers, glucocorticoids and potential secretagogues, have been associated with hypercalcitoninemia. An association between calcitonin levels and chronic auto-immune thyroiditis remains controversial. Patients with calcitonin levels >100 pg/mL have a high risk for medullary thyroid carcinoma (approximately 90%-100%), whereas patients with values from 10 to 100 pg/mL (normal values: <8.5 pg/mL for men, <5.0 pg/mL for women; immunochemiluminometric assay) have a <25% risk for medullary thyroid carcinoma.In multiple endocrine neoplasia type 2 (MEN2), RET mutation analysis is the gold-standard for the recommendation of total preventive thyroidectomy to relatives at risk of harboring a germline RET mutation (50%). False-positive calcitonin results within MEN2 families have led to incorrect indications of preventive total thyroidectomy to RET mutation negative relatives. In this review, we focus on the differential diagnosis of hypercalcitoninemia, underlining its importance for the avoidance of misdiagnosis of medullary thyroid carcinoma and consequent incorrect recommendation for thyroid surgery.
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“Examples of common drugs that may increase calcitonin include omeprazole and other proton pump inhibitors, glucocorticoids, beta-blockers, and glucagon”
From Anti-Obesity Medications and Investigational Agents: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2022 (2022) · cites this paper as [54]
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“Especially at marginal to mild elevations in calcitonin blood levels, hypercalcitoninemia is not pathognomonic of medullary thyroid cancer.”
From Anti-Obesity Medications and Investigational Agents: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2022 (2022) · cites this paper as [54]
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“Calcitonin is a polypeptide secreted by thyroid C-cells that is involved with bone and calcium metabolism.”
From Anti-Obesity Medications and Investigational Agents: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2022 (2022) · cites this paper as [54]
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“Some reports suggest that mild elevation in calcitonin levels can be due to thyroid disease other than medullary thyroid cancer”
From Anti-Obesity Medications and Investigational Agents: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2022 (2022) · cites this paper as [54]
In the citing paper
“Especially in the absence of family history otherwise suggesting genetic predisposition to medullary thyroid cancer, and especially in the absence of abnormal thyroid gland physical findings (i.e., nodules or goiter), modestly elevated calcitonin levels are more likely due to other non-thyroid causes, such as neuroendocrine tumors”
From Anti-Obesity Medications and Investigational Agents: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2022 (2022) · cites this paper as [54]
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Citations
Cites
CONSENSUS: Guidelines for Diagnosis and Therapy of MEN Type 1 and Type 2
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Germ-line mutations of the RET proto-oncogene in multiple endocrine neoplasia type 2A
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Cited by
Wells, S. A., Asa, S. L., Dralle, H., Elisei, R., Evans, D. B., Gagel, R. F., Lee, N., Machens, A., Moley, J. F., Pacini, F., et al. (2015) · Thyroid · doi:10.1089/thy.2014.0335 · Cited by 2,444
Electrochemical Methods for the Analysis of Clinically Relevant Biomolecules
Labib, M., Sargent, E. H., & Kelley, S. O. (2016) · Chemical Reviews · doi:10.1021/acs.chemrev.6b00220 · Cited by 976
Multiple Endocrine Neoplasia Type 2 and Familial Medullary Thyroid Carcinoma: An Update
Wells, S. A., Pacini, F., Robinson, B. G., & Santoro, M. (2013) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2013-1204 · Cited by 338
American Thyroid Association Statement on Optimal Surgical Management of Goiter
Chen, A. Y., Bernet, V. J., Carty, S. E., Davies, T. F., Ganly, I., Inabnet, W. B., & Shaha, A. R. (2013) · Thyroid · doi:10.1089/thy.2013.0291 · Cited by 205
MIP-Based Sensors: Promising New Tools for Cancer Biomarker Determination
Selvolini, G., & Marrazza, G. (2017) · Sensors · doi:10.3390/s17040718 · Cited by 194
Metadata
- Authors
- Toledo, S. P., Lourenço, D. M., Santos, M. A., Tavares, M. R., Toledo, R. A., & de Menezes Correia-Deur, J. E.
- Affiliations
- Universidade de São Paulo (BR)
- Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (BR)
- Corresponding author
- Tavares, Marcos R
- Venue
- Clinics
- Publisher
- Elsevier BV
- Published
- 2009-07
- Volume
- 64
- Issue
- 7
- Pages
- 699-706
- ISSN
- 1807-5932 (ISSN-L)
- PMC
- PMC2710445
- OpenAlex
- W2170408697
- Cited by
- 154
- References
- 55
- Citations by year
- 2026: 4 · 2025: 9 · 2024: 11 · 2023: 14 · 2022: 11 · 2021: 16 · 2020: 13 · 2019: 3 · 2018: 6 · 2017: 9 · 2016: 11 · 2015: 12 · 2014: 8 · 2013: 12 · 2012: 8
- FWCI
- 0.61
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- creativecommons.org/licenses/by-nc/3.0/ (vor, 20 d)
- Locations
- Clinics (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (publishedVersion, other-oa)
- Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) (publishedVersion)
- Americanae (AECID Library) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, other-oa)
- Funders
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Health Sciences › Medicine › Surgery › Thyroid and Parathyroid Surgery
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Keywords
- hypercalcitoninemia, medullary thyroid carcinoma, calcitonin, differential diagnosis, multiple endocrine neoplasia type 2, RET mutations, thyroid nodules, omeprazole, beta-blockers, glucocorticoids, autoimmune thyroiditis, misdiagnosis
- MeSH terms
- Calcitonin, Diagnosis, Differential, Female, Humans, Male, Multiple Endocrine Neoplasia, Risk, Thyroid Neoplasms, Thyroidectomy, Biomarkers, Tumor, Carcinoma, Medullary
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- Toledo, S. P., Lourenço, D. M., Santos, M. A., Tavares, M. R., Toledo, R. A., & de Menezes Correia-Deur, J. E. (2009). Hypercalcitoninemia is not Pathognomonic of Medullary Thyroid Carcinoma. Clinics. https://doi.org/10.1590/s1807-59322009000700015
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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