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PubMed2002

Effectiveness of thyroid hormone suppressive therapy in benign solitary thyroid nodules: a meta-analysis.

The effectiveness of thyroid hormone suppressive therapy in reducing the volume of benign thyroid nodules is controversial. It is important to clarify this therapeutic effect of thyroid hormone, because its prolonged use needs to be carefully weighed against its potential deleterious effects in the skeletal and cardiovascular systems. To evaluate the best available evidence, we conducted a systematic review and meta-analysis of the randomized controlled trials that fulfill the following inclusion criteria: single thyroid nodules proven benign by fine needle aspiration, treatment, and follow-up of at least 6 months; documented suppression of TSH; measurement of thyroid nodule volume by ultrasound; and response to therapy defined as more than 50% volume reduction from baseline. Six randomized clinical trials published between 1987 and 1999, with 346 patients, were included in the meta-analysis. Ninety percent of the participants were female. Using a random effects model, the overall effect size showed a relative risk of 1.9 (95% confidence interval, 0.95-3.81) favoring a treatment effect. A sensitivity analysis showed significant changes in the results. Suppressive thyroid hormone therapy for longer than 6 months is associated with a trend toward a reduction of more than 50% in volume of benign thyroid nodules, without achieving statistical significance. The results are highly sensitive to changes in the statistical analysis, especially if the method used ignores heterogeneity among the effect sizes. More studies are needed before this therapy can be widely recommended.

Humans↗

PubMed1993

Multiple genetic factors in the heterogeneity of thyroid hormone resistance.

Generalized resistance to thyroid hormone (GRTH), a syndrome of inherited tissue hyposensitivity to thyroid hormone, is linked to thyroid hormone receptor (TR) mutations. A typical feature of GRTH is variable severity of organ involvement among families that, surprisingly, does not correlate with the degree of T3-binding impairment of the corresponding in vitro synthesized mutant TRs. Furthermore, variations in the clinical severity among family members harboring identical TR beta mutations have been reported. We compared serum levels of thyroid hormones that maintained a normal TSH in members of a large family with GRTH divided in three groups: Group A, 8 affected subjects with a mutation replacing arginine-320 with a histidine in the T3-binding domain of TR beta; Group B, 11 first degree relatives (sibs and children of affected subjects) with no TR beta mutation; Group C, 16 controls related by marriage. TSH values were not different among the three groups. As expected, total and free T4 and T3, and rT3 levels were significantly higher in Group A vs Groups B and C. However, with the exception of T3, the same tests were also significantly higher in Group B vs Group C. The latter differences are not due to thyroid hormone transport in serum since TBG concentrations were not different. It is postulated that genetic variability of factors that contribute to the action of thyroid hormone modulate the phenotype of GRTH associated with TR beta mutations.

Adult↗

PubMed2003

The molecular actions of thyroid hormone in bone.

Thyroid hormone (T(3)) is essential for the normal development of endochondral and intramembranous bone and plays an important role in the linear growth and maintenance of bone mass. Childhood T(3) deficiency results in retardation of skeletal development and growth arrest, whereas T(3) excess leads to accelerated growth and bone formation. In adult thyrotoxicosis, there is increased bone remodelling, characterized by an imbalance between bone resorption and formation, which results in net bone loss and an increased risk for posteoporotic fracture. These clinical observations demonstrate the importance of T(3) in skeletal development and metabolism. Nevertheless, the molecular mechanisms of T(3) action in bone are poorly understood. Here, we provide an overview of T(3) regulation of chondrocytes, osteoblasts and osteoclasts, and the actions of thyroid hormone receptor (TR) isoforms in skeletal development. The possible roles of T(3) and TRs in nuclear receptor crosstalk, prereceptor ligand metabolism, heparan sulfate proteoglycan synthesis and angiogenesis are also considered.

Adolescent↗

PubMed2004

Multiple messenger ribonucleic acid variants regulate cell-specific expression of human thyroid hormone receptor beta1.

