DOCSLIB.ORG

211 L.A. Erickson, Atlas of Endocrine Pathology, Atlas of Anatomic

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
211 L.A. Erickson, Atlas of Endocrine Pathology, Atlas of Anatomic Index A tumor size and weight , 174 ACC. See Adrenal cortical carcinoma (ACC) unilateral tumors , 165 ACTH. See Adrenocorticotropic hormone (ACTH) Adrenal cortical hyperplasia Acute thyroiditis , 14 autosomal dominant disorder , 159 Adenomatoid tumor description , 159 asymptomatic and identifi ed , 204 diffuse cortical cells and focal lipomatous ectopic ACTH production , 160 metaplasia , 205 enlargement , 161 spaces, small glandular , 205 pancreatic neuroendocrine tumor , 160 Adrenal cortical carcinoma (ACC) secondary hyperplasia , 160 aldosteronism , 168 zona fasciculata , 160 alveolar pattern , 169 nodular cellular and nuclear pleomorphism , 167 defi nition , 161 cystic degeneration , 171 endocrine atypia , 162 cytotoxic chemotherapy , 173 macro- and micronodules , 161, 162 description , 173 PPNAD ( see Primary pigmented nodular adrenocortical eosinophilic cells , 167, 168 disease (PPNAD)) eosinophilic cytoplasm , 170, 172, 179, 180 PRKAR1A gene , 159 feminizing/virilizing tumors , 165 Adrenal cysts histologic features , 173 CD31-immunostained sample , 156 insulin-like growth factor 2 , 173 endothelial-lined adrenal cysts , 156 keratin , 181 fi brous-walled adrenal pseudocyst , 156 lipid-rich adrenal cortical adenoma cells , 168 pheochromocytomas , 155 lipofuscin , 171 pseudocysts , 155, 156 lipomatous/myelolipomatous , 167 vague symptoms , 155 lymphoma , 177 Adrenal gland mitotic fi gures , 175 abnormalities and pathogenic processes , 147 multivariate analysis , 165 adipocytes and lymphocytes , 151 myxoid change central adrenal vein , 150 and epithelioid cells , 170 chromaffi n cells , 150 and spindle cells , 170 encapsulated cortical extrusions , 151 necrosis , 175 formalin , 148 nuclear-to-cytoplasmic ratios heterotopia ( see Heterotopia) and cellular monotony , 174 medullary hyperplasia , 147 monotonous cells , 176 pheochromocytomas , 147 mucin , 178 right and left adrenal glands , 148 pleomorphism , 176 scattered adipocyte , 150 oncocytic adenomas , 171 zona pale lipid-rich cell , 166 fasciculata , 149 pale-staining cells , 167 glomerulosa , 148 pediatric tumors , 173 reticularis , 149 polymorphous cells , 176 Adrenal gland tumors primary hyperaldosteronism , 168 adenomatoid , 204–205 pseudoglandular growth pattern , 169 angiosarcoma , 202 pseudoglandular pattern , 177 leiomyosarcoma , 203 punctate microscopic foci , 175 teratoma , 204 small cell cytomorphology , 178 Adrenal medullary hyperplasia spindle cell change , 179 description , 187 spironolactone bodies , 169 MEN2A, MEN2B and cystic subclinical Cushing syndrome , 166 fi brosis , 188 trabecular growth pattern , 176 pheochromocytoma , 188 tumor behavior , 170 trabecular growth pattern , 188 L.A. Erickson, Atlas of Endocrine Pathology, Atlas of Anatomic Pathology, 211 DOI 10.1007/978-1-4939-0443-3, © Springer Science+Business Media New York 2014 212 Index Adrenal myelolipoma colloid , 34 adjacent adrenal cortical tissue , 184 cystic-appearing lymph node metastasis , 36 bilateral , 183 growth patterns , 34 cortical tissue , 184 intranuclear holes , 34 description , 183 invasive , 32 hematopoietic elements , 184 low-power photomicrograph , 35 hypersecretion , 183 multiple ill-defi ned fi rm masses , 32 trilineage hematopoietic cells , 185 “Orphan