Table of Contents

Total Page:16

File Type:pdf, Size:1020Kb

Table of Contents CONTENTS 1. Normal Thyroid Gland .................................................................................................... 1 Embryology .................................................................................................................. 1 Anatomy ...................................................................................................................... 3 Histology ...................................................................................................................... 4 The Follicular Cell ........................................................................................................ 8 Thyroid Hormones ................................................................................................... 10 The C-Cell .................................................................................................................... 11 Calcitonin and Calcitonin Gene-Related Peptide .................................................... 14 Solid Cell Nests ............................................................................................................ 15 2. Genes Involved in Thyroid Tumorigenesis ..................................................................... 23 TSH Receptor/cAMP Pathway ...................................................................................... 25 MAPK Pathway ............................................................................................................ 31 Tyrosine Kinase Receptors (RET, NTK1, MET) .......................................................... 31 RAS............................................................................................................................ 36 BRAF ......................................................................................................................... 37 P13K/PTEN/AKT Pathway ............................................................................................ 39 PPARg Rearrangement .................................................................................................. 41 ß-Catenin/APC/Wnt Signaling ................................................................................... 42 TERT ............................................................................................................................. 43 Tumor Protein p53 ....................................................................................................... 45 3. General Features of Thyroid Tumors ............................................................................... 57 Incidence of Thyroid Carcinoma ................................................................................ 57 Thyroid Tumors and Iodine Deficiency....................................................................... 57 Thyroid Tumors and Radiation Exposure .................................................................... 57 Thyroid Tumors in Childhood .................................................................................... 58 4. Classification of Thyroid Tumors .................................................................................... 61 Primary Tumors ........................................................................................................... 62 Secondary Tumors and Tumor-Like Lesions ................................................................ 62 5. Follicular Thyroid Adenoma and Variants ...................................................................... 65 Follicular Adenoma ...................................................................................................... 65 Adenoma Variants ....................................................................................................... 73 Adenoma with Bizarre Nuclei .................................................................................. 73 Hyalinizing Trabecular Adenoma............................................................................. 73 Adenolipoma and Adenochondroma ...................................................................... 78 Atypical Adenoma (Including Spindle Cell Adenoma) ........................................... 78 Adenoma with Papillary Features ............................................................................ 79 “Toxic” Adenoma ..................................................................................................... 81 xi Tumors of the Thyroid and Parathyroid Glands 6. Follicular Thyroid Carcinoma ......................................................................................... 85 Minimally Invasive (Encapsulated) Type .................................................................... 86 Widely Invasive Type ................................................................................................... 97 7. Papillary Thyroid Carcinoma and Variants ..................................................................... 103 Papillary Carcinoma .................................................................................................... 103 Papillary Carcinoma Variants ...................................................................................... 127 Papillary Microcarcinoma ........................................................................................ 127 Encapsulated Variant ................................................................................................ 130 Follicular Variant ...................................................................................................... 131 Encapsulated Follicular Variant of PTC and the “Uncertain Malignant Potential (UMP)” Concept .................................................................................... 135 Solid/Trabecular Variant ........................................................................................... 139 Diffuse Sclerosing Variant ........................................................................................ 141 Oncocytic and Warthin-Like Variants ..................................................................... 143 Tall and Columnar Cell Variants .............................................................................. 146 Cribriform/Morular Variant ..................................................................................... 149 8. Poorly Differentiated Thyroid Carcinoma ...................................................................... 165 Insular Carcinoma ....................................................................................................... 165 Other Poorly Differentiated Carcinomas..................................................................... 172 9. Undifferentiated (Anaplastic) Thyroid Carcinoma ......................................................... 177 10. Thyroid Tumors with Oncocytic (Hürthle Cell) Features ............................................... 199 General Considerations ............................................................................................... 199 Oncocytic Adenoma (Hürthle Cell Adenoma) ............................................................ 203 Oncocytic Carcinoma (Hürthle Cell Carcinoma) ........................................................ 209 Papillary Oncocytic Neoplasms ................................................................................... 215 11. Thyroid Tumors with Clear Cell, Squamous, and Mucinous Features ........................... 221 Tumors with Clear Cell Features .................................................................................. 221 General Considerations ............................................................................................ 221 Tumor Types ............................................................................................................. 222 Other Conditions ..................................................................................................... 227 Tumors with Squamous Features ................................................................................. 228 Tumors with Mucinous Features ................................................................................. 233 12. Medullary Thyroid Carcinoma and C-Cell Hyperplasia ................................................. 241 Medullary Thyroid Carcinoma .................................................................................... 241 Medullary Carcinoma Variants .................................................................................... 261 Papillary Variant ....................................................................................................... 261 Follicular (Tubular) Variant ...................................................................................... 261 Small Cell Variant ..................................................................................................... 261 Giant Cell Variant .................................................................................................... 261 xii Contents Clear Cell Variant ..................................................................................................... 262 Melanotic Variant ..................................................................................................... 262 Oncocytic Variant .................................................................................................... 262 Squamous Cell Variant ............................................................................................. 264 Amphicrine Cell Variant .........................................................................................
