Search PubMedSearch

SEARCH · Search PubMed

Results for “thyroid”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Corticosteroids and thyroid function. Different effects on plasma volume, thyroid hormones and thyroid hormone-binding proteins after oral and intravenous administration.

The influence of glucocorticosteroids on plasma volume, thyroid hormones and thyroid hormone-binding proteins was studied in 17 patients. Plasma volume was not affected either by i.v. beta-methasone (6 mg daily) or by oral prednisolone (45--180 mg daily) given for 5 days. The serum T3 concentration decreased while rT3 increased independently of the route of administration of corticosteroids. Serum T4 concentration decreased after i.v. but not after oral administration of corticosteroids. Oral steroids as compared to i.v. increased the 125I-triiodothyronine uptake test value. The serum TBG concentration decreased independently of the route of administration, while the serum TBPA concentration increased after oral corticosteroids but was unchanged after i.v. treatment. The serum TSH concentration was slightly reduced. About half of the patients were given both corticosteroids and nutrition i.v. and the other half were given all treatment by mouth. The part played by the route of administration of corticosteroids and calories, respectively, cannot be evaluated at present but these factors seem to be of importance.

Administration, Oral

Altered thyroidal responsivity to thyrotropin induced by circulating thyroid hormones. A "short-loop" regulatory mechanism?

We studied the effect of thyroid hormone administration on responsivity of murine thyroid to exogenous thyrotropin (TSH) in order to explore the possibility that the thyroid gland might be directly inhibited by its own hormones. In the rat both L-thyroxine (T4) and 3,5,3'-L-triiodothyronine (T3) pretreatment inhibited TSH-induced thyroidal ornithine decarboxylase (ODC) activity in vivo in a dose-related manner (half-maximal inhibition, 1.7 mug/rat and 0.6 mug/rat, respectively). Other structurally related compounds exhibited the following inhibitory potencies compared to T4: T3, 283%; triiodothyroacetic acid, 40%; D-T4, 18%; 3,5-L-diiodothyronine, 9%. Monoiodotyrosine, diiodotyrosine, and iodide were not inhibitory. The full inhibitory effect of T4 or T3 was observed when thyroid hormone was administered from 96 to 12 h before TSH and was also seen in hypophysectomized animals. Pretreatment with T4 or T3 in divided doses over 2 1/2 days inhibited TSH-induced increase in [1-14C]glucose oxidation to 14C02 and [3H] leucine incorporation into protein in rat thyroid. In the mouse T4 or T3 pretreatment (0.25-25 mug daily) caused dose-related inhibition of both thyroidal ODC activity and 131I release induced by TSH in vivo. In mice on a low-iodine diet (LID) but not in animals on a regular diet (RD) NaI pretreatment also blunted TSH-induced thyroidal ODC activation and 131I release. When LID or RD mice were pretreated with 12.5-125 mug of T4 or T3 over 2 1/2 days, TSH-induced in vitro stimulation of thyroid cyclic 3',5'-adenosine monophosphate formation was inhibited in a dose-related manner; NaI pretreatment was inhibitory in the LID mouse only. Prior administration of exogenous TSH blunted the activation of thyroid ODC and thyroid hormone release induced by subsequent TSH administration in rat and mouse. These studies indicate altered thyroid responsivity to TSH under the influence of circulating thyroid hormones and suggest the existence of a "short-loop" negative feedback regulating thyroid function.

Animals

Effect of adrenal hormones on thyroid secretion and thyroid hormones on adrenal secretion in the sheep.

1. Previous work has shown that after stressful stimuli, sheep initially secrete increased amounts of thyroid hormone, at a time when adrenal secretion is also elevated. 2. This study was designed to evaluate (a) any short-term activation or inhibition of thyroid secretion by exogenous cortisol or ACTH administered in quantities comparable to those secreted after stress in sheep and (b) any short-term effect that exogenous thyroxine or triiodothyronine may have on the concentration of plasma cortisol in the sheep. 3. Thyroid activity was measured by determination of plasma protein bound 125I (PB125I) and total 125I in thyroid vein and mixed venous (jugular) blood. Plasma cortisol and thyroxine concentrations were measured by a competitive protein-binding assay at intervals for up to 5 hr after commencement of the experiment. 4. No evidence of an activation of thyroid secretion was found during cortisol or ACTH infusion, as monitored by thyroid vein PB125I. Similarly there was no evidence of any inhibition of thyroid function, as measured by continued secretion of thyroid hormones into thyroid vein blood. 5. No effect on plasma cortisol concentration due to thyroid hormone treatment was observed. 6. It was concluded that (a) elevated circulating corticosteroids in physiological concentrations have no short-term effects on thyroid activity in the sheep and (b) the short-term alterations in thyroid and adrenal cortical secretion observed during stress in the sheep could not be attributed to direct interaction of elevated thyroid hormone concentrations with adrenal cortical secretion.

