LINGUAL AND SUBLINGUAL THYROID GLANDS IN EUTHYROID CHILDREN

PEDIATRICS ◽  
1966 ◽  
Vol 38 (4) ◽  
pp. 647-651
Author(s):  
Wellington Hung ◽  
Judson G. Randolph ◽  
Domenic Sabatini ◽  
Theodore Winship

Five clinically euthyroid children with lingual or sublingual thyroid glands were seen during a 12-month period. Certain recommendations have been formulated based upon our experience with these patients. A careful physical examination should be performed to demonstrate the presence of a normally located thyroid gland in all children presenting with midline masses in the lingual or sublingual areas. When the thyroid gland cannot be palpated with certainty in these children, a scintiscan with I-131 should be carried out to determine if the mass is an ectopic thyroid gland and if a normally located thyroid gland is present. All children with lingual on sublingual thyroid glands should have a trial of full replacement thyroid hormone therapy before excision is contemplated. Thyroid therapy will prevent further hypertrophy and hyperplasia. Surgical intervention should be reserved for those children in whom there is dysphagia, dysphonia, ulceration, or hemorrhage due to a lingual thyroid gland or if the ectopic thyroid gland fails to decrease in size following a course of treatment with thyroid hormones.

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Inès Riahi ◽  
Rim Fradi ◽  
Ibtissem Ben Nacef ◽  
Ahlem Blel

Abstract Background Ectopic thyroid is a developmental anomaly of the thyroid gland of embryological origin. Instead of having a pretracheal situation, thyroid tissue is elsewhere, most commonly in the median cervical line along the course of the thyroglossal duct. Lingual thyroid is the most common presentation. Ectopic thyroid tissue in the submandibular region has been rarely reported. Case presentation We report herein a case of a 65-year-old man admitted to our department with a complaint of a painless swelling in the left submandibular region. Conclusions Thyroid gland ectopia should be considered among the differential diagnoses of submandibular swelling. Ectopic thyroid tissue can present with the same pathology affecting the normal thyroid gland such as malignancy and hyperthyroidism.


Iodine (I2) is essential in the synthesis of thyroid hormones T4 and T3 and functioning of the thyroid gland. Both T3 and T4 are metabolically active, but T3 is four times more potent than T4. Our body contains 20-30 mg of I2, which is mainly stored in the thyroid gland. Iodine is naturally present in some foods, added to others, and available as a dietary supplement. Serum thyroid stimulating hormone (TSH) level is a sensitive marker of thyroid function. Serum TSH is increased in hypothyroidism as in Hashimoto's thyroiditis. In addition to regulation of thyroid function, TSH promotes thyroid growth. If thyroid hormone synthesis is chronically impaired, TSH stimulation eventually may lead to the development of a goiter. This chapter explores the iodide metabolism and effects of Hashimoto's disease.


1999 ◽  
pp. 625-629 ◽  
Author(s):  
M Tamura ◽  
B Matsuura ◽  
S Miyauchi ◽  
M Onji

We previously reported that serum interleukin-12 (IL-12) levels were significantly increased in patients with hyperthyroid Graves' disease and in normal subjects after administration of thyroid hormone. In the present study, we investigated which cells produce IL-12 and the interactions between IL-12 and thyroid hormones, using a hyperthyroid mouse model. Thyroid hormones induced IL-12 production, and IL-12 was mainly produced by dendritic cells outside the thyroid glands in a hyperthyroid state.


