scholarly journals Modern concepts of primary thyroid gland failure

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.

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.


2021 ◽  
Vol 12 ◽  
Author(s):  
Maria C. Opazo ◽  
Juan Carlos Rivera ◽  
Pablo A. Gonzalez ◽  
Susan M. Bueno ◽  
Alexis M. Kalergis ◽  
...  

Fetus and infants require appropriate thyroid hormone levels and iodine during pregnancy and lactation. Nature endorses the mother to supply thyroid hormones to the fetus and iodine to the lactating infant. Genetic variations on thyroid proteins that cause dyshormonogenic congenital hypothyroidism could in pregnant and breastfeeding women impair the delivery of thyroid hormones and iodine to the offspring. The review discusses maternal genetic variations in thyroid proteins that, in the context of pregnancy and/or breastfeeding, could trigger thyroid hormone deficiency or iodide transport defect that will affect the proper development of the offspring.


Endocrinology ◽  
2006 ◽  
Vol 147 (3) ◽  
pp. 1306-1313 ◽  
Author(s):  
Lutz Schomburg ◽  
Cornelia Riese ◽  
Marten Michaelis ◽  
Emine Griebert ◽  
Marc O. Klein ◽  
...  

The thyroid gland is rich in selenium (Se) and expresses a variety of selenoproteins that are involved in antioxidative defense and metabolism of thyroid hormones (TH). Se deficiency impairs regular synthesis of selenoproteins and adequate TH metabolism. We recently generated mice that lack the plasma Se carrier, selenoprotein P (SePP). SePP-knockout mice display decreased serum Se levels and manifest growth defects and neurological abnormalities partly reminiscent of thyroid gland dysfunction or profound hypothyroidism. Thus, we probed the TH axis in developing and adult SePP-knockout mice. Surprisingly, expression of Se-dependent 5′-deiodinase type 1 was only slightly altered in liver, kidney, or thyroid at postnatal d 60, and 5′-deiodinase type 2 activity in brain was normal in SePP-knockout mice. Thyroid gland morphology, thyroid glutathione peroxidase activity, thyroid Se concentration, and serum levels of TSH, T4, or T3 were within normal range. Pituitary TSHβ transcripts and hepatic 5′-deiodinase type 1 mRNA levels were unchanged, indicating regular T3 bioactivity in thyrotropes and hepatocytes. Cerebellar granule cell migration as a sensitive indicator of local T3 action during development was undisturbed. Collectively, these findings demonstrate that low levels of serum Se or SePP in the absence of other challenges do not necessarily interfere with regular functioning of the TH axis. 5′-deiodinase isozymes are preferentially supplied, and Se-dependent enzymes in the thyroid are even less-dependent on serum levels of Se or SePP than in brain. This indicates a top priority of the thyroid gland and its selenoenzymes with respect to the hierarchical Se supply within the organism.


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.


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.


Author(s):  
Michela Del Prete ◽  
Fabrizio Muratori ◽  
Irene Campi ◽  
Gianleone Di Sacco ◽  
Federico Vignati ◽  
...  

Summary Resistance to thyroid hormone (RTH) is a rare hereditary syndrome with impaired sensitivity to thyroid hormones (TH) and reduced intracellular action of triiodothyronine (T3) caused by genetic variants of TH receptor beta (TRB) or alpha (TRA). RTH type beta (RTHβ) due to dominant negative variants in the TRB gene usually occurs with persistent elevation of circulating free TH, non-suppressed serum TSH levels responding to a thyrotropin-releasing hormone (TRH) test, an absence of typical symptoms of hyperthyroidism and goiter. Here, we present a rare variant in the TRB gene reported for the first time in an Italian patient with generalized RTHβ syndrome. The patient showed elevated TH, with non-suppressed TSH levels and underwent thyroid surgery two different times for multinodular goiter. The genetic test showed a heterozygous mutation in exon 9 of the TRB gene resulting in the replacement of threonine (ACG) with methionine (ATG) at codon 310 (p.M310T). RTHβ syndrome should be considered in patients with elevated TH, non-suppressed TSH levels and goiter. Learning points Resistance to thyroid hormone (RTH) is a rare autosomal dominant hereditary syndrome with impaired tissue responsiveness to thyroid hormones (TH). Diagnosis of RTH is usually based on the clinical finding of discrepant thyroid function tests and confirmed by a genetic test. RTH is a rare condition that must be considered for the management of patients with goiter, elevation of TH and non-suppressed serum TSH levels in order to avoid unnecessary treatments.


