Clinical, Laboratory, Ultrasound and FNAB Aspects of Subclinical Thyroid Diseases (Hypo and Hyperthyroidism)

Case Report

Austin Endocrinol Diabetes Case Rep. 2019; 4(1): 1016.

Clinical, Laboratory, Ultrasound and FNAB Aspects of Subclinical Thyroid Diseases (Hypo and Hyperthyroidism)

Alves MLD*

Medicine Course of Ribeirão Preto University, UNAERP, Ribeirão Preto São Paulo, Brazil

*Corresponding author: Maria Lúcia D’arbo Alves, Medicine Course of Ribeirão Preto University, UNAERP, Ribeirão Preto São Paulo, Brazil

Received: April 02, 2019; Accepted: May 01, 2019; Published: May 08, 2019


Hypothyroidism; Hyperthyroidism; Subclinical Thyroid Disease; Subclinical Hypothyroidism; Subclinical Hyperthyroidism; Thyroid


The thyroid gland is the first gland to appear in the human embryo, exhibiting a highly organized structure and being able to synthesize and excrete its secretion products, the Thyroid Hormones (TH) triiodothyronine (T3) and thyroxine (T4), which are important for the development, growth and maintenance of the quality of life of human beings. The thyroid is one of the largest glands in the human body, weighing 15 to 20 grams during adult life, containing two lobes 2 to 2.5cm3 in volume, and containing about 3 million follicles of various sizes [1].

The evaluation of thyroid dysfunctions is part of the investigation of many specialties. In general, thyroid function can be determined in a direct manner by palpation of the gland or using specific tests [2-5].

Non-thyroid diseases, pregnancy, various medications (especially amiodarone and lithium) and age may affect the extra-thyroid metabolism, the transport, absorption and/or action of TH, and may mimic dysfunction of this gland. The presence of anti-TSH or anti- TH antibodies results in abnormal findings [6-12]. The synthesis and secretory activities of TH are controlled or stimulated by thyrotropin hormone, which is produced by the thyrotrophic cells of the anterior pituitary. These activities also involve the presence of iodine and of a glycoprotein - thyroglobulin (Tg) - which is responsible for 70 to 80% of the entire protein content of the thyroid and is the site of TH synthesis. Tg levels increase in the individuals by accompanying the increase in gland volume (goiter) [13,14].

Hashimoto’s thyroiditis is associated with the presence of antithyroperoxidase and/or anti-thyroglobulin titers and is accompanied by diffuse or nodular goiter and/or by heterogeneity of the thyroid parenchyma, being the main cause of acquired hypothyroidism [15- 18].

Hypothyroidism is the syndrome induced by TH deficiency and by increased levels of TSH and of thyroid antibody titers (anti- thyroperoxidase and/or anti-thyroglobulin) and is associated with Hashimoto’s thyroiditis [19,20].

Hyperthyroidism is the syndrome caused by excess TH, suppression of TSH, increased levels of antithyroid antibodies (antithyroperoxidase, anti-thyroglobulin and anti-TSH receptor) and is associated with Graves’ disease [21].

Subclinical thyroid dysfunctions are characterized by normal TH levels and altered (increased or decreased) TSH levels. They are highly prevalent in the general population and their significance and the need for drug treatment are topics of debate in clinical practice.

The increasing number of prospective population and metaanalysis studies about the effect of subclinical disease on the cardiovascular system and on life expectancy has led to a new consensus regarding the indications of treatment for these two clinical entities.

Case Presentation

The study was conducted on 145 patients (27 men and 118 women) with subclinical hypothyroidism (TSH value > 4.5μIU/L and normal free T4 and T3 values) and 45 patients (8 men and 37 women) with subclinical hyperthyroidism (TSH value < 0.1μIU/L and normal free T4 and T3 values) (Table 1). Age ranged from 23 to79 years (mean: 50.18 years) for hypothyroid men and from 20 to 84 years (mean: 41.61 years) for hypothyroid women, and from 54 to 86 years (mean: 70.75 years) for hyperthyroid men and from 27 to 89 years (mean: 62.37 years) for hyperthyroid women (Table 2).