Recommended publications
  • Thyroid Follicular Adenoma: Benign Or Malignant?
    Volume 4 Number 3 Medical Journal of the ['ayiz1369 Islamic Repuhlit of Imn Rabiolawwal141 I F:llll990 THYROID FOLLICULAR ADENOMA: BENIGN OR MALIGNANT? HOSSEIN GHARIB, M.D. From fhe Division of Endocrillology and !lIlernal Medicine, Mayo Clinic and Mayo FOll1uiafion, Rochester, MillllCSOla, U.S.A. ABSTRACT Four patients are described in whom a follicular carcinoma developed following thyroidectomy for a benign follicular neoplasm. It is possible that the initial thyroid neoplasm was a well- differentiated follicular carcinoma which was microscopically indistinguishable from a benign adenoma. Realizing this pathologic pitfall in thyroid diagnosis, the need for meticulous examination of the pathologic specimen is emphasized. Long- term postop­ erative reassessment is recommended. MIIRI, Vol. 4, No.3, 173-176, 1990 INTRODUCTION CASE REPORTS Follicular adenoma is the most common type of Case I cellular thyroid adenomas. 1 There is considerable de­ A 49-year-old woman was referred for evaluation of bate whether follicular adenoma of the thyroid, a metastatic thyroid carcinoma. She was in good health benign neoplasm, is a precancerous lesion which occa­ until six months earlier when she complained of ins om- sionally may be mistaken for a carcinoma2.30n the nia and nervousness. Two months before admission a other hand, several published reports indicate that a routine chest x-ray revealed metastatic nodules in both follicular adenoma which appears benign by conven­ lungs. Extensive laboratory tests and radiographic tional histologic criteria, may demonstrate malignant studies were negative. A diagnostic left thoracotomy behavior."·() showed ,dow grade thyroid cancep. and she was refer­ This report describes four patients whose thyroid red for further examination.