Annie” nuclei , 32 yellow adipose tissue , 184 papillae with fi brovascular cores and cystic change , 32, 33 Adrenal tumors, metastatic prominent papillae with fi brovascular cores , 32, 33 breast cancer , 209 psammoma bodies , 33 cortical , 207 Columnar variant of PTC , 47 medullary , 207 Composite pheochromocytoma melanoma , 208 composition , 194 neuroendocrine , 207 ganglioneuroma , 194 primary , 207 Cowden syndrome , 25 renal cell carcinoma , 208 Cribriform-morular variant of PTC Adrenocorticotropic hormone (ACTH) aberrant nuclear and cytoplasmic staining, β-catenin , 41 in congenital adrenal hyperplasia , 159 arches and anastomosing bars , 40 cortical hyperplasia , 159 autosomal dominant syndrome , 40 neuroendocrine tumor , 160 morules , 41 Amiodarone thyroid , 5–6 nuclear staining, TTF1 , 41 Amyloid goiter , 25, 28–29 spindle/oval tumor cells , 41 Anaplastic thyroid carcinoma adjacent structures, invasion , 72 atypical spindle cells , 73 D composition , 71, 73 de Quervain thyroiditis. See Granulomatous distant metastases , 71 (de Quervain) thyroiditis hemorrhage and necrosis areas , 72 Diffuse hyperplasia. See Graves disease Hurthle cell carcinoma, dedifferentiation , 74 Diffuse sclerosing variant of PTC , 43 papillary thyroid carcinoma (PTC) , 74–75 Dyshormonogenetic goiter , 27–28 Rhabdoid features , 74 Riedel (fi brous) thyroiditis , 71, 73 TTF1 , 71 F vascular invasion , 72 Familial isolated hyperparathyroidism (FIH) , 131 Angiosarcoma , 92, 202 Fibrous (Riedel) thyroiditis , 13, 16, 71, 73 Atypical parathyroid adenoma FIH. See Familial isolated hyperparathyroidism (FIH) composition , 128 Focal lymphocytic thyroiditis , 13, 18 hypercellular and fi brosis , 128 Follicular adenoma indolent behavior , 128 adipocytes , 57 irregular growth and fi brous bands , 129 clear cell change , 56, 57 Ki67 labeling index , 129 degenerative feature and hyalinization , 59 monotonous growth , 129 description , 55 parathyroid carcinoma , 128 extensive signet ring cell change , 58 immunoperoxidase markers , 56 medium-power view , 59 B metaplastic bone/ossifi cation , 59 Breast cancer , 209 microfollicular and macrofollicular architectural Brown tumor of bone , 113 pattern , 56 mucin , 57 prominent spindle cell change , 58 C signet ring cell change , 58 Calcifi cations , 81 thyroid , 56 Carcinoembryonic antigen (CEA) , 84 Follicular carcinoma Carcinoma showing thymus-like differentiation (CASTLE) , 94–95 capsular invasion , 60 CASTLE. See Carcinoma showing thymus-like clear cell change , 61, 62 differentiation (CASTLE) description , 60 C cells, tumors mushroom-like area , 60 hyperplasia , 78 signet ring cell change , 62 medullary thyroid microcarcinoma , 78–79 spindle cell change , 62 MTC ( see Medullary thyroid carcinoma (MTC)) thrombus , 61 CEA. See Carcinoembryonic antigen (CEA) vascular invasion , 60, 61 Chief cells, parathyroid histology , 103–104 Follicular thyroid neoplasms Classic PTC adenomas ( see Follicular adenoma) cervical and ipsilateral lymph nodes , 35 carcinomas ( see Follicular carcinoma) characteristic cytologic features , 33 cytologic specimens , 55 Index 213 histologic patterns , 55 extracellular eosinophilic hyaline fi brosis , 52 malignancy , 55 prominent eosinophilic intranuclear tumors with extensive vascular invasion , 55 inclusions , 52 Follicular variant of papillary thyroid RET/PTC rearrangements , 51 carcinoma (FVPTC) tumor cells , 52 characteristic features , 38 Hyperparathyroidism–jaw