Thyroid hormones are essential for development, growth, and metabolism and act via T3 receptors (TR) alpha and beta. The THRA and THRB genes have discrete physiological roles but their mRNAs are expressed widely in overlapping patterns. There is poor correlation between TR mRNA and protein, indicating that expression may be regulated by posttranscriptional mechanisms. Differences in the relative levels of expressed TRalpha and beta proteins have been suggested to modulate tissue T3 responsiveness. We determined the structure of the human THRB gene, cloned seven alternately spliced 5'-untranslated region (5'-UTR) TRbeta1 mRNAs, and identified five polyadenylation position elements in the 3'-UTR. At least six TRbeta1 mRNAs between 1.35 and 7.5 kb in length were expressed in discrete temporospatial patterns in fetal and adult human tissues. The 5'-UTRs contained up to seven upstream short open reading frames, which did not influence the structure of the TRbeta1 protein. In transfection studies, 5'-UTRs exerted cell-specific effects on mRNA expression but consistently reduced protein expression. Furthermore, each 5'-UTR strongly inhibited translation in vitro. Thus, developmental and tissue-specific expression of human thyroid hormone receptor beta1 5'-UTR mRNAs may regulate T3-responsiveness in target tissues by modulating TRbeta protein translation and thereby controlling the ratio of expressed TRalpha and -beta proteins.

3' Untranslated Regions↗

PubMed1989

Value of thyroid hormone determination.

Free thyroid hormone assays have broadened the repertoire in thyroid diagnosis. At elevated binding protein levels they provide more reliable information on the metabolic state than do total hormone determinations; yet under estrogen contraception free T4 may yield test specifically falsely too high data. As a rule, there is accordance between free hormone concentrations and the indices, being equivalent in establishing the free thyroid hormone fraction. In this light the Thyroid Section of the German Endocrinologic Society recommended in 1986 to consider determinations of free or total hormone concentrations with calculation of the indices as being of equal value. In borderline situations the TRH test, the hypersensitivity TSH assay as well as checkups establishing the course of development of the disorder are substantiated.

Adolescent↗

PubMed1971

Control of mitochondrial turnover under the influence of thyroid hormone.

The effect of thyroid hormone on the turnover of mitochondrial DNA and protein was studied in rat heart and liver. Changes in turnover were observed in both thyroidectomized and normal rats following administration of thyroid hormone. In heart and liver the turnover of mitochondrial DNA and protein was slower in thyroidectomized rats than in normal rats. The turnover of mitochondrial DNA and protein was affected similarly following the administration of thyroid hormone, suggesting that mechanisms which control turnover of mitochondrial constituents may be predicated upon a major part of the mitochondrion. In heart a decreased rate of degradation contributes to the increase in total mitochondrial protein. Mitochondrial DNA, labeled before administration of thyroid hormone, turns over, after the start of thyroid hormone administration, at a different rate from that in newly synthesized DNA. The different turnover rates suggest that in liver the pre-existing population of mitochondria is being replaced by another population synthesized under new physiological conditions.

Animals↗

PubMed1987

Thyroid hormone reserve in asymptomatic autoimmune thyroiditis.

Basal (B) and peak (P) serum levels of thyroxine (T4), free thyroxine (FT4), triiodothyronine (T3), free triiodothyronine (FT3), and TSH were measured before and after oral TRH (40 mg) administration in 79 subjects affected with asymptomatic autoimmune thyroiditis (AAT) and in 69 normal subjects. The area under the curve (AUC) and peak values of T4, FT4, T3 and FT3 were considered as parameters of thyroid hormone reserve. Intrathyroidal iodine (ITI) was measured by the X-ray fluorescence method. The AAT subjects were divided into three groups on the basis of their basal and peak TSH values. In group I, these parameters were similar to those in the normal controls; in group II, basal TSH remained normal but peak TSH was significantly increased, and in group III both values were significantly increased. Group I differed from the controls by a decrease in P FT4 and AUC FT4, whereas in groups II and III B FT4 was also significantly lowered. T3 levels were similar in all groups except in group III, in whom they dropped. ITI was already lower in group I than in the controls. Its decline went further in groups II and III. An inverse correlation with significant r values was evidenced between log B and P TSH on one hand and log B FT4, P FT4 and AUC FT4 on the other. When group III was excluded, log P TSH was positively correlated with log B T3, P T3, AUC T3, and AUC F T3.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMedDate not supplied

Impact of PCBs on thyroid hormone directed brain development.