    [Show full text]
  • Comprehensive Assessment of TERT Mrna Expression Across a Large Cohort of Benign and Malignant Thyroid Tumours
    cancers Article Comprehensive Assessment of TERT mRNA Expression across a Large Cohort of Benign and Malignant Thyroid Tumours Ana Pestana 1,2,3, Rui Batista 1,2,3, Ricardo Celestino 1,2,3,4 , Sule Canberk 1,2,5, Manuel Sobrinho-Simões 1,2,3,6 and Paula Soares 1,2,3,7,* 1 Institute of Molecular Pathology and Immunology of the University of Porto (Ipatimup), 4200-135 Porto, Portugal; [email protected] (A.P.); [email protected] (R.B.); [email protected] (R.C.); [email protected] (S.C.); [email protected] (M.S.-S.) 2 i3S-Instituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200-135 Porto, Portugal 3 Medical Faculty of University of Porto (FMUP), 4200-139 Porto, Portugal 4 School of Allied Health Technologies, Polytechnic of Porto, 4200-072 Porto, Portugal 5 Abel Salazar Biomedical Sciences Institute (ICBAS), University of Porto, 4050-313 Porto, Portugal 6 Department of Pathology, Centro Hospitalar São João, 4200-139 Porto, Portugal 7 Department of Pathology, Medical Faculty of the University of Porto, 4200-139 Porto, Portugal * Correspondence: [email protected]; Tel.: +351-220-408-800 Received: 10 June 2020; Accepted: 6 July 2020; Published: 9 July 2020 Abstract: The presence of TERT promoter (TERTp) mutations in thyroid cancer have been associated with worse prognosis features, whereas the extent and meaning of the expression and activation of TERT in thyroid tumours is still largely unknown. We analysed frozen samples from a series of benign and malignant thyroid tumours, displaying non-aggressive features and low mutational burden in order to evaluate the presence of TERTp mutations and TERT mRNA expression in these settings.
    [Show full text]
  • Nonfunctional Metastatic Parathyroid Carcinoma in the Setting of Multiple Endocrine Neoplasia Type 2A Syndrome
    Hindawi Publishing Corporation Surgery Research and Practice Volume 2014, Article ID 731481, 4 pages http://dx.doi.org/10.1155/2014/731481 Case Report Nonfunctional Metastatic Parathyroid Carcinoma in the Setting of Multiple Endocrine Neoplasia Type 2A Syndrome María Posada-González,1 Joaquín Gómez-Ramírez,2 Manuel Luque-Ramírez,3 Mercedes Guijarro,4 Elena Martín-Pérez,1 Ana Rodríguez-Sánchez,1 Iñigo García-Sanz,1 and Eduardo Larrañaga1 1 Department of General and Gastrointestinal Surgery, La Princesa University Hospital, 62 Diego de Leon Street, 28006 Madrid, Spain 2 Department of General and Gastrointestinal Surgery, Fundacion´ Jimenez´ D´ıaz Hospital, 2 Reyes Catolicos Avenue, 28040 Madrid, Spain 3 Department of Endocrinology and Clinical Nutrition, Ramon´ y Cajal University Hospital, Colmenar Viejo Road 9.100 Km, 28034 Madrid, Spain 4 Department of Pathology, La Princesa University Hospital, 62 Diego de Leon Street, 28006 Madrid, Spain Correspondence should be addressed to Mar´ıa Posada-Gonzalez;´ [email protected] Received 28 August 2013; Accepted 26 September 2013; Published 20 February 2014 AcademicEditors:C.Foroulis,G.Lal,andF.Turegano´ Copyright © 2014 Mar´ıa Posada-Gonzalez´ et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Parathyroid carcinoma is a very rare malignancy. It has been associated with hyperparathyroidism-jaw tumour syndrome, familial isolated primary hyperparathyroidism, and multiple endocrine neoplasia type 1 (MEN-1) and 2A (MEN-2A) syndromes. We report a 54-year-old man with a MEN-2A which presents with a nonfunctional metastatic parathyroid carcinoma and a pheochromocytoma in the absence of medullary thyroid carcinoma.