tumor syndrome classic PTC , 37, 39 (HP-JT) , 131 cumulative diagnosis , 37 elongated follicles , 38 encapsulated tumors , 37 L HBME-1 immunostain , 40 Langerhans cell histiocytosis , 91 low-power photomicrograph , 39 Leiomyosarcoma , 203 numerous patterns , 38 Lipoadenomatous hyperplasia , 114 photomicrograph shows , 38 Lipohyperplasia , 109 thyroid parenchyma , 39 Low-grade fi bromyxoid sarcoma , 93 Lymphoma , 90 G Ganglioneuroma M adrenal gland , 198 Medullary thyroid carcinoma (MTC) needle core biopsy , 198 acinar growth pattern , 82 recognizable tumor , 197 amyloid , 79 spindled Schwann cells , 199 calcifi cations , 81 stroma-rich , 198 calcitonin , 83 Granulomatous (de Quervain) thyroiditis CEA , 84 multinucleated giant cells , 15 composition , 81 noncaseating granulomas , 15 epithelioid cells , 80 patchy areas, neutrophils and microabscesses , 14 growth patterns , 80 patients , 13, 14 intranuclear pink holes , 80 Graves disease neuroendocrine markers , 83 complications , 21 oxyphilic , 82 cut section , 22 papillary architectural pattern , 83 diffuse hyperplasia , 23 recognization , 82 diffusely enlarged thyroid , 22 solid growth, necrosis , 81 follicular epithelium , 24 spindle cells , 80 hyperthyroidism , 21 syndromic , 79 low-power photomicrograph , 22 TTF1 , 83, 84 papillae , 22, 23 Metastases to parathyroid patients treatment with iodine , 24 carcinoma , 144 thyroid carcinomas , 21 medullary thyroid carcinoma , 144 thyroid parenchyma , 22 primary thyroid tumors , 143 thyroid tumors , 144 Metastases to thyroid H breast cancer metastatic , 100 Hashimoto thyroiditis melanoma metastatic , 101 fi brous variant , 18 primary tumors , 99 prominent lymphoid follicles , 17 renal cell carcinoma metastatic , 100 solid cell nests , 18 resection , 99 thyroid , 13 Minocycline thyroid , 5–6 H&E. See Hematoxylin and eosin (H&E) MTC. See Medullary thyroid Hematoxylin and eosin (H&E) , 1, 4 carcinoma (MTC) Heterotopia Multinodular goiter , 26–27 adipocytes and foci, lymphocytes , 152 Multiple endocrine neoplasia (MEN) types cortical nodule , 152 1 and 2A , 109 embryologic path , 152 subcapsular space , 152 Hobnail variant of PTC , 48 N HP-JT. See Hyperparathyroidism–jaw tumor Nephrolithiasis , 121 syndrome (HP-JT) Neuroblastoma Hurthle cell adenoma , 63, 64 children , 197 Hurthle cell carcinoma , 65 classifi cation , 197, 199 Hurthle cell thyroid neoplasms , 63–65 ganglion and Schwann cells , 197 Hyalinizing trabecular tumor malignant , 197 Carney’s group , 51 nests , 200 description , 51 primordial neural crest cells , 199 encapsulation and separation , 52 sporadic , 197 214 Index Normal thyroid glandular growth pattern , 135 central lumen containing colloid , 3 hemosiderin deposition , 134 chromogranin immunostain , 4 HRPT2 tumor suppressor gene , 131 cut section , 2 hyperplasia and , 133 fat cells , 4 intrathyroidal , 133 follicles , 3 invasive
Load more

Recommended publications
  • 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]
  • View Its Management Considering the Recent Relevant Literature