1996 ◽  
Vol 16 (3) ◽  
pp. 259-267 ◽  
Author(s):  
J H Mitchell ◽  
F Nicol ◽  
G J Beckett ◽  
J R Arthur

ABSTRACT The stimulation of thyroid hormone synthesis in iodine deficiency may increase the requirement for the selenoproteins which are involved in thyroid hormone synthesis in the thyroid gland. Selenoenzyme activity and expression were investigated in the thyroid and liver of second generation selenium-and/or iodine-deficient rats. Selenium deficiency caused substantial decreases in hepatic seleniumcontaining type I iodothyronine deiodinase (ID-I) and cytosolic glutathione peroxidase (cGSHPx) activities and mRNA abundances, but phospholipid hydroperoxide glutathione peroxidase (phGSHPx) activity was only 55% of selenium-supplemented control levels, despite the absence of change in its mRNA abundance. Selenoenzyme mRNA concentrations were maintained at control levels in thyroid glands from the selenium-deficient rat pups. Despite this, a differential effect was observed in selenoenzyme activities: ID-I activity was decreased to 61%, cGSHPx activity to 45% and phGSHPx to 29% of that in selenium-adequate controls. In iodine-deficient thyroid glands, mRNA levels were increased 2·2, 50 and 2·8 times for ID-I, cGSHPx and phGSHPx respectively. ID-I and cGSHPx enzyme activities were also increased but the activity of phGSHPx was decreased despite the high mRNA abundance. Thyroid selenoprotein mRNA levels were also increased in combined selenium and iodine deficiency but again there were differential effects on enzyme activities, with ID-I activity increased, cGSHPx unchanged and phGSHPx decreased. Thus, iodine deficiency may produce an oxidant stress on the thyroid gland, increasing the requirement for selenium to maintain selenoenzyme activity. When dietary supplies of selenium are limiting, thyroid selenoprotein mRNA levels are increased to compensate for overall lack of the micronutrient. Furthermore, there is a preferential supply of available selenium to ID-I and cGSHPx to allow maintenance of thyroid function.


1997 ◽  
Vol 9 (5) ◽  
pp. 489 ◽  
Author(s):  
Conrad Sernia ◽  
Tang Zeng ◽  
Robert T. Gemmell

Newborn marsupials do not have a thyroid gland at birth. The gland develops while the young marsupial is in the mother’s pouch. The young brushtail possum initiates secretion of thyroid hormones from its own thyroid at about Day 65 post partum. However, during the first three weeks of pouch life thyroxine is passed from the mother to the young via the milk. To determine if this maternal thyroxine can effect organ development in the young possum before it initiates secretion of thyroxine from its own thyroid, the ontogeny of thyroid hormone receptors was determined in nuclear extracts of lung, liver and kidney by radioreceptor assay, using125I-labelled tri-iodothyronine as ligand. Receptor density was calculated for tissues removed from young possums at Days 25 (n = 5), 50 (n = 4), 100 (n = 3) and 150 (n = 4) and from adults (n = 5). Receptors were found in possums of all age groups, including the small 25-day pouch young. Significant differences were not found in the receptor density between different tissues or at various ages. The association constant Ka (4 ·0 ± 2· 6 L nmol-1 for lung) was similar in different tissues and at the various ages examined. The passage of thyroid hormones from the mother to the developing marsupial via the milk may have a role in the slow development of organ systems early in pouch life by acting on thyroid receptors in the pouch young. However, the functional maturation of the thyroid gland of the young possum, not an increase in receptors, appears to coincide with the rapid increase in the rate of growth and development which occurs in later pouch life.


2011 ◽  
Vol 210 (1) ◽  
pp. 3-4 ◽  
Author(s):  
Marian Ludgate

A paper published in this issue of the Journal of Endocrinology has revisited the hypothesis that thyroid hormones may be generated by tissues outside the thyroid gland in higher organisms including mammals. This commentary appraises the strengths and weaknesses of the study, the alternative explanations for the findings and possible future measures to investigate further. The concept of extrathyroidal thyroxine and triiodothyronine synthesis has previously been proposed; by assuming that Nagao et al. and earlier authors are correct, the plausibility and possible mechanisms underlying the hypothesis are discussed.


2015 ◽  
Vol 2015 ◽  
pp. 1-4 ◽  
Author(s):  
Khaled Khamassi ◽  
Habib Jaafoura ◽  
Fahmi Masmoudi ◽  
Rim Lahiani ◽  
Lobna Bougacha ◽  
...  