    [Show full text]
  • MEN1 Gene Mutation with Parathyroid Carcinoma: First Report of a Familial Case
    6 8 L Cinque, A Sparaneo et al. MEN1familial familialcase and caseparathyroid andcarcinoma 886–8916:8 8866–891:886 Research parathyroid carcinoma Open Access MEN1 gene mutation with parathyroid carcinoma: first report of a familial case Luigia Cinque1,*, Angelo Sparaneo2,*, Antonio S Salcuni3, Danilo de Martino4, Claudia Battista3, Francesco Logoluso5, Orazio Palumbo1, Roberto Cocchi6, Evaristo Maiello7, Paolo Graziano8, Geoffrey N Hendy9, David E C Cole10, Alfredo Scillitani3 and Vito Guarnieri1 1Medical Genetics, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy 2Laboratory of Oncology, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy 3Endocrinology, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy 4Thoracic Surgery, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy 5Department of Emergency and Organ Transplantation, Unit of Endocrinology, University Medical School of Bari ‘Aldo Moro’, Bari, Italy 6Maxillofacial Surgery, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy 7Oncoematology, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy 8Pathology, IRCCS Casa Sollievo della Sofferenza Hospital, San Giovanni Rotondo (FG), Italy 9Departments of Medicine, Physiology and Human Genetics, McGill University and Metabolic Disorders and Correspondence Complications, McGill University Health Centre Research Institute, Montreal, Quebec, Canada should be addressed 10Departments
    [Show full text]
  • Synchronous Primary Hyperparathyroidism and Papillary Thyroid Carcinoma in a 50-Year-Old Female, Who Initially Presented with Uncontrolled Hypertension
    Open Access http://www.jparathyroid.com Journal of Journal of Parathyroid Disease 2014,2(2),69–70 Epidemiology and Prevention Synchronous primary hyperparathyroidism and papillary thyroid carcinoma in a 50-year-old female, who initially presented with uncontrolled hypertension Seyed Seifollah Beladi Mousavi1, Hamid Nasri2*, Saeed Behradmanesh3 hough, the association between parathyroid and Implication for health policy/practice/research/ thyroid diseases is not uncommon, however medical education concurrent presence of parathyroid adenoma An association between parathyroid adenoma Tand thyroid cancer is rare (1,2). The association between and thyroid cancer is rare. Awareness of this concurrent thyroid and parathyroid disease was firstly situation will enable clinicians to consider for explained by Kissin et al. in 1947 (2). Awareness of possible thyroid pathology in patients with primary this situation will enable clinicians to consider for hyperparathyroidism. Both of these endocrine diseases possible thyroid pathology in patients with primary could then be managed with a single surgery involving hyperparathyroidism. While thyroid follicular cells and concomitant resection of the thyroid and involved parathyroid cells are embryologically different. It is evident parathyroid glands. that presence of parathyroid adenoma leading to primary hyperparathyroidism and coexistent of thyroid papillary cancer is rare. Both of these endocrine diseases could then coincidence of papillary thyroid carcinoma. After surgery, be managed with a single surgery involving concomitant serum parathormone and calcium returned to their normal resection of the thyroid and involved parathyroid glands. values and patient was referred to an endocrinologist for A 50-year-old female, referred to the nephrology clinic for continuing the treatment of papillary carcinoma.
    [Show full text]
  • Parathyroid Carcinoma Presenting As an Acute Pancreatitis
    International Journal of Radiology & Radiation Therapy Case Report Open Access Parathyroid carcinoma presenting as an acute pancreatitis Abstract Volume 3 Issue 3 - 2017 Parathyroid carcinoma is the cause of only 1% of hyperparathyroidism cases. The Enrique Cadena,1,2,3 Alfredo Romero-Rojas1,3 incidence of acute pancreatitis in patients with hyperparathyroidism was reported to 1Department of Head and Neck Surgery and Pathology, be only 1.5%. The occurrence of pancreatitis in patients with parathyroid carcinoma National Cancer Institute, Colombia is unusual, ranging from 0% to 15%. Here, we report a very rare case of parathyroid 2Department of Surgery, National University of Colombia, carcinoma presenting as an acute pancreatitis in a 45years old woman, who was Colombia suspected for hypercalcemia and higher levels of intact parathyroid hormone. The 3Department of Head and Neck Surgery and Pathology, Marly parathyroid carcinoma was verified with ultrasound, CT Scan, and single-photon Clinic, Colombia emission computed tomography. The pathological anatomy report showed a minimally invasive parathyroid carcinoma. Following surgery, the patient was free after almost Correspondence: Enrique Cadena, Department of Head and a 4years follow up. Neck Surgery and Pathology, National Cancer Institute, Bogotá, 1st Street # 9-85, Colombia, Tel 5713341111, 5713341478, Keywords: acute necrotizing pancreatitis, hypercalcemia, primary Email [email protected] hyperparathyroidism, parathyroid carcinoma Received: May 29, 2017 | Published: June 27, 2017 Abbreviations: HPT, hyperparathyroidism; PHPT, primary (2.5mg/dl) levels. Kidney and liver function tests, albumin and hyperparathyroidism; SPECT, single-photon emission computed to- triglyceride levels were all within normal limits. The patient was mography; CT, computed tomography; iPTH, intact parathyroid hor- treated initially with intravenous fluids and H2 blockers, and no oral mone.