    Ferraro et al. BMC Endocrine Disorders 2019, 19(Suppl 1):46 https://doi.org/10.1186/s12902-019-0368-1 RESEARCH Open Access Current concepts in parathyroid carcinoma: a single Centre experience Valentina Ferraro1†, Lucia Ilaria Sgaramella1†, Giovanna Di Meo1, Francesco Paolo Prete2, Francesco Logoluso2, Francesco Minerva1, Marica Noviello1, Giuseppina Renzulli3, Angela Gurrado1 and Mario Testini1* Abstract Background: Parathyroid carcinoma is a rare neoplasm that may present sporadically or in the context of a genetic syndrome. Diagnosis and management are challenging due to the lack of clinical and pathological features that may reliably distinguish malignant from benign disease. Methods: From January 2013 to December 2017, from 358 consecutive patients affected by parathyroid diseases, 3 patients with parathyroid carcinoma were treated at our academic Department of General Surgery. We present our experience as illustrative of the different features of clinical presentation of parathyroid carcinoma and review its management considering the recent relevant literature. Results: Case 1: A 62-year-old man was hospitalized for left-sided palpable neck mass, hypercalcemia and elevated PTH. US-guided FNA was suspect for parathyroid carcinoma. A large cystic mass was excised in bloc with total thyroidectomy and central neck dissection. Genetic studies framed a pathologically confirmed parathyroid carcinoma within MEN1 syndrome. Case 2: A 48-year-old woman with hypothyroidism had total thyroidectomy performed for a suspect for right follicular thyroid lesion. Pathology revealed parathyroid carcinoma. Case 3: A47 year-old man was admitted for hypercalcaemic crisis and renal failure in the context of PHPT. A lesion suggestive on US and MIBI scan for parathyroid adenoma in the right lower position was removed by mini-invasive approach.
    [Show full text]
  • NCCN Neuroendocrine Tumors Guidelines Are Divided Into 6 Endocrine Systems, Which Produce and Secrete Regulatory Hormones
    NCCN Clinical Practice Guidelines in Oncology™ Neuroendocrine Tumors V.1.2007 Continue www.nccn.org Guidelines Index ® Practice Guidelines Neuroendocrine TOC NCCN in Oncology – v.1.2007 Neuroendocrine Tumors MS, References NCCN Neuroendocrine Tumors Panel Members * Orlo H. Clark, MD/Chair ¶ John F. Gibbs, MD ¶ Thomas W. Ratliff, MD † UCSF Comprehensive Cancer Center Roswell Park Cancer Institute St. Jude Children's Research Hospital/University of Tennessee Jaffer Ajani, MD †¤ Martin J. Heslin, MD ¶ Cancer Institute The University of Texas M. D. University of Alabama at Anderson Cancer Center Birmingham Comprehensive Leonard Saltz, MD † Cancer Center Memorial Sloan-Kettering Cancer Al B. Benson, III, MD † Center Robert H. Lurie Comprehensive Fouad Kandeel, MD Cancer Center of Northwestern City of Hope Cancer Center David E. Schteingart, MD ð University University of Michigan Anne Kessinger, MD † Comprehensive Cancer Center David Byrd, MD ¶ UNMC Eppley Cancer Center at The Fred Hutchinson Cancer Research Nebraska Medical Center Manisha H. Shah, MD † Center/Seattle Cancer Care Alliance Arthur G. James Cancer Hospital & Matthew H. Kulke, MD † Richard J. Solove Research Gerard M. Doherty, MD ¶ Dana-Farber/Partners CancerCare Institute at The Ohio State University of Michigan Comprehensive University Cancer Center Larry Kvols, MD † H. Lee Moffitt Cancer Center & Stephen Shibata, MD † Paul F. Engstrom, MD † Research Institute at the University City of Hope Cancer Center Fox Chase Cancer Center of South Florida David S. Ettinger, MD † John A. Olson, Jr., MD, PhD ¶ The Sidney Kimmel Comprehensive Duke Comprehensive Cancer Cancer Center at Johns Hopkins Center * Writing Committee Member ¶ Surgery/Surgical oncology † Medical oncology ¤ Gastroenterology ð Endocrinology Continue Version 1.2007, 03/14/07 © 2007 National Comprehensive Cancer Network, Inc.