2019 ◽  
Vol 51 (06) ◽  
pp. 381-388 ◽  
Author(s):  
Jorge Tapia-Martínez ◽  
Alejandra Paola Torres-Manzo ◽  
Margarita Franco-Colín ◽  
Marisol Pineda-Reynoso ◽  
Edgar Cano-Europa

AbstractEnvironmental stimuli during critical developmental stages establish long-term physiological and structural patterns that “program” health during adult life. Little is known about how alterations in hormonal supply might have consequences in metabolic and thyroid programming. This work aims to prove that alterations in the supply of thyroid hormones during gestation and lactation have long-term consequences in the metabolic and thyroid programming of the offspring. Female Wistar rats were divided into euthyroid, hypothyroid, and hypothyroid with 20 μg/day of s.c. thyroxine (T4), replacement wet nurses. Rats were mating, and after birth, pups were grouped according to their wet nurses group. Milk quality of wet nurses was assessed on days 7, 14, and 21. Body mass gain and energy intake of the offspring were monitored for 28 weeks after weaning. At sacrifice, we extracted and weighed their thyroid gland and adipose reserves, and collected blood to measure its metabolic and thyroid profiles. Hypothyroid wet nurses presented a persistent low quality of milk, while both male and female hypothyroid offspring presented lower body mass gain, higher blood glucose, dyslipidemia, hyperinsulinemia, and hyperleptinemia, as well as lower total adipose reserves, but higher visceral reserve, diminished T3 and T4 concentrations, and lower weight of thyroid gland. Thyroxine replacement prevented all changes in both wet nurses and pups. We conclude that maternal thyroid hormone deficiency during congenital and lactation stages alters the metabolic and thyroid programming of the offspring, while the reestablishment of maternal thyroid status during critical periods of development can prevent these alterations.


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.


1988 ◽  
Vol 118 (1) ◽  
pp. 45-50 ◽  
Author(s):  
Gen Komaki ◽  
Hajime Tamai ◽  
Takahiro Mori ◽  
Tetsuya Nakagawa ◽  
Shu Mori

Abstract. We investigated changes in the serum angiotensin-converting enzyme, as an index of thyroid hormone action, before, during and after fasting in 15 non-obese, hospitalized patients. Serum angiotensinconverting enzyme decreased significantly from 14.6 ± 1.1 U/l before fasting to 13.2 ± 1.1 U/l on the 5th day (P < 0.05, N = 15) during fasting, and to 10.6 ± 1.0 U/l on the 10th day (P < 0.05, N = 8). The serum TSH and T3 levels decreased significantly to below the normal range, and the serum T4 level decreased gradually during fasting, whereas free T4 (Amerlex) changed slightly, but within normal range. Although re-feeding did not lead to any reduction in the serum TSH, T3, or T4 level, the serum angiotensin-converting enzyme further decreased to 8.7 ± 0.9 U/l on the 5th day of re-feeding compared with that on the 10th day of fasting (P < 0.01, N = 8). There was a delay in the re-elevation of serum angiotensin-converting enzyme following a rise in serum T3. No correlations were found between serum angiotensin-converting enzyme levels and thyroid hormone levels throughout the study period. It is concluded that a significant reduction in the serum angiotensin-converting enzyme level occurs under a 'low T3' state during acute starvation, although there is no clear association between serum angiotensinconverting enzyme and thyroid hormone levels.


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.


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