Thyroid hormones regulate neuronal proliferation, migration, process outgrowth, synaptic development, and myelin formation in specific brain regions. Because brain development occurs during discrete windows of time, inappropriate levels of thyroid hormones in definitive periods can produce permanent damage, the nature of which depends upon the timing and magnitude of the insult. Thyroid hormones cross the placenta and enter the brain primarily as thyroxine (T4); therefore, conditions selectively lowering serum T4 levels alter brain hormone availability. Triiodothyronine (T3) is the predominant form of the hormone that binds to the receptor. T3 is produced from T4 in the brain by the enzyme type II, 5'-deiodinase. Polychlorinated biphenyls (PCBs) are synthetic environmental toxicants that bear a striking structural resemblance to the active thyroid hormones and can, depending upon the species, dosage, and congener used, act as agonists, antagonists, and partial agonists to thyroid hormones.

Animals↗

PubMed1996

Insulin-like growth factor I alters peripheral thyroid hormone metabolism in humans: comparison with growth hormone.

Insulin-like growth factor I (IGF-I) is considered to mediate some of the growth-promoting and metabolic effects of growth hormone (GH). Growth hormone treatment of healthy and GH-deficient subjects is accompanied by increased conversion of thyroxine (T4) to triiodothyronine (T3) in peripheral tissues. Whether these effects are mediated by IGF-I is unknown. To assess the respective roles of these hormones on thyroid hormone metabolism we have treated two groups of subjects. The first group consisted of eight healthy subjects who were treated with IGF-I (10 micrograms.kg-1.h-1 sc for 5 days). The second group consisted of eight subjects with combined GH and thyrotropin (TSH) deficiency due to acquired pituitary disease. They were treated with IGF-I (10 micrograms.kg-1.h-1 sc for 7 days), GH (2 IU m-2 sc q.i.d.) or both hormones together. The IGF-I treatment in healthy subjects led to an increase in free T3 (FT3) and a reduction in TSH levels, whereas FT4 and total T4 (TT4) levels remained unchanged. In the second group-in which all subjects were substituted with oral L-thyroxine-treatment with IGF-I led to an elevation of FT3 in the face of unchanged T4 levels. Growth hormone alone and GH plus IGF-I resulted in a more pronounced elevation in T3 level. The results suggest that IGF-I partially mediates the well-known effects of GH on peripheral conversion of T4 to T3. However, GH has more pronounced effects on thyroid hormones that apparently are not mediated by IGF-I.

Adult↗

PubMed1995

Steroid hormone receptors selectively affect transcriptional activation but not basal repression by thyroid hormone receptors.

Thyroid hormone receptors (TRs) and steroid hormone receptors belong to a large superfamily of nuclear hormone receptors. The interactions between these receptor subfamilies are poorly understood. In this study, cotransfection assays were used to examine the effects of estrogen and glucocorticoid receptors on TR-mediated repression of basal transcription by unliganded TR and transcriptional activation by liganded TR with two different thyroid hormone response element-containing reporter plasmids. Surprisingly, it was found that steroid hormone receptors blocked T3-mediated transcriptional activation with little or no effect on basal repression by unliganded TR. The mechanism for blocking TR-mediated transcriptional activation does not require steroid hormone receptor binding to the thyroid hormone response element but, rather, may involve titration of a critical coactivator(s) required for T3-mediated transcriptional activation. These studies strongly suggest divergent pathways for transcriptional activation and basal repression by TRs. Additionally, these studies raise the potential for nuclear hormone receptors to modulate TR-mediated transcriptional activation in steroid hormone-responsive tissues.