Adrenal Glands

Thyroid-joint crosstalk: a systematic review and meta-analysis of thyroid autoimmunity and dysfunction in juvenile idiopathic arthritis.

BACKGROUND: Recent observational studies outlined the concomitant presence of autoimmune diseases in children with juvenile idiopathic arthritis (JIA), including endocrine autoimmunity. Despite the growing evidence of thyroid involvement in JIA, available data are heterogeneous and fragmented. We aimed to systematically review the available evidence on the prevalence of thyroid autoantibody positivity and thyroid dysfunction in patients with JIA. METHODS: PubMed/Medline, Cochrane, and Scopus databases were approached to identify studies reporting data on thyroid autoantibody positivity and dysfunction in children with JIA. RESULTS: A total of 15 studies were included in the final analysis, encompassing 19 015 children with JIA (13 225 females, 69.6%) with a weighted mean age of 8.0 years (range 1.8-21 years). The pooled prevalence estimates of antithyroid antibody positivity and thyroid dysfunction were 0.04 (95% CI: 0.03-0.05) and 0.04 (95% CI: 0.03-0.08), respectively. The risk difference for thyroid autoantibody positivity between children with JIA and controls was 0.08 (95% CI: 0.02-0.14). Possible risk factors were analyzed: the presence of family history for thyroid autoimmune disease (odds ratio - OR 3.91, 95% CI 1.86-8.25), concurrent Antinuclear Antibodies (ANA) positivity (OR 1.62, 95% CI 1.13-2.31), and older age (MD 2.10 years, 95% CI 1.32-2.89) were associated with thyroid autoantibody positivity and/or thyroid dysfunction in children with JIA. No significant difference emerged for the specific JIA form. CONCLUSION: Thyroid dysfunction may be detected in children with JIA, with a significant risk difference in comparison to healthy controls. Specific clinical characteristics, such as family history, ANA positivity, and older age at JIA onset, may suggest which patients should benefit from thyroid autoantibody screening.

Humans

The Thyroid-Brain Network: Exploring Inflammation, Immune Mechanisms and Common Triggers in Thyroid-Related Neurological Dysfunction.

Autoimmune thyroid diseases (AITD), including Hashimoto's thyroiditis and Graves' disease, represent the most prevalent endocrine disorders worldwide, affecting hundreds of millions with profound but often under recognized neurological consequences. There are emerging lines of evidence establishing inflammation and immunity as the critical missing link connecting peripheral thyroid dysfunction to central nervous system manifestations. Thyroid hormones function as essential neuromodulators governing neurodevelopment, synaptic plasticity, and cognitive processing through integrated genomic and non-genomic mechanisms, with region-specific cerebral metabolic disturbances correlating with distinct neuropsychiatric symptoms. The immunological perspective reveals that AITD propagates neuroinflammation through convergent pathways: molecular mimicry enabling cross-reactivity between thyroid and neural antigens, cytokine-mediated disruption of neurotransmitter metabolism, HMGB1-driven glial activation, and blood-brain barrier compromise facilitating immune cell infiltration. The thyroid-gut-microbiota axis emerges as a critical mediator wherein dysbiosis perpetuates both thyroid autoimmunity and neuroinflammation through impaired serotonin precursor availability and increased intestinal permeability. Mitochondrial dysfunction represents an energetic common denominator, as thyroid hormone dysregulation directly impairs oxidative phosphorylation, producing region-specific cerebral metabolic disturbances. Simultaneous compromise of monoamine systems, cholinergic signaling abnormalities, and glutamate excitotoxicity creates a particularly toxic neurochemical state in untreated thyroid dysfunction. Common triggers such as psychological stress, gut dysbiosis, and mitochondrial impairment may activate interconnected pathways that simultaneously compromise thyroid and brain function, revealing that these disorders share fundamental mechanistic origins. These insights have been discussed in the current review to enhance the understanding of thyroid-brain function, the core mechanisms and consequences of functional deficits.