    [Show full text]
  • Genetic Landscape of Papillary Thyroid Carcinoma and Nuclear Architecture: an Overview Comparing Pediatric and Adult Populations
    cancers Review Genetic Landscape of Papillary Thyroid Carcinoma and Nuclear Architecture: An Overview Comparing Pediatric and Adult Populations 1, 2, 2 3 Aline Rangel-Pozzo y, Luiza Sisdelli y, Maria Isabel V. Cordioli , Fernanda Vaisman , Paola Caria 4,*, Sabine Mai 1,* and Janete M. Cerutti 2 1 Cell Biology, Research Institute of Oncology and Hematology, University of Manitoba, CancerCare Manitoba, Winnipeg, MB R3E 0V9, Canada; [email protected] 2 Genetic Bases of Thyroid Tumors Laboratory, Division of Genetics, Department of Morphology and Genetics, Universidade Federal de São Paulo/EPM, São Paulo, SP 04039-032, Brazil; [email protected] (L.S.); [email protected] (M.I.V.C.); [email protected] (J.M.C.) 3 Instituto Nacional do Câncer, Rio de Janeiro, RJ 22451-000, Brazil; [email protected] 4 Department of Biomedical Sciences, University of Cagliari, 09042 Cagliari, Italy * Correspondence: [email protected] (P.C.); [email protected] (S.M.); Tel.: +1-204-787-2135 (S.M.) These authors contributed equally to this paper. y Received: 29 September 2020; Accepted: 26 October 2020; Published: 27 October 2020 Simple Summary: Papillary thyroid carcinoma (PTC) represents 80–90% of all differentiated thyroid carcinomas. PTC has a high rate of gene fusions and mutations, which can influence clinical and biological behavior in both children and adults. In this review, we focus on the comparison between pediatric and adult PTC, highlighting genetic alterations, telomere-related genomic instability and changes in nuclear organization as novel biomarkers for thyroid cancers. Abstract: Thyroid cancer is a rare malignancy in the pediatric population that is highly associated with disease aggressiveness and advanced disease stages when compared to adult population.
    [Show full text]
  • Multiple Endocrine Neoplasia Type 1 (MEN1)
    Lab Management Guidelines v2.0.2019 Multiple Endocrine Neoplasia Type 1 (MEN1) MOL.TS.285.A v2.0.2019 Introduction Multiple Endocrine Neoplasia Type 1 (MEN1) is addressed by this guideline. Procedures addressed The inclusion of any procedure code in this table does not imply that the code is under management or requires prior authorization. Refer to the specific Health Plan's procedure code list for management requirements. Procedures addressed by this Procedure codes guideline MEN1 Known Familial Mutation Analysis 81403 MEN1 Deletion/Duplication Analysis 81404 MEN1 Full Gene Sequencing 81405 What is Multiple Endocrine Neoplasia Type 1 Definition Multiple Endocrine Neoplasia Type 1 (MEN1) is an inherited form of tumor predisposition characterized by multiple tumors of the endocrine system. Incidence or Prevalence MEN1 has a prevalence of 1/10,000 to 1/100,000 individuals.1 Symptoms The presenting symptom in 90% of individuals with MEN1 is primary hyperparathyroidism (PHPT). Parathyroid tumors cause overproduction of parathyroid hormone which leads to hypercalcemia. The average age of onset is 20-25 years. Parathyroid carcinomas are rare in individuals with MEN1.2,3,4 Pituitary tumors are seen in 30-40% of individuals and are the first clinical manifestation in 10% of familial cases and 25% of simplex cases. Tumors are typically solitary and there is no increased prevalence of pituitary carcinoma in individuals with MEN1.2,5 © eviCore healthcare. All Rights Reserved. 1 of 9 400 Buckwalter Place Boulevard, Bluffton, SC 29910 (800) 918-8924 www.eviCore.com Lab Management Guidelines v2.0.2019 Prolactinomas are the most commonly seen pituitary subtype and account for 60% of pituitary adenomas.
