Causes and laboratory investigations of thyrotoxicosis

Author(s):  
Francesco Latrofa ◽  
Paolo Vitti ◽  
Aldo Pinchera

The term thyrotoxicosis identifies the clinical syndrome caused by elevated circulating thyroid hormones of all sources, while the term hyperthyroidism includes only the disorders due to an increased secretion of hormones by the thyroid gland. Hyperthyroidism is the most frequent cause of thyrotoxicosis. Destructive processes involving the thyroid gland that induce unregulated discharge of preformed thyroid hormones (destructive thyrotoxicosis) and circulating thyroid hormone of extrathyroidal origin (exogenous or extrathyroidal thyrotoxicosis) are less common causes of thyrotoxicosis. Although careful history taking and physical examination often allows a diagnosis of thyrotoxicosis to be made, laboratory confirmation by measurement of thyroid-stimulating hormone (TSH) and thyroid hormone is always needed. Once thyrotoxicosis is confirmed, laboratory testing and thyroid imaging are required to identify the cause of thyrotoxicosis.

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.


Author(s):  
Claudio Marcocci ◽  
Filomena Cetani ◽  
Aldo Pinchera

The term thyrotoxicosis refers to the clinical syndrome that results when the serum concentrations of free thyroxine, free triiodothyronine, or both, are high. The term hyperthyroidism is used to mean sustained increases in thyroid hormone biosynthesis and secretion by the thyroid gland; Graves’ disease is the most common example of this. Occasionally, thyrotoxicosis may be due to other causes such as destructive thyroiditis, excessive ingestion of thyroid hormones, or excessive secretion of thyroid hormones from ectopic sites; in these cases there is no overproduction of hormone by thyrocytes and, strictly speaking, no hyperthyroidism. The various causes of thyrotoxicosis are listed in Chapter 3.3.5. The clinical features depend on the severity and the duration of the disease, the age of the patient, the presence or absence of extrathyroidal manifestations, and the specific disorder producing the thyrotoxicosis. Older patients have fewer symptoms and signs of sympathetic activation, such as tremor, hyperactivity, and anxiety, and more symptoms and signs of cardiovascular dysfunction, such as atrial fibrillation and dyspnoea. Rarely a patient with ‘apathetic’ hyperthyroidism will lack almost all of the usual clinical manifestations of thyrotoxicosis (1). Almost all organ systems in the body are affected by thyroid hormone excess, and the high levels of circulating thyroid hormones are responsible for most of the systemic effects observed in these patients (Table 3.3.1.1). However, some of the signs and symptoms prominent in Graves’ disease reflect extrathyroidal immunological processes rather than the excessive levels of thyroid hormones produced by the thyroid gland (Table 3.3.1.2).


2021 ◽  
Vol 53 (04) ◽  
pp. 272-279
Author(s):  
Chaochao Ma ◽  
Xiaoqi Li ◽  
Lixin Liu ◽  
Xinqi Cheng ◽  
Fang Xue ◽  
...  

AbstractThyroid hormone reference intervals are crucial for diagnosing and monitoring thyroid dysfunction during early pregnancy, and the dynamic change trend of thyroid hormones during pregnancy can assist clinicians to assess the thyroid function of pregnant women. This study aims to establish early pregnancy related thyroid hormones models and reference intervals for pregnant women. We established two derived databases: derived database* and derived database#. Reference individuals in database* were used to establish gestational age-specific reference intervals for thyroid hormones and early pregnancy related thyroid hormones models for pregnant women. Individuals in database# were apparently healthy non-pregnant women. The thyroid hormones levels of individuals in database# were compared with that of individuals in database* using nonparametric methods and the comparative confidence interval method. The differences in thyroid stimulating hormone and free thyroxine between early pregnant and non-pregnant women were statistically significant (p<0.0001). The reference intervals of thyroid stimulating hormone, free thyroxine and free triiodothyronine for early pregnant women were 0.052–3.393 μIU/ml, 1.01–1.54 ng/dl, and 2.51–3.66 pg/ml, respectively. Results concerning thyroid stimulating hormone and free thyroxine reference intervals of early pregnancy are comparable with those from other studies using the same detection platform. Early pregnancy related thyroid hormones models showed various change patterns with gestational age for thyroid hormones. Early pregnancy related thyroid hormones models and reference intervals for pregnant women were established, so as to provide accurate and reliable reference basis for the diagnosing and monitoring of maternal thyroid disfunction in early pregnancy.


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.


2000 ◽  
Vol 19 (8) ◽  
pp. 11-26 ◽  
Author(s):  
Denise Kirsten

The thyroid gland contains many follicular cells that store the thyroid hormones within the thyroglobulin molecule until they are needed by the body. The thyroid hormones, often referred to as the major metabolic hormones, affect virtually every cell in the body. Synthesis and secretion of the thyroid hormones depend on the presence of iodine and tyrosine as well as maturation of the hypothalamic-pituitary-thyroid system. Interruption of this development, as occurs with premature delivery, results in inadequate production of thyroid-stimulating hormone and thyroxine, leading to a variety of physiologic conditions. Pathologic conditions occur in the presence of insufficient thyroid production or a defect in the thyroid gland. Laboratory tests are important in diagnosing conditions of the thyroid gland. A thorough history in combination with clinical manifestations and radiologic findings are also useful in diagnosing specific thyroid conditions. Nurses play an important role in identifying and managing thyroid disorders and in providing supportive care to infants and their families.


