Value of routine measurement of serum calcitonin concentrations in patients with nodular thyroid disease: A multicenter study

Papi, Giampaolo; Corsello, Salvatore Maria; Cioni, Katia; Am, Pizzini; Corrado, Stefania; Carapezzi, C; Fadda, Guido; Baldini, Alessandra; Carani, Cesare; Pontecorvi, Alfredo; Roti, Elio

doi:10.1007/bf03344126

Cited by 63 publications

(57 citation statements)

References 37 publications

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“…Despite the ever increasing number of publications recommending routine calcitonin measurements in patients with thyroid nodules to diagnose medullary thyroid cancer in an early and therefore curable stage (Pacini et al 1994, Rieu et al 1995, Niccoli et al 1997, Vierhapper et al 1997, 2005, Ozgen et al 1999, Hahm et al 2001, Elisei et al 2004, Papi et al 2006, Costante et al 2007, 'calcitonin screening' is not recommended in daily practice (Hegedus 2004). Differences exist in the literature (Scheuba et al 1999, Iacobone et al 2002, Costante et al 2007) regarding calcitonin cut-off levels, indication, time, and extent of surgery.…”

Section: Introductionmentioning

confidence: 99%

Sporadic hypercalcitoninemia: clinical and therapeutic consequences

Scheuba¹,

Kaserer²,

Moritz³

et al. 2009

Endocrine-Related Cancer

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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 (O10 pg/ml) and stimulated calcitonin levels (O100 pg/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 with basal and stimulated calcitonin levels. All patients were subsequently followed biochemically. C-cell hyperplasia (CCH) 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, CCH:4). In 56 (46%) of 122 patients, sporadic CCH was classified neoplastic ('carcinoma in situ'). Of 97 (72%; 10 with hereditary medullary thyroid cancer) had pT1 (International Union against Cancer recommendations 2002) and 33 (25%) had pT2 or pT3 and 4 (3%) pT4 tumors. Of 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 O64 pg/ml and stimulated calcitonin O560 pg/ml have medullary thyroid cancer. Medullary thyroid cancer was documented in 20% of patients with basal calcitonin O10 pg/ml but !64 pg/ml and stimulated calcitonin O100 pg/ml but !560 pg/ml.

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Section: Introductionmentioning

confidence: 99%

Sporadic hypercalcitoninemia: clinical and therapeutic consequences

Scheuba¹,

Kaserer²,

Moritz³

et al. 2009

Endocrine-Related Cancer

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“…Compared with FNAB, the sensitivity of the calcitonin measurement for preoperative diagnosis of MTC is higher (approximately 100% sensitivity and 95% specificity) (18,40,41) (B). Individuals with MTC that was diagnosed from a calcitonin measurement during the investigation of thyroid nodules exhibit better postoperative outcomes than do those diagnosed by FNAB, with 10-year survival rates of 86.8% and 43.7%, respectively (42) (B).…”

Section: (C)mentioning

confidence: 99%

Diagnóstico, tratamento e seguimento do carcinoma medular de tireoide: recomendações do Departamento de Tireoide da Sociedade Brasileira de Endocrinologia e Metabologia

Maia

Siqueira

Kulcsar

et al. 2014

Arq Bras Endocrinol Metab

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Introduction: Medullary thyroid carcinoma (MTC) originates in the thyroid parafollicular cells and represents 3-4% of the malignant neoplasms that affect this gland. Approximately 25% of these cases are hereditary due to activating mutations in the REarranged during Transfection (RET) proto-oncogene. The course of MTC is indolent, and survival rates depend on the tumor stage at diagnosis. The present article describes clinical evidence-based guidelines for the diagnosis, treatment, and follow-up of MTC. Objective: The aim of the consensus described herein, which was elaborated by Brazilian experts and sponsored by the Thyroid Department of the Brazilian Society of Endocrinology and Metabolism, was to discuss the diagnosis, treatment, and follow-up of individuals with MTC in accordance with the latest evidence reported in the literature. Materials and methods: After clinical questions were elaborated, the available literature was initially surveyed for evidence in the MedLine-PubMed database, followed by the Embase and Scientific Electronic Library Online/Latin American and Caribbean Health Science Literature (SciELO/Lilacs) databases. The strength of evidence was assessed according to the Oxford classification of evidence levels, which is based on study design, and the best evidence available for each question was selected. Results: Eleven questions corresponded to MTC diagnosis, 8 corresponded to its surgical treatment, and 13 corresponded to follow-up, for a total of 32 recommendations. The present article discusses the clinical and molecular diagnosis, initial surgical treatment, and postoperative management of MTC, as well as the therapeutic options for metastatic disease. Conclusions: MTC should be suspected in individuals who present with thyroid nodules and family histories of MTC, associations with pheochromocytoma and hyperparathyroidism, and/or typical phenotypic characteristics such as ganglioneuromatosis and Marfanoid habitus. Fine-needle nodule aspiration, serum calcitonin measurements, and anatomical-pathological examinations are useful for diagnostic confirmation. Surgery represents the only curative therapeutic strategy. The therapeutic options for metastatic disease remain limited and are restricted to disease control. Judicious postoperative assessments that focus on the identification of residual or recurrent disease are of paramount importance when defining the follow-up and later therapeutic management strategies. Arq Bras Endocrinol Metab. 2014;58(7):667-700

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“…No se registró mortalidad durante el seguimiento. [17][18][19][20] sugieren la medición de calcitonina en pacientes con enfermedad tiroidea nodular para aumentar la tasa de diagnóstico preoperatorio de CMT. La medición de calcitonina sérica para el tamizaje puede detectar Hiperplasia de células C y CMT en etapas tempranas, lo que podría mejorar la sobrevida global.…”

Section: Seguimiento a Largo Plazounclassified

Cáncer medular de tiroides: Experiencia quirúrgica en 10 años

et al. 2013

Rev. méd. Chile

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Value of routine measurement of serum calcitonin concentrations in patients with nodular thyroid disease: A multicenter study

Cited by 63 publications

References 37 publications

Sporadic hypercalcitoninemia: clinical and therapeutic consequences

Sporadic hypercalcitoninemia: clinical and therapeutic consequences

Diagnóstico, tratamento e seguimento do carcinoma medular de tireoide: recomendações do Departamento de Tireoide da Sociedade Brasileira de Endocrinologia e Metabologia

Cáncer medular de tiroides: Experiencia quirúrgica en 10 años

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