    [Show full text]
  • Multiple Endocrine Neoplasia Type 2: an Overview Jessica Moline, MS1, and Charis Eng, MD, Phd1,2,3,4
    GENETEST REVIEW Genetics in Medicine Multiple endocrine neoplasia type 2: An overview Jessica Moline, MS1, and Charis Eng, MD, PhD1,2,3,4 TABLE OF CONTENTS Clinical Description of MEN 2 .......................................................................755 Surveillance...................................................................................................760 Multiple endocrine neoplasia type 2A (OMIM# 171400) ....................756 Medullary thyroid carcinoma ................................................................760 Familial medullary thyroid carcinoma (OMIM# 155240).....................756 Pheochromocytoma ................................................................................760 Multiple endocrine neoplasia type 2B (OMIM# 162300) ....................756 Parathyroid adenoma or hyperplasia ...................................................761 Diagnosis and testing......................................................................................756 Hypoparathyroidism................................................................................761 Clinical diagnosis: MEN 2A........................................................................756 Agents/circumstances to avoid .................................................................761 Clinical diagnosis: FMTC ............................................................................756 Testing of relatives at risk...........................................................................761 Clinical diagnosis: MEN 2B ........................................................................756
    [Show full text]
  • A Marker to Distinguish Follicular Thyroid Adenoma from Carcinoma'
    [CANCERRESEARCH57.2144-2147. June I, 1997) Advances in Brief Telomerase Activity: A Marker to Distinguish Follicular Thyroid Adenoma from Carcinoma' Christopher B. Umbricht, Motoyasu Saji, William H. Westra, Robert Udelsman, Martha A. Zeiger, and Saraswati Sukumar@ Breast Cancer Program. Oncology Center (C. B. U., S. SI. Division of Surgical Oncology and Endocrine Surgery (M. S.. R. U., M. A. 1], and Department of Pathology 1W. H. WI, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205 Abstract Finally, activation of one of the three ras oncogenes appears to be a fairly common and early event (5) but is detected in adenomas as well The inability to distinguish microinvasivefollicular thyroid cancer as in carcinomas. More importantly, less than 50% of follicular from benign follicular tumors preoperatively presents an important sur carcinomas in any published series show these changes (6, 7). Thus, gical dilemma. We examined 44 folilcular tumors and found telomerase no molecular markers that can reliably distinguish adenomas from activity in all 11 folllcular carcinomas and in S of 33 benign fofficular tumors. It was undetectable in 22 normal thyroid tissues adjacent to the carcinomas have yet been found. Recently, activation of the ribonu tumors. Telomerase activity may thus provide a diagnostic marker dis cleoprotein telomerase has been found in a wide variety of carcinomas tinguishing benign from malignant follicular thyroid tumors. The ability (8—li). Telomerase is an enzyme that maintains the stability and to identify invasive follicular thyroid tumors could avert over 14,000 integrity of chromosomal ends composed of telomeres (12). Although thyroidectomies annually in the United States, thereby significantly de telomerase activity is repressed in almost all nonneoplastic somatic creasing morbidity and health care costs.