Cell Line↗

PubMed1994

[Cloning and characterization of the human thyrotropin-releasing hormone receptor: regulation of thyrotropin-releasing hormone receptor mRNA levels by thyroid hormone].

1) We successfully cloned a human thyrotropin-releasing hormone receptor (TRH-R) gene. The human TRH-R consists of 398 amino acids and is a member of the G protein-coupled receptor family. The gene has a single intron in the coding sequence. Although highly homologous to the rat and mouse TRH-Rs, the human TRH-R has several differences in the carboxyl-terminal structure. 2) We next studied the effect of thyroid status on TRH-R mRNA levels both in vivo and in vitro. TRH-R mRNA levels in hypothyroid rats were increased significantly, while no significant changes were observed in vitro. The data indicate that thyroid hormone may regulate TRH-R mRNA levels in different manners in vitro and in vivo.

Amino Acid Sequence↗

PubMed1989

Relationship between serum free thyroid hormone concentrations and target organ responsiveness in thyroid disease patients before and after treatment.

Relationship between serum free thyroid hormone concentrations and several markers of peripheral tissue response to thyroid status was studied in 24 patients with hyperthyroidism, 17 with euthyroidism with goiter and 10 with primary hypothyroidism before and after the initiation of standard forms of treatment. Before treatment, serum free T4 correlated significantly, either positively or negatively, with the basal metabolic rate (BMR), duration of the achilles tendon reflex (ATR), resting pulse rate (RPR), serum total cholesterol (T-cholesterol), ratio of the pre-ejection period to the left ventricular ejection time (PEP/LVET), serum high density lipoprotein (HDL) and creatine phosphokinase (CPK) in the descending order. Serum free T3 also correlated significantly all the these parameters. After treatment, changes in both serum free T4 and free T3 correlated well with those of the BMR and ATR in the patients with hyperthyroidism, and with those of the ATR, serum CPK and T-cholesterol in the patients with hypothyroidism. These results indicate that these peripheral parameters correlated well with serum free thyroid hormone concentrations in thyroid disease patients. Therefore, these parameters can be used to assess thyroid functions in patients with thyroid hormone resistance.

Adult↗

PubMed2003

Thyroid Hormone Resistance in children.

Thyroid Hormone Resistance (RTH) is characterized by the diminished response of thyroid hormone-responsive tissues in varying degrees in association with elevated serum levels of total and free T4 and T3 and inappropriately normal or elevated TSH levels. In almost all cases it is due to different mutations in only one allele of the thyroid hormone receptor beta gene which blocks the action of normal allele thus producing dominantly inherited RTH. In RTH, varying degrees of target tissue responsiveness result in a heterogenous clinical presentation. Resistance in the thyrotrophs and the peripheral tissues is assessed by the evaluation of TSH secretion and changes in peripheral markers of thyroid hormone action after administration of L-T3, respectively. The treatment decision depends on the individual characteristics of each patient. Patients with hypothyroid and hyperthyroid symptoms may require treatment with thyroid hormone and with agents such as beta blockers, antithyroid drugs and thyroid hormone analogues.

Biomarkers↗

PubMed2002

Heterogeneity of the thyroglobulin epitopes associated with circulating thyroid hormone autoantibodies in hashimoto's thyroiditis and non-autoimmune thyroid diseases.

