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Congress Report: 16th Latin American Thyroid Society (LATS)

PART OF Manage Thyroid Online FEATURE
Congress Report: 16th Latin American Thyroid Society (LATS)
  • Endocrinology and metabolism
  • Thyroid disorder


Resource type



Regional conference
Latin America
thyroid disease
thyroid cancer



Highlights from the 16th Latin American Thyroid Society (LATS) Congress, Rio de Janeiro, Brazil, 15-18 June 2017

The 1600 attendees of the XVI LATS Congress in Rio de Janeiro were immersed in clinical, translational and basic thyroid research for 4 days, while surrounded by the spirit of Vinicius de Moraes and his famous Bossa Nova.

During the meeting, several changes in the clinical management of thyroid nodules and thyroid cancer were announced. Also, a new trend in treatment has been identified for the large group of patients with indolent thyroid lesions – the patients with the highest risk of progression are now actively sought and identified, thus providing more personalised treatment for those who need it most.

Among the new proposals discussed at the meeting by Professor Paula Suarez (Porto, Portugal) was the removal of noninvasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP) from the list of thyroid cancers and its inclusion among the non-malignant thyroid lesions. This will probably modify the management of patients with this diagnosis and, once the NIFTP tumours are excluded from the malignancy list, lead to revision downwards of the published rates of malignancy within the indeterminate cytology categories.

Other modifications to clinical management include a patient age cutoff for the TNM stratification of thyroid cancer at 55 years to predict disease-specific survival presented by Professor Fabian Pitoia (Buenos Aires, Argentina). This will eventually result in the down-staging of several patients who will now receive far less invasive treatment1 as well as the implementation of a dynamic recurrence risk stratification, rather than a static initial risk classification as follow up. The use of this stratification risk system has been further validated for those thyroid cancer patients with lobectomy or who have not received radioiodine treatment.2

Similarly, the management of microcarcinomas may change into ‘active surveillance’ rather than thyroidectomy explained Professor Gregory Randolph (Harvard Medical School, USA). The age of the patient, the tumour location and the presence of lymph node involvement are all factors to be considered for this decision.

Professor Enrico Papini (Rome, Italy), reported that patients with localized thyroid cancer metastases might receive local treatments that include radiofrequency or laser thermal ablation. For those with distant metastases who are refractory to radioiodine, the use of multikinase inhibitors, of which several (eg., sorafenib, vandetanib and lenvantinib) are already licensed by the public health organizations in some Latam countries, was discussed by Professor Martin Schlumberger (Paris, France).

In the field of translational research, the advances in thyroid cancer include the use of microRNAs (miRNAs) - small, highly conserved non-coding RNA molecules involved in the regulation of gene expression. Low expression of miR-451a has been shown to correlate with aggressive clinical-pathological features of papillary thyroid cancer (PTC) -  tall cell variant, advanced stage and extrathyroid extension.3 Marked down-regulation of 14q32-encoded miRNAs in an in vivo model of PTC progression suggested that these miRNAs could play a key role in the pathophysiology of PTC and therefore be relevant for the development of new therapeutic strategies.4

Professor George Kahaly (Mainz, Germany) presented several of the latest European Group on Graves’ orbitopathy (EUGOGO) recommendations including the use of intravenous glucocorticoids in moderate to severe orbitopathy.5 Furthermore, new therapeutic opportunities are available for patients with active ophthalmopathy, including teprotumumab, a monoclonal antibody that inhibits the insulin-like growth factor I receptor (IGF-IR), which was more effective in reducing proptosis and the Clinical Activity Score than placebo in clinical trials.6

Professor Leonidas Duntas (Ulm, Germany and Athens, Greece), introduced novel concepts including the industrial use of chemicals such as polychlorinated biphenyls, polybrominated diphenyl ethers, and bisphenol A, among others, which all act as thyroid hormones disruptors. He also described the effects of dysbiosis (the result of alteration of the gut microbiota) on induction of thyroid autoimmunity.

Thyroid regulation of metabolism was covered by Professor Gregory Brent (Los Angeles, USA), who presented the effects of thyroid hormones on receptor variants within different tissues. The mutation of these receptors produces different phenotypes which affect metabolism, as observed in animal models with defects in these receptors. Patients with resistance to thyroid hormones have been identified, but these people are believed to be underdiagnosed. Selective thyroid hormone receptor agonists, such as sobetirome, are being investigated to take a similar role as those for the correction of the biochemical abnormality in X-linked adrenoleukodystrophy.7 Another strategy to impact on metabolic disorders has been the engineering of chemical conjugates of glucagon and T3 to synergize and correct hyperlipidaemia, steatohepatitis, atherosclerosis, glucose intolerance and obesity in metabolically compromised mice.8 Conversely, the role of thyroid hormones on longevity may be related to the decreased signaling shown in long-lived mouse strains which have reduced thyroid hormone action.9

Professor Antonio Bianco (Chicago, USA), described the effects of polymorphisms in the deiodinases (DIO) that regulate the passage of T4 to T3. In animal models, these types of polymorphisms are responsible for mitochondrial damage, opening the debate as to possible implications in humans. Controversy regarding the use of combination T4 and T3 treatment continues, although some studies in thyroidectomized patients who carry polymorphism DIO2 Thr92Ala show that these particular patients are at increased risk of reduced intracellular and serum T3 concentrations that are not adequately compensated for by levothyroxine.10

The normal serum level of thyroid stimulating hormone (TSH) in pregnancy is still a matter of debate and the lower cutoff values proposed by past guidelines have been recently questioned. According to the most recent guidelines,11 TSH reference ranges should ideally be determined in each population of pregnant women. Levothyroxine therapy is recommended for:

  • TPO antibody positive women with a TSH greater than the pregnancy-specific reference range
  • TPO antibody negative women with a TSH greater than 10.0 mU/L

and ‘may’ be considered for:

  • TPO antibody positive women with TSH concentrations >2.5 mU/L and below the upper limit of the pregnancy specific reference range
  • TPO antibody negative women with TSH concentrations greater than the pregnancy specific reference range and below 10.0 mU/L.


1. Tuttle RM, et al. Thyroid 2017;27(6):751-6.

2. Momesso DP, et al. J Clin Endocrinol Metab 2016;101(7):2692-2700.

3. Minna E, et al. Oncotarget 2016;7(11):12731-47.

4. Geraldo MV, et al. Oncotarget 2017;8(6):9597-9607.

5. Perros P, et al. Orphanet J Rare Dis 2017;12(1):72.

6. Smith TJ, et al. N Engl J Med 2017;376(18):1748-61.

7. Hartley MD, et al. Endocrinology 2017;158(5):1328-38.

8. Finan B, et al. Cell 2016;167(3):843-857.

9. Hine C, et al. Cell Metab 2017;25(6):1320-33.

10. Castagna MG, et al. J Clin Endocrinol Metab 2017;102(5):1623-30.

11. Alexander EK, et al. Thyroid 2017;27(3):315-389.

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