2005 ◽  
Vol 184 (2) ◽  
pp. 407-416 ◽  
Author(s):  
Michael Muchow ◽  
Ioannis Bossis ◽  
Tom E Porter

Increased thyroid hormone production is essential for hatching of the chick and for the increased metabolism necessary for posthatch endothermic life. However, little is known about the ontogeny and distribution of pituitary thyrotrophs during this period or whether pituitary thyroid-stimulating hormone (TSH) production is regulated by endogenous thyroid hormones during chick embryonic development. This study assessed the abundance and location of pituitary thyrotrophs and the regulation of TSHβ peptide and mRNA levels by endogenous thyroid hormones prior to hatching. TSHβ-containing cells were first detected on embryonic day (e) 11, and the thyrotroph population increased to maximum levels on e17 and e19 and then decreased prior to hatching (d1). Thyrotroph distribution within the cephalic lobe of the anterior pituitary was determined on e19 by whole-mount immunocytochemistry for TSHβ peptide and by whole-mount in situ hybridization for TSHβ mRNA. Thyrotroph distribution within the cephalic lobe was heterogeneous among embryos, but most commonly extended from the ventral medial region to the dorsal lateral regions, along the boundary of the cephalic and caudal lobes. Inhibition of endogenous thyroid hormone production with methi-mazole (MMI) decreased plasma thyroxine (T4) levels and increased pituitary TSHβ mRNA levels on e19 and d1. However, control pituitaries contained significantly more TSHβ peptide than MMI-treated pituitaries on e17 and e19, suggesting higher TSH secretion into the blood in MMI-treated groups. We conclude that thyrotroph abundance and TSH production increase prior to hatching, that thyrotrophs are localized heterogenenously within the cephalic lobe of the anterior pituitary at that time, and that TSH gene expression and secretion are under negative feedback regulation from thyroid hormones during this critical period of development.


1996 ◽  
Vol 17 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Anna Capaldo ◽  
Vincenza Laforgia ◽  
Rosaria Sciarrillo ◽  
Antimo Cavagnuolo

AbstractInsulin was administered to Podarcis sicula in winter, when the thyroid gland is inhibited. The activity of the thyroid increased, plasma concentrations of thyroid hormones and hepatic 5'-monodeiodinase activity (MDA) increased, and thyroid stimulating hormone (TSH) concentrations fell to undetectable values. This result confirms the influence of insulin on the activity of the thyroid gland in the lizard species studied. The mechanisms are still unclear, although there is evidence which leads us to believe that insulin is directly responsible for thyroid activation.


Author(s):  
Bo Hyun Park ◽  
Sun Jung Baik ◽  
Hye Ah Lee ◽  
Young Sun Hong ◽  
Hae Soon Kim ◽  
...  

AbstractHypertension is the leading cause of cardiovascular disease worldwide, and both high and low blood pressures are associated with various chronic diseases. Thyroid hormones have profound effects on cardiovascular function, including on blood pressure. Recent studies have shown that childhood hypertension can lead to adult hypertension. Therefore, adequate blood pressure control is important from early life. Employing a life-course approach, we aimed to investigate the association between thyroid hormones and blood pressure in children.A total of 290 children from the Ewha Woman’s University Hospital birth cohort participated in a preadolescent check-up program. We assessed the levels of serum thyroid-stimulating hormone (TSH) and free thyroxine (FT4) and the blood pressure status in these children. Thyroid hormone concentrations were measured using an electro-chemiluminescence immunoassay (ECLIA), and hypertension was defined according to the guideline of the Korea Centers for Disease Control and Prevention.The sex-, age-, and height-adjusted prevalence of hypertension was 27.0% in the present study. On regression analysis, serum FT4 showed significantly negative association with diastolic blood pressure (DBP; β=–8.24, 95% CI: –14.19–2.28, p=0.007). However, these relationships were not significant after adjustment for sex, age, and current body mass index. The levels of serum TSH showed no relationship with mean systolic blood pressure (SBP) and diastolic blood pressure (DBP) after adjustment. No significant differences in serum TSH and FT4 levels according to hypertension status were found.These findings suggest that thyroid hormone is not independently associated with increased blood pressure in euthyroid preadolescents.


2006 ◽  
Vol 26 (11) ◽  
pp. 4311-4315 ◽  
Author(s):  
Chin-Hsing Lin ◽  
Stephen J. Tapscott ◽  
James M. Olson

ABSTRACT Mice lacking neuroD2, a basic helix-loop-helix transcription factor involved in brain development, show growth retardation and other abnormalities consistent with hypothalamic-pituitary-thyroid (HPT) axis dysfunction. neuroD2 is expressed in the paraventricular hypothalamic nuclei, the anterior lobe of pituitary, and the thyroid gland. In neuroD2-deficient mice, thyrotropin-releasing hormone, thyroid-stimulating hormone, and thyroid hormone are decreased in these three regions, respectively. neuroD2-null mice typically die 2 to 3 weeks after birth, but those treated with replacement doses of thyroxine survived more than 8 weeks. These data indicate that neuroD2 is expressed throughout the HPT axis and that all levels of the axis are functionally affected by its absence in mice.


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.


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