We previously implicated TG leakage from fine-needle aspiration biopsy (FNAB) as responsible for circulating thyroid hormone autoantibodies (THAb). However, THAb were not always associated with TGAb. In the literature these negative findings have been interpreted against a role of TG as the antigen for THAb. To evaluate the TGAb status more fully and to gain information on TG epitopes involved in THAb development, we measured: 1) TGAb with an independent hemagglutination assay (HA), and 2) epitope specificity in a competitive ELISA using 2 monoclonal Abs (mAb) against TG: mAb 42C3 and mAb 134C2. MAb 42C3 recognizes a cross-reactive iodinated epitope, whereas 134C2 is specific for human TG. We tested 12 Hashimoto's thyroiditis (HT) and 35 non-HT patients sampled prior to, 1 and 3 months after FNAB. We found that, irrespective of thyroid disease or post-FNAB THAb status, certain patients previously classified as TGAb negative by IRMA tested TGAb positive by HA or by competition ELISA and vice versa. A post FNAB positive response to the 42C3 iodinated epitope in only one THAb IgM-T4+ve HT and a few THAb negative non-HT patients was observed. Furthermore, we observed that the 3 non-HT patients who expressed IgM-T3 THAb failed to bind either TG-mAb epitope. We conclude that a single TGAb assay is not sufficient to define the TGAb status, which can be achieved reliably only by using multiple TGAb assays. In addition, the TG-iodinated epitope recognized by 42C3 is not a major epitope in post-FNAB THAb, and the T3-epitope involved in THAb remains distinct from the mAb epitopes. In light of recent data in the literature, we further suggest that the responsible epitopes are more likely to be expressed in leaked TG fragments, rather than leaked intact TG.

Antibodies, Monoclonal↗

PubMed2006

Cloning and characterization of cDNAs for hormones and/or receptors of growth hormone, insulin-like growth factor-I, thyroid hormone, and corticosteroid and the gender-, tissue-, and developmental-specific expression of their mRNA transcripts in fathead minnow (Pimephales promelas).

Growth hormone (GH), insulin-like growth factor-I (IGF-I), thyroid hormones, and corticosteroids play central roles in a wide range of body functions but, in fish, information on their interactions is limited. These axes of the endocrine system are also potential targets for disruption of signaling pathways by hormone-mimicking chemicals, but have received little study. Molecular approaches offer an effective way to help unravel these endocrine interactions but require the appropriate gene-specific assays to do so. In this study, the cDNAs for a suite of hormones and/or receptors involved in signaling for the effects of GH and IGF-I [GH, GH receptor (GHR), IGF-I, IGF-I receptor (IGF-IR)], thyroid hormones [thyroid hormone receptor alpha (TRalpha) and beta (TRbeta)], and corticosteroids [glucocorticoid receptor (GR)] were cloned from the fathead minnow (Pimephales promelas; fhm), and the tissue-, developmental-, and gender-related expression of their mRNA transcripts established. By polymerase chain reaction (PCR) strategy, we obtained full-length 1123-bp GH, 817-bp IGF-I, 1584-bp TRbeta, and 2571-bp GR cDNAs, coding for 210 amino acid (aa) GH, 161 aa IGF-I, 378 aa TRbeta, and 745 aa GR putative proteins, and partial-length 158-bp GHR, 811-bp IGF-IR, and 446-bp TRalpha cDNAs. Real-time PCR analyses revealed broad tissue expression for the target mRNAs; all targets were expressed in brain, pituitary, gill, liver, gonad, intestine, and muscle, with the exception of GH that was expressed only in the pituitary and gonad. Expression patterns in both juvenile and adult fhm were complex, with both temporal-, tissue-, and sex-specific characteristics. For example, hepatic expressions of GHR, IGF-I, and IGF-IR were far higher in males than in females, possibly reflecting the sex-related dimorphism in growth that occurs in this species, and TRalpha and TRbeta showed divergent expression patterns during development (where TRbeta predominated) and in adult tissues implying some distinct roles for the two TR subtypes.

Adrenal Cortex Hormones↗

PubMed2003

Effect of perinatal asphyxia on thyroid-stimulating hormone and thyroid hormone levels.