    [Show full text]
  • Non-Functioning Parathyroid Carcinoma: a Case Report
    Suganuma et al. Surgical Case Reports (2017) 3:81 DOI 10.1186/s40792-017-0357-4 CASE REPORT Open Access Non-functioning parathyroid carcinoma: a case report Nobuyasu Suganuma1* , Hiroyuki Iwasaki1, Satoru Shimizu1, Tatsuya Yoshida1, Takashi Yamanaka1, Izumi Kojima1, Haruhiko Yamazaki1, Soji Toda2, Hirotaka Nakayama2, Katsuhiko Masudo2, Yasushi Rino2, Kae Kawachi1, Yohei Miyagi1, Akio Miyake2, Kenichi Ohashi2 and Munetaka Masuda2 Abstract Background: Non-functioning parathyroid carcinoma is a rare disease that is difficult to distinguish from other diseases based on the lack of hyperparathyroidism. This is a report of non-functioning parathyroid carcinoma diagnosed by reverse transcription polymerase chain reaction (RT-PCR) targeting parathyroid hormone (PTH) messenger RNA. Case Presentation: The patient is a 67-year-old male who visited our hospital for the chief complaint of hoarseness. A 5-cm mass was observed in the right lobe of the thyroid gland, and poorly differentiated thyroid carcinoma was suspected according to the fine-needle biopsy results. The laboratory data for thyroid functions, thyroglobulin, anti-thyroglobulin antibodies, calcium, phosphorus, and intact-PTH were all within the normal range. Right recurrent nerve paralysis was observed preoperatively. The patient was diagnosed with poorly differentiated thyroid carcinoma, and total thyroidectomy and central node dissection with partial resection of the right recurrent nerve and esophageal muscle were performed. The pathological findings revealed atypical cells containing clear cells in solid and alveolar structures with broad fibrosis. Mitosis, focal coagulative necrosis, and vascular and capsular invasions were observed. A slightly positive PTH immunohistochemical stain was noted, whereas the RT-PCR results were positive. We finally diagnosed this tumor as non-functioning PTC.
    [Show full text]
  • Case Report Ectopic Secretion of Parathyroid Hormone in a Neuroendo- Crine Tumor: a Case Report and Review of the Literature
    Int J Clin Exp Med 2011;4(3):234-240 www.ijcem.com /ISSN:1940-5901/IJCEM1103003 Case Report Ectopic secretion of parathyroid hormone in a neuroendo- crine tumor: a case report and review of the literature Emad Kandil1, Salem Noureldine1, Mohamed Abdel Khalek1, Philip Daroca2; Paul Friedlander3 1Division of Endocrine and Oncologic Surgery, Department of Surgery; 2Department of Pathology, Tulane University School of Medicine, New Orleans, LA; 3Department of Otolaryngology; Tulane University School of Medicine, New Orleans, LA, USA. Received March 30, 2011; accepted August 19, 2011; Epub September 15, 2011; published September 30, 2011 Abstract: Very few cases have been reported in which the production and secretion of intact PTH by a non-parathyroid tumor has been authenticated. This paper describes the case of a 73 year old white female with a clinical and bio- chemical profile characteristic of primary hyperparathyroidism. Sestamibi scan and comprehensive neck ultrasono- graphy failed to localize a cervical lesion. Because the clinical manifestations were striking, neck exploration was performed. Dissection of the central compartment identified a lesion. PTH levels dropped to normal within ten min- utes after its removal. Intraoperative parathyroid hormone assays facilitated the successful surgical removal of the lesion. Pathological examination yielded a diagnosis of a neuroendocrine tumor. These results document the ectopic production of intact PTH by a neuroendocrine tumor and present a novel neoplastic cause of primary hyperparathy- roidism. This is the second report of an ectopic neuroendocrine tumor in the head and neck which secreted intact PTH. Keywords: Ectopic neuroendocrine tumor, ectopic PTH, primary hyperparathyroidism, intraoperative PTH assays Introduction approach has an equivalent rate of complica- tions as well as of persistent and recurrent dis- Primary hyperparathyroidism is a common dis- ease when compared to bilateral cervical explo- ease, with approximately 100,000 new cases ration [6, 10].