Ectopy of the thyroid gland is an abnormal embryological development. Its occurrence in children is rare. In this study, we report the case of a 12-year-old girl that presented with dysphagia and nocturnal dyspnea. Magnetic resonance imaging confirmed the presence of a lingual thyroid. Thyroid scintigraphy showed intense and elective uptake of radiotracer at the base of the tongue. Hormonal tests revealed hypothyroidism. Treatment consisted of opotherapy based on levothyroxine. Evolution has been favourable and the patient showed significant improvement with reduction of the dyspnea and the dysphagia and normalization of thyroid hormone tests.


Author(s):  
Ferruccio Santini ◽  
Aldo Pinchera

Hypothyroidism is the clinical state that develops as a result of the lack of action of thyroid hormones on target tissues (1). Hypothyroidism is usually due to impaired hormone secretion by the thyroid, resulting in reduced concentrations of serum thyroxine (T4) and triiodothyronine (T3). The term primary hypothyroidism is applied to define the thyroid failure deriving from inherited or acquired causes that act directly on the thyroid gland by reducing the amount of functioning thyroid tissue or by inhibiting thyroid hormone production. The term central hypothyroidism is used when pituitary or hypothalamic abnormalities result in an insufficient stimulation of an otherwise normal thyroid gland. Both primary and central hypothyroidism may be transient, depending on the nature and the extent of the causal agent. Hypothyroidism following a minor loss of thyroid tissue can be recovered by compensatory hyperplasia of the residual gland. Similarly, hypothyroidism subsides when an exogenous inhibitor of thyroid function is removed. Peripheral hypothyroidism may also arise as a consequence of tissue resistance to thyroid hormones due to a mutation in the thyroid hormone receptor. Resistance to thyroid hormones is a heterogeneous clinical entity with most patients appearing to be clinically euthyroid while some of them have symptoms of thyrotoxicosis and others display selected signs of hypothyroidism. The common feature is represented by pituitary resistance to thyroid hormones, leading to increased secretion of thyrotropin that in turn stimulates thyroid growth and function. The variability in clinical manifestations depends on the severity of the hormonal resistance, the relative degree of tissue hyposensitivity, and the coexistence of associated genetic defects (see Chapter 3.4.8).


1996 ◽  
Vol 42 (1) ◽  
pp. 179-182 ◽  
Author(s):  
E C Ridgway

Abstract Primary thyroid gland failure is a common medical disorder occurring in mild or severe forms in 10% to 15% of our population. Symptoms may be classical and easy to recognize or very subtle, escaping clinical detection. This disorder is more common in females and increases with advancing age. The most important diagnostic test is measurement of the serum thyrotropin (TSH) concentration, which will increase above the normal range in both mild and severe cases. Most clinical effects of thyroid hormone deficiency can be explained by the "nuclear thyroid hormone hypothesis," which states that thyroid hormones act predominantly by effecting the transcription of key genes in affected tissues. Therapy of hypothyroidism is easy, inexpensive, and precise, involving pure L-thyroxine and measuring dose requirements and efficacy by monitoring serum TSH concentrations.


1978 ◽  
Vol 26 (12) ◽  
pp. 1121-1124 ◽  
Author(s):  
M Wilson ◽  
K R Hitchcock ◽  
R A DeLellis

Direct and indirect immunofluorescence techniques were used to localize the thyroid hormones triidothyronine (T3) and thyroxine (T4) in adult rat thyroid gland. Optimum dilutions of the antisera were established and four tissue fixatives were investigated for usefulness in this technique. Use of antibodies specific for either T3 or T4 resulted in brilliant fluorescence in the colloid pools and apical cytoplasm of follicular cells. In all cases, the adjacent parathyroid gland was devoid of fluorescence. This report demonstrates that these dipeptide hormones can be localized by using immunofluorescence techniques.


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