AIM: To compare serum concentrations of thyroid hormones--T4, T3, free T4 (FT4) and reverse T3 (rT3)--and thyroid-stimulating hormone (TSH) found in the umbilical cord blood of term newborns with and without asphyxia and those found in their arterial blood collected between 18 and 24 h after birth. A further aim of the study was to assess the association between severity of hypoxic-ischemic encephalopathy and altered thyroid hormone and TSH levels, and between mortality and FT4 levels in the arterial blood of newborns between 18 and 24 h of life. METHODS: A case-control study was carried out. The case group comprised 17 term newborns (Apgar score < or = 3 and < or = 5 at the first and fifth minutes; umbilical cord blood pH < or = 7.15) who required bag and mask ventilation for at least one minute immediately after birth. The control group consisted of 17 normal, term newborns (Apgar score > or = 8 and > or = 9 at the first and fifth minutes; umbilical cord blood pH > or = 7.2). Cord blood and arterial blood samples were collected immediately after birth and 18 to 24 h after birth, respectively, and were used in the blood gas analysis and to determine serum concentrations of T4, T3, FT4, rT3 and TSH by radioimmunoassay. All newborns were followed-up until hospital discharge or death. RESULTS: Gestational age, birthweight, sex, size for gestational age, mode of delivery and skin color (white and non-white) were similar for both groups. No differences were found in mean levels of cord blood TSH, T4, T3 and FT4 between the groups. In the samples collected 18 to 24 h after birth, mean levels of TSH, T4, T3 and FT4 were significantly lower in the asphyxiated group than in the control group. Mean concentrations of arterial TSH, T4 and T3 between 18 and 24 h of life were lower than concentrations found in the cord blood analysis in asphyxiated newborns, but not in controls. In addition, asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy presented significantly lower mean levels of TSH, T4, T3 and FT4 than those of controls. None of the asphyxiated newborns with FT4 > or = 2.0 ng/dl died; 6 out of the 11 asphyxiated newborns with FT4 < 2.0 ng/dl died. CONCLUSIONS: Serum concentrations of TSH, T4, T3 and FT4 are lower in asphyxiated newborns than in normal newborns between 18 and 24 h of life; this suggests central hypothyroidism secondary to asphyxia. Asphyxiated newborns with moderate/severe hypoxic-ischemic encephalopathy present a greater involvement of the thyroid function and consequently a greater risk of death.

Asphyxia Neonatorum↗

PubMedDate not supplied

Prostate-thyroid axis: prostatic TRH is one of the stimulators of thyroid hormone.

Ventral prostatectomy decreased serum thyroid hormones and histology of the thyroid gland indicate that hypothyroid condition. Co-culture of thyroid gland and ventral prostate stimulates thyroid hormone secretion. In the present study we report prostatic thyrotropin releasing hormone (TRH) is the stimulating factor of thyroid hormone secretion. Mature rat (90 days old) ventral prostate, anterior pituitary and thyroid glands were co-cultured in vitro with or without TRH antibody to assess the direct influence ofprostatic TRH on thyroid hormone secretion. Total thyroxine (T4) and triiodothyronine (T3) were increased significantly in the culture media of ventral prostate, anterior pituitary and thyroid gland when compared with thyroid gland plus anterior pituitary culture media. However, media T4 and T3 concentration decreased significantly in thyroid gland alone; also in thyroid gland plus ventral prostate, thyroid gland plus anterior pituitary and thyroid gland plus anterior pituitary plus ventral prostate were co-cultured with TRH antibody (Ab) in a dose dependent manner. The results suggest that ventral prostatic TRH is one ofthe stimulating factors of thyroid hormone secretion under these in vitro conditions.

Animals↗

PubMed1988

Effect of simultaneously administered iopanoic acid and thyrotropin releasing hormone (TRH) on thyroid hormone metabolism in euthyroid subjects.

The cause of serum T4 elevation after iopanoic acid administration was searched in euthyroid subjects. 3 gr iopanoic acid was given per os to 9 healthy volunteers (group I), in other 5 volunteers a TRH test was performed prior to iopanoic acid administration (group II). In group I TSH, T4, FT4I and rT3 levels increased, in group II T3 and FT3I decreased, but no TSH, T4, FT4I increase was seen, obviously, because of the exhaustion of pituitary TSH content by TRH. On the ground of the findings T4 elevation caused by iopanoic acid is predominantly consequence of TSH release and not that of inhibited T4 conversion rate.

Adult↗