    [Show full text]
  • Downloaded from Bioscientifica.Com at 09/25/2021 10:48:16PM Via Free Access
    25 2 Endocrine-Related C Guerin et al. MEN2 and non-MEN2 PHEO 25:2 T15–T28 Cancer and HPTH THEMATIC REVIEW Looking beyond the thyroid: advances in the understanding of pheochromocytoma and hyperparathyroidism phenotypes in MEN2 and of non-MEN2 familial forms Carole Guerin1, Pauline Romanet2, David Taieb3, Thierry Brue4, André Lacroix5, Frederic Sebag1, Anne Barlier2 and Frederic Castinetti4 1Department of Endocrine Surgery, Aix Marseille University, Assistance Publique Hopitaux de Marseille, La Conception Hospital, Marseille, France 2Department of Molecular Biology, Aix Marseille University, CNRS UMR 7286, Assistance Publique Hopitaux de Marseille, La Conception Hospital, Marseille, France 3Department of Nuclear Medicine, Aix Marseille University, Assistance Publique Hopitaux de Marseille, La Timone Hospital, Marseille, France 4Department of Endocrinology, Aix Marseille University, CNRS UMR7286, Assistance Publique Hopitaux de Marseille, La Conception Hospital, Marseille, France 5Endocrine Division, Department of Medicine, Centre hospitalier de l’Université de Montréal, Montreal, Quebec, Canada Correspondence should be addressed to F Castinetti: [email protected] This paper is part of a thematic review section on 25 Years of RET and MEN2. The guest editors for this section were Lois Mulligan and Frank Weber. Abstract Over the last years, the knowledge of MEN2 and non-MEN2 familial forms of Key Words pheochromocytoma (PHEO) has increased. In MEN2, PHEO is the second most frequent f pheochromocytoma disease: the penetrance and age at diagnosis depend on the mutation of RET. Given f hyperparathyroidism the prevalence of bilateral PHEO (50% by age 50), adrenal sparing surgery, aimed f multiple endocrine at sparing a part of the adrenal cortex to avoid adrenal insufficiency, should be neoplasia systematically considered in patients with bilateral PHEO.
    [Show full text]
  • Parafibromin Immunostainings of Parathyroid Tumors in Clinical Routine
    Modern Pathology (2019) 32:1082–1094 https://doi.org/10.1038/s41379-019-0252-6 ARTICLE Parafibromin immunostainings of parathyroid tumors in clinical routine: a near-decade experience from a tertiary center 1,2 3,4 3,5 1,3,4 C. Christofer Juhlin ● Inga-Lena Nilsson ● Kristina Lagerstedt-Robinson ● Adam Stenman ● 3,4 3,5 1,2 Robert Bränström ● Emma Tham ● Anders Höög Received: 21 November 2018 / Revised: 20 February 2019 / Accepted: 26 February 2019 / Published online: 28 March 2019 © United States & Canadian Academy of Pathology 2019 Abstract The cell division cycle 73 gene is mutated in familial and sporadic forms of primary hyperparathyroidism, and the corresponding protein product parafibromin has been proposed as an adjunct immunohistochemical marker for the identification of cell division cycle 73 mutations and parathyroid carcinoma. Here, we present data from our experiences using parafibromin immunohistochemistry in parathyroid tumors since the marker was implemented in clinical routine in 2010. A total of 2019 parathyroid adenomas, atypical adenomas, and carcinomas were diagnosed in our department, and parafibromin staining was ordered for 297 cases with an initial suspicion of malignant potential to avoid excessive numbers 1234567890();,: 1234567890();,: of false positives. The most common inclusion criteria for immunohistochemistry were marked tumor weight (146 cases) and/or fibrosis (77 cases) and/or marked pleomorphism (58 cases). In total, 238 cases were informatively stained, and partial or complete loss of nuclear parafibromin immunoreactivity was noted in 40 cases; 10 out of 182 adenomas (5%), 27 out of 46 atypical adenomas (59%), and 7 out of 10 carcinomas (70%), with positive and negative predictive values of 85 and 90%, respectively for the detection of atypical adenomas/carcinomas versus adenomas, and 18 and 98%, respectively for carcinomas versus atypical adenomas/adenomas.
