ERC Society for Endocrinology Archive
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
 QUICK SEARCH:   [advanced]


     


Accepted Preprint first posted online on 5 November 2008

Endocrine-Related Cancer 2009;16:243.

DOI: 10.1677/ERC-08-0059
Copyright © 2008 by the Society for Endocrinology.
This Article
Right arrow Accepted manuscript (PDF)
Right arrow All Versions of this Article:
ERC-08-0059v1
16/1/243    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Scheuba, C.
Right arrow Articles by Niederle, B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Scheuba, C.
Right arrow Articles by Niederle, B.

RESEARCH

Sporadic hypercalcitoninemia: clinical and therapeutic consequences

Christian Scheuba, Klaus Kaserer, Anne Moritz, Ralph Drosten, Heinrich Vierhapper, Christian Bieglmayer, Oskar Haas and Bruno Niederle

C Scheuba, Section of Endocrine Surgery, Division of General Surgery, Department of Surgery, Medical University of Vienna, Vienna, Austria
K Kaserer, Department of Clinical Pathology, Medical University of Vienna, Vienna, Austria
A Moritz, Medgen Vienna, Vienna, Austria
R Drosten, Radiology Department, University of Utah, Salt Lake City, United States
H Vierhapper, Division of Endocrinology and Metabolism, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
C Bieglmayer, Clinical Institute for Medical and Chemical Laboratory Diagnostics, Medical University of Vienna, Vienna, United Kingdom
O Haas, Vienna, Austria
B Niederle, Section of Endocrine Surgery, Division of General Surgery, Department of Surgery, Medical University of Vienna, Vienna, Austria

Correspondence: Christian Scheuba, Email: christian.scheuba{at}meduniwien.ac.at

Abstract

Calcitonin screening is not accepted as the standard of care in daily practice. The clinical and surgical consequences of "calcitonin screening" in a series of patients with mildly elevated basal calcitonin and pentagastrin stimulated calcitonin levels are presented. 260 patients with elevated basal (>10pg/ml) and stimulated calcitonin levels (>100pg/ml) were enrolled in this prospective study. None of the patients was member of a known medullary thyroid carcinoma family. Thyroidectomy and bilateral central and lateral neck dissections were performed. Testing for the presence of germ line mutations was performed in all patients. Histological and immunohistochemical findings were compared to basal and stimulated calcitonin levels. All patients were subsequently followed biochemically. C-cell hyperplasia was found in 126 (49%) and medullary thyroid cancer was found in 134 (51%) patients. RET proto-oncogen mutations were documented in 22 (8%) patients (medullary thyroid cancer:18, C-cell hyperplasia:4). In 56 (46%) of 122 patients, sporadic C-cell hyperplasia was classified neoplastic (carcinoma in situ). 81 (60%; 8 with hereditary medullary thyroid cancer) had pT1 (UICC 1997) and 38 (29%) had pT2 or pT3 and 15 (11%) pT4 tumors. 39 (29.1%) had lymph node metastases. 106 (79.1%; 15 [38.5%] with lymph node metastases) patients were cured. Evaluation of basal and stimulated calcitonin levels enables the prediction of medullary thyroid cancer. All patients with basal calcitonin >64pg/ml and stimulated calcitonin >560pg/ml have medullary thyroid cancer. Medullary thyroid cancer was documented in 20% of patients with basal calcitonin >10pg/ml but <64pg/ml and stimulated calcitonin >100pg/ml but <560pg/ml.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2008 by the Society for Endocrinology.