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3 results

  • Chapter 26 - Anesthesia for laryngoplasty

  • from Section 4 - Anesthesia for laryngotracheal surgery
  • Edited by Basem Abdelmalak, John Doyle
  • Book:
    Anesthesia for Otolaryngologic Surgery
    Published online:
    05 November 2012
    Print publication:
    18 October 2012, pp 245-254

  • Summary

    There are several specific issues that significantly affect the anesthetic management for patients undergoing thyroid surgery. In addition to the general considerations pertaining to anesthesia, specific attention should be directed to the assessment of thyroid function, the size and location of the thyroid gland, its relationship to the trachea and adjacent vascular structures, and the co-existence of a multiple endocrine neoplasia. Hyperparathyroidism due to an adenoma or hyperplasia is the most common presenting symptom of multiple endocrine neoplasia 1 syndrome. Patients at risk of iatrogenic hypoparathyroidism should have ionized calcium levels monitored postoperatively until calcium levels demonstrate that parathyroid function is intact. Primary hyperparathyroidism may result from benign parathyroid adenoma, multiple gland hyperplasia and carcinoma of the parathyroid glands. Clinical signs include carpopedal spasm during cuff inflation, facial twitching by tapping over the facial nerve at the parotid gland, and a prolonged QT interval on the ECG.

  • Chapter 14 - Tight glucose control using intensive insulin therapy in the critically ill

  • from Section 3 - Endocrine disorders in the critically ill
  • Edited by George M. Hall, St George's Hospital, London, Jennifer M. Hunter, University of Liverpool, Mark S. Cooper, University of Birmingham
  • Book:
    Core Topics in Endocrinology in Anaesthesia and Critical Care
    Published online:
    06 July 2010
    Print publication:
    01 April 2010, pp 134-143

  • Summary

    Multiple endocrine neoplasia (MEN) is a rare autosomal dominant disorder characterised by primary tumours in at least two different endocrine glands. In the early twentieth century, a syndrome that involved the concurrence of tumours of the parathyroid glands, the pancreatic islets and the anterior pituitary gland was described. The gene that codes for menin is located on chromosome 11q12-13 and transcribes an mRNA consisting of 10 exons which encodes the 610 amino acid protein, menin. MEN 2 is a rare disorder with a prevalence of one in 20,000, and like MEN 1, is an dominant syndrome. The RET protooncogene, located on chromosome 10q11.2, transcribes an mRNA consisting of 21 exons. Molecular information has revolutionised the understanding and treatment of MEN 2. The increasing knowledge of the molecular mechanisms of MEN coupled with the clinical outcome and the availability of genetic testing has greatly reduced its morbidity and mortality.

  • New presentation of familial medullary thyroid carcinoma in 87-year-old patient with high-risk RET proto-oncogene codon 620 mutation

  • M K J Jaggard, C MacRae, S Ifeacho, S Robinson, N S Tolley
  • Journal:
    The Journal of Laryngology & Otology / Volume 123 / Issue 7 / July 2009
    Published online by Cambridge University Press:
    04 September 2008, pp. 796-800
    Print publication:
    July 2009
  • Objective:

    We report a case of familial medullary thyroid carcinoma in an 87-year-old woman, despite the patient having a high-risk codon 620 mutation.

    Method:

    Medline and PubMed were searched for cases and literature reviews relating to the following keywords: ‘codon 620’, ‘medullary thyroid carcinoma’, ‘multiple endocrine neoplasia’ and ‘RET proto-oncogene’.

    Results:

    We report the case of an 87-year-old woman who presented with a goitre, later identified as medullary thyroid carcinoma. Genetic analysis revealed a RET proto-oncogene codon 620 mutation. Genetic testing has revolutionised the management of medullary thyroid carcinoma. The genetic basis of hereditary medullary thyroid carcinoma lies with the RET proto-oncogene. Several disease-causing mutations of this gene have been identified and their clinical prognosis described. The penetrance of these mutations is high; as such, carriers progress to develop medullary thyroid carcinoma at a young age. Mutations at the codon 620 position are classified as high-risk for early development of medullary thyroid carcinoma; thus, the current recommendation is for prophylactic thyroidectomy at five years of age.

    Conclusions:

    In this case, the progress of hereditary medullary thyroid carcinoma was unique, considering the late presentation of medullary thyroid carcinoma despite the presence of the high-risk RET proto-oncogene codon 620 mutation. The authors wish to highlight the importance of this case, as it may present a counter-argument to the current recommendations for early, prophylactic thyroidectomy in codon 620 mutation carriers in order to prevent early development of medullary thyroid carcinoma.