    [Show full text]
  • Cancer Mortality in Women with Thyroid Disease1
    (CANCER RESEARCH 50. 228.1-2289. April 15. 1990| Cancer Mortality in Women with Thyroid Disease1 Marlene B. Goldman,2 Richard R. Monson, and 1aralio Maloof Department of Epidemiology, Harvard School of Public Health, Boston 02115 [M. B. 6"..R. K. M.J, and Thyroid I'nil, Massachusetts Ornerai Hospital, Boston 02114 /F. M.I, Massachusetts ABSTRACT in a study of American women (4). A mechanism for a causal relationship between the two diseases is not established, al A retrospective follow-up study of 7338 women with either nontoxic though thyroid hormones are known to influence the breast nodular goiter, thyroid adenoma, hyperthyroidism, hypothyroidism, Hashimoto's thyroiditis, or no thyroid disease was conducted. All women either directly or through effects on thyroid-stimulating hor patients at the Massachusetts General Hospital Thyroid Clinic who were mone, prolactin, estrogens, or androgens. Researchers sug seen between 1925 and 1974 and who were treated for a minimum of 1 gested that a deficit of thyroid hormone altered the hormonal year were traced. A total of 2231 women (30.4%) were dead and 2012 milieu in a way that permitted the growth of malignant cells (1, women (27.4%) were alive as of December 31, 1978. Partial follow-up 5, 6). It is just as reasonable to hypothesize, however, that an information was available for the remaining 3095 women (42.2%). The excess of thyroid hormone may promote tumor growth. A average length of follow-up was 15.2 years. When losses to follow-up number of biochemical and clinical studies have been con were withdrawn at the time of their loss, the standardized mortality ratios ducted, but no consensus has been reached as to the role of (SMR) for all causes of death were 1.2 |95% confidence interval (CI), thyroid hormones in the initiation or promotion of cancer.
    [Show full text]
  • Carotid Body Tumor Associated with Primary Hyperparathyroidism
    DOI: 10.30928/2527-2039e-20212755 _______________________________________________________________________________________Relato de caso CAROTID BODY TUMOR ASSOCIATED WITH PRIMARY HYPERPARATHYROIDISM TUMOR DO CORPO CAROTÍDEO ASSOCIADO COM HIPERPARATIREOIDISMO PRIMÁRIO Duilio Antonio Palacios1; Ledo Massoni1; Climério Pereira do Nascimento1; Marilia D'Elboux Brescia, TCBC-SP1; Sérgio Samir Arap, TCBC-SP1; Fabio Luiz de Menezes Montenegro, TCBC-SP1. ABSTRACT Introduction: Carotid body tumors (CBT) are an uncommon tumor of head and neck. The associa- tion between this entity with primary hyperparathyroidism (PHPT) is even rarer and few cases have been reported. Case Report: We described two cases of association between CBT and PHPT. The first case was a 55-year-old male patient with Shambling type III malignant paraganglioma and PHPT sin- gle adenoma. The second one was a 56-year-old male patient with Shambling type III paraganglioma and double parathyroid adenoma. Conclusion: The adequate preoperative evaluation allowed to iden- tify and treat simultaneously both neoplasms in these patients without compromising the appropriate treatment. Treatment of the two neoplasms when identified could be performed satisfactorily at the same surgical time. Keywords: Carotid Body Tumor. Hyperparathyroidism. Hypercalcemia. Treatment Outcome. RESUMO Introdução: O paraganglioma de corpo carotídeo (PCC) é um dos tumores menos frequente da cabeça e do pescoço. A associação entre essa entidade e o hiperparatireoidismo primário (HPT) é ainda mais rara e poucos casos foram relatados. Relato do Caso: Relatam-se dois novos casos de PCC e HPT. O primeiro é um paciente de 55 anos com um paraganglioma maligno que envolvia as artérias carótidas interna e externa (Shambling III) e um adenoma de paratireoide. O segundo trata-se de paciente mas- culino de 56 anos, também com tumor Shambling III, mas com duplo adenoma de paratireoide.
    [Show full text]