    [Show full text]
  • Endocrine Neoplasms in Familial Syndromes of Hyperparathyroidism
    236 Y Li and W F Simonds Hyperparathyroidism-associated 23:6 R229–R247 Review neoplasms Endocrine neoplasms in familial syndromes of hyperparathyroidism Correspondence Yulong Li and William F Simonds should be addressed to W F Simonds Metabolic Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Email National Institutes of Health, Bethesda, Maryland, USA [email protected] Abstract Familial syndromes of hyperparathyroidism, including multiple endocrine Key Words neoplasia type 1 (MEN1), multiple endocrine neoplasia type 2A (MEN2A), f multiple endocrine and the hyperparathyroidism-jaw tumor (HPT-JT), comprise 2–5% of primary neoplasia type 1 (MEN1) hyperparathyroidism cases. Familial syndromes of hyperparathyroidism are also f multiple endocrine neoplasia type 2A associated with a range of endocrine and nonendocrine tumors, including potential (MEN2A) malignancies. Complications of the associated neoplasms are the major causes of f hyperparathyroidism-jaw morbidities and mortalities in these familial syndromes, e.g., parathyroid carcinoma tumor (HPT-JT) in HPT-JT syndrome; thymic, bronchial, and enteropancreatic neuroendocrine tumors f malignant tumor in MEN1; and medullary thyroid cancer and pheochromocytoma in MEN2A. Because f neuroendocrine tumor of the different underlying mechanisms of neoplasia, these familial tumors may have different characteristics compared with their sporadic counterparts. Large-scale clinical trials are frequently lacking due to the rarity of these diseases. With technological advances and the development of new medications, the natural history, diagnosis, Endocrine-Related Cancer Endocrine-Related and management of these syndromes are also evolving. In this article, we summarize the recent knowledge on endocrine neoplasms in three familial hyperparathyroidism syndromes, with an emphasis on disease characteristics, molecular pathogenesis, recent developments in biochemical and radiological evaluation, and expert opinions on surgical and medical therapies.
    [Show full text]
  • Primary Hyperparathyroidism and Thyroid Cancer: a Case Series
    Central JSM Head and Neck Cancer Cases and Reviews Bringing Excellence in Open Access Case Report *Corresponding author Rodrigo Arrangoiz, Department of surgery, Centro Médico ABC, Mexico City, Av. Carlos Graef Fernández Primary Hyperparathyroidism #154 Consultorio 515 Col. Tlaxala, Delg, Cuajimalpa, México, D.F. 05300, Tel: 1103-1600 Ext: 4515 to 4517; Fax: 1664-7164; Email: and Thyroid Cancer: A Case Submitted: 09 January 2017 Accepted: 21 January 2017 Series Published: 23 January 2017 Copyright Arrangoiz R*, Lambreton-Hinojosa F, Cordera F, Caba D, Cruz- © 2017 Arrangoiz et al. González E, Luque-de-León E, Moreno E, and Muñoz M OPEN ACCESS Department of surgery, Centro Médico ABC, Mexico Keywords Abstract • Primary hyperparathyroidism • Papillary thyroid carcinoma Primary hyperparathyroidism (PHTP) is the most common cause of outpatient • Surgical treatment hypercalcemia and has a prevalence of about one to seven cases per 1,000 adults. • Preoperative evaluation Concurrent thyroid disease and PHPT has been reported in 20% to 84% of the cases, although no causal relationship has been established. Malignant tumors of the thyroid are identified in approximately 2% to 20% of these cases. Papillary thyroid carcinoma (PTC) is the most common thyroid malignancy. Certain situations undoubtedly contribute to the development of both of these diseases, such as the use of therapeutic neck radiation for various clinical indications used in the past. Outside of these special situations with a clear etiology, the wide variation in reports of concomitant parathyroid and thyroid disease fuel debate as to the necessity and extent of thyroid evaluation prior to surgical treatment of PHPT. We report on 5 patients with thyroid cancer that was detected or suspected during work-up for surgical treatment of PHPT.
    [Show full text]