Endocrine surgery

2021 ◽  
pp. 327-364

This chapter outlines the clinically relevant anatomy and physiology of the thyroid and parathyroid glands. The assessment and management of a patient with a thyroid goitre and post-operative complications are described in detail. Conditions such as thyrotoxicosis, thyroid malignancies, hyperparathyroidism, adrenal incidentaloma, cushing’s syndrome, conn’s syndrome, phaeochromocytoma and multiple endocrine neoplasia are discussed in this chapter.

2017 ◽  
Vol 8 (5) ◽  
pp. 5-11
Author(s):  
Zoya S. Matveeva ◽  
Anatoliy F. Romanchishen ◽  
Alexandr V. Gostimsky ◽  
Kristina V. Vabalayte

The article presents results of diagnostics, surgical treatment and follow-up of patients with rare hereditary-conditioned forms of thyroid cancer – medullary thyroid carcinoma in content of multiple endocrine neoplasia syndrome. Particular attention is paid to the examination and tactics of treatment of children and adolescents with family genetically confirmed Sipple syndrome. The disease is diagnosed in 4 families. Syndrome of multiple endocrine neoplasia 2a type we found in 7 (0.024%) of 29,325 children and adult patients. All the children were from families in which one of the blood relatives suffered medullary thyroid cancer. The family nature of the disease was confirmed by molecular genetic studies that revealed mutations in C634 (T1900C) in the 11 exon of the RET gene. Only in 3 out of 7 cases thyroidectomy was prophylactic. Four children were fond foci of medullary carcinoma in the removed thyroid gland. In total, 22 operations were performed for the members of 4 families suffering from the family syndrome MEN-2a. The article shows that if a patient is diagnosed Sippl's syndrome, all his blood relatives need to be checked for the mutation of the RET gene to identify familial medullary thyroid cancer, adenomas of parathyroid glands and pheochromocytomas. Early removal of the thyroid gland (in children under the age of 5 years) prevents medullary cancer, and timely diagnosis and adequate surgical removal of neoplasms of parathyroid glands and adrenal glands ensure recovery of the patients. Closest relatives should be checked for the level of calcium and calcitonin, catecholamines, vanillylmandelic acid and metanephrine, ACTH, cancer-embryonic antigen.


2012 ◽  
Vol 58 (3) ◽  
pp. 323-327 ◽  
Author(s):  
André Fernandes d’Alessandro ◽  
Fábio Luiz de Menezes Montenegro ◽  
Lenine Garcia Brandão ◽  
Delmar Muniz Lourenço ◽  
Sérgio de Almeida Toledo ◽  
...  

Author(s):  
Matthew D. Gardiner ◽  
Neil R. Borley

This chapter begins by discussing the basic principles of oncology, cancer diagnosis and classification, and cancer treatment, before focusing on the key areas of knowledge, namely disorders of breast development and involution, breast cancer assessment and management, goitre, altered thyroid state, thyroid cancer, parathyroid conditions, adrenal conditions, and multiple endocrine neoplasia. The chapter concludes with relevant case-based discussions.


2018 ◽  
Vol 13 ◽  
pp. 117727191878512 ◽  
Author(s):  
Fatemeh Khatami ◽  
Seyed Mohammad Tavangar

Multiple endocrine neoplasia (MEN) syndromes are infrequent inherited disorders in which more than one endocrine glands develop noncancerous (benign) or cancerous (malignant) tumors or grow excessively without forming tumors. There are 3 famous and well-known forms of MEN syndromes (MEN 1, MEN 2A, and MEN 2B) and a newly documented one (MEN4). These syndromes are infrequent and occurred in all ages and both men and women. Usually, germ line mutations that can be resulted in neoplastic transformation of anterior pituitary, parathyroid glands, and pancreatic islets in addition to gastrointestinal tract can be an indicator for MEN1. The medullary thyroid cancer (MTC) in association with pheochromocytoma and/or multiple lesions of parathyroid glands with hyperparathyroidism can be pointer of MEN2 which can be subgrouped into the MEN 2A, MEN 2B, and familial MTC syndromes. There are no distinct biochemical markers that allow identification of familial versus nonfamilial forms of the tumors, but familial MTC usually happens at a younger age than sporadic MTC. The MEN1 gene (menin protein) is in charge of MEN 1 disease, CDNK1B for MEN 4, and RET proto-oncogene for MEN 2. The focus over the molecular targets can bring some hope for both diagnosis and management of MEN syndromes. In the current review, we look at this disease and responsible genes and their cell signaling pathway involved.


1987 ◽  
Vol 114 (1) ◽  
pp. 12-17 ◽  
Author(s):  
Lars Benson ◽  
Jonas Rastad ◽  
Sverker Ljunghall ◽  
Claes Rudberg ◽  
Göran Åkerström

Abstract. Hyperparathyroidism (HPT) in the syndrome of multiple endocrine neoplasia type 1 (MEN-1) exhibits a different picture regarding its propensity for recurrence compared with sporadic primary HPT. In order to shed further light on the MEN-1 syndrome an investigation in vitro was made of parathyroid hormone (PTH) release of dispersed parathyroid cell from 11 patients with parathyroid hyperplasia associated with MEN-1, 10 patients with single parathyroid adenomas, and 10 preparations of normal bovine parathyroid glands. The two patient groups had the same average serum calcium value prior to surgery. Immunoreactive concentrations of PTH were measured after 2-h incubations at extracellular calcium concentrations of 0.5–3.0 mmol/l. Compared with the normal bovine parathyroid cells, the cells of the MEN-1 patients had a reduced calcium sensitivity of the PTH release and secreted smaller amounts of hormone at both low and high extracellular calcium concentrations. A similar abnormality of the PTH release was found for the cells of the hyperplastic and adenomatous parathyroid glands. Although individual parathyroid glands were investigated in only three MEN-1 patients, the results suggested the secretory regulation to be less defective in the small glands of each patient. It is concluded that in patient groups matched for serum calcium, the parathyroid tissue of MEN-1 patients has an abnormality of the PTH release similar to that of parathyroid adenomas.


Sign in / Sign up

Export Citation Format

Share Document