2023 European Thyroid Association Clinical Practice Guidelines for thyroid nodule management

Abstract

With the widespread use of sensitive imaging techniques, which include neck visualization, a conspicuous number of thyroid nodules emerge and demand attention. Most lesions are benign, asymptomatic, and do not warrant treatment. In case of cancer diagnosis, most are small, intrathyroidal and indolent neoplasms that can safely be managed conservatively. There is a pronounced need for more cost-effective, risk-adapted approaches to the management of this highly prevalent condition, taking the voice of the patient into consideration. Thus, the present guidelines aim at providing a clinical practice guide for the initial work-up and the subsequent management of adult individuals harbouring thyroid nodules. Importantly, these guidelines are not intended to cover the management of thyroid malignancy. The manuscript and the specific recommendations were developed by reconciling the best available research evidence with the knowledge and clinical experience of the panellists and updates aspects of a number of previous European Thyroid association guidelines.

Use of thyroid hormones in hypothyroid and euthyroid patients: A survey of members of the Endocrine Society of Australia

“…[13][14][15][16][17][18][19] Only eleven percent of respondents considered prescribing thyroid hormones for a simple goitre growing over time, which is consistent with clinically insignificant benefit and the risks associated with lowering TSH. 34 This number was lower than most surveyed European countries and similar to Latin America, Denmark and the United Kingdom. 10,[12][13][14][15][16][17][18][19][20][21][22] Reassuringly, use of thyroid hormone for euthyroid patients with depression, severe hypercholesterolaemia and unexplained fatigue were not considered by most respondents.…”

Are there specific cytologic features that can predict BRAFV600E mutational status of papillary thyroid carcinoma in fine‐needle aspiration specimens?

“…6 In addition, molecular testing of thyroid FNAs outside the United States is currently mainly limited to local laboratory-developed research settings in Europe and East Asia, and a publicly funded test in Canada. 20 Immunohistochemistry for BRAF antibody (clone VE1) has been successfully used in surgical pathology specimens to screen for BRAF V600E alterations and shown excellent concordance with molecular tests. 21 The utilization of BRAFVE1 immunocytochemistry in PTC cytology specimens has shown high sensitivity and specificity.…”

The C55A Single Nucleotide Polymorphism in CTLA-4 Gene, a New Possible Biomarker in Thyroid Autoimmune Pathology Such as Hashimoto’s Thyroiditis

“…The case group included patients diagnosed by endocrinologists, based on clinical criteria (fatigue and sluggishness, constipation, dry skin, increased sensitivity to cold, etc.) and paraclinical criteria all values for thyroid markers, such as thyroid stimulating hormone (TSH), free thyroxine (FT4), anti-thyroid peroxidase (ATPO), and anti-thyroglobulin antibodies (ATG), according to the European and national guidelines for hypothyroidism [21][22][23][24]. The control group included healthy persons, without clinical manifestations regarding thyroid diseases and with normal reference values for TSH, FT4, ATPO, and ATG.…”

“…The fact that the healthy siblings of AITDs patients with positive autoantibodies demonstrates that the genetic locus responsible for seropositivity is different from the one involved in the control of the clinical manifestations of AITDs (fatigue, dry skin, constipation, increased sensitivity to cold, etc.) [21][22][23][24]. The locus of the gene involved in the synthesis of the Cytotoxic T-Lymphocyte Antigen (CTLA-4) is located on the long arm, band 33 of chromosome 2 [25,26].…”

“…The production of anti-TG and anti-TPO thyroid autoantibodies is a specific feature of AITDs [1,10,33]. These autoantibodies are used as markers for the evaluation of various forms of AITDs, such as hypothyroidism, HT, and postpartum thyroiditis (PPT) [1,[21][22][23][24]34]. Another study proved that anti-TPO and TG antibodies develop in HT as a result of follicular cells damages, produced by T lymphocytes mediated cytotoxicity [18,32].…”