Journal Article

Adsorption of thyroid-stimulating antibody (TSAb) of Graves' disease by homologous and heterologous thyroid tissue.

Immunoglobulin G purified from the serum of patients with Graves' disease, stimulated the thyroid of man, calf, and guinea pig (cAMP accumulation as the end-point) in vitro, and the thyroid of the mouse in vivo (LATS bioassay). The stimulatory effect on the thyroids of all four species was removed by adsorption of the immunoglobulin G to human thyroid membranes and was diminished to a proportionately similar degree by adsorption with bovine thyroid membranes. All activity, as assessed by stimulation of the human thyroid in vitro. was recovered from both human and bovine membranes by elution with 2 M NaSCN solution. The data support the concept that the thyroid-stimulating antibody of Graves' disease is homologous to a human thyroid antigen and, in some instances, cross-reacts with a similar antigen in the thyroid of a distant species and so stimulates the heterologous gland.

Adsorption

Thyroidal triiodothyronine and thyroxine in Graves' disease: correlation with presurgical treatment, thyroid status, and iodine content.

To evaluate the potential contribution of thyroidal secretion to the relative excess of triiodothyronine (T3) production in hyperthyroidism and to investigate the effects of treatment, iodine (127I), T3 and thyroxine (T4) were measured in digests of thyroid tissue obtained at surgery from 13 patients with Graves' disease. In 11 normal human thyroid glands, 127I content was 630 +/- 60 (all values mean +/- SE in mug/ wet weight) T4, 254 +/- 39 and T3 21 +/-3. The T4I was 26 +/- 3% of the total iodine and the molar ratio T4/T3 was 11 +/- 1. The 13 patients with Graves' disease were divided into three groups. Eleven were clinically euthyroid (Groups I and II) and had received either iodide or iodide plus a thiourea derivative before surgery. Two subjects (Group III) received only propranolol. In Group I (n = 8), mean thyroidal 127I content was 320 +/- 50, T4 was 115 +/- 9 and T3 22 +/- 4. The molar ratio T4/T3 was 5.9 +/- 1 and T4I was 26 +/- 2% of the total. Group II patients (3) had the lowest preoperative serum T4 (less than 2.5 mug/dl) and T3 (less than ng/dl) concentrations with TSH elevated in only one (7 muU/ml). Thyroidal 127I was 100 +/- 26, T49 +/- and T3 1.3 +/- 0.3. The % T4I was 5 +/-2. The two chemically hyperthyroid subjects had a mean tissue 127I of 450; T4, 295 and T3, 56, the T4/T3 ratio was 4.5 and % T4I was 42. There was no correlation between tissue 127I and T4/T3 within either the normal or Graves' disease group. Since adequate clinical and chemical control of hyperthyroidism with antithyroid drugs and iodine was attained in the 8 Group I subjects without a decrease in the % T4I or T3I below that of normal thyroids, it suggests that inhibition of iodotyrosine coupling is not required for this effect. The % T4I was below normal only in patients with marked suppression of serum T4 and T3 concentraions. The lack of correlation between tissue 127I and T4/T3 ratio in the treated patients suggests that the lower T4/T3 ratio in Graves' thyroids is independent of intrathyroidal iodine concentrations. This hypothesis is strengthened by the similarly low T4/T3 ratio in untreated subjects with near normal tissue 127I content. Assuming that the thyroid hormones are secreted in the ratios present in these digests, one can estimate that direct secretion by the thyroid could contribute most, of not all, of the excess T3 production in Graves' disease.

Adolescent

The role of the pentose phosphate shunt in thyrotropin-induced thyroid hormone secretion: in vivo and vitro studies with 6-aminonicotinamide in mouse thyroids.

The possible role of the pentose phosphate shunt in thyroid hormone secretion was investigated in vivo and in vitro with mouse thyroid glands. Thyroidal endocytosis in response to TSH, a step of thyroid hormone secretion, was evaluated for its dependency upon the pentose phosphate shunt by using 6-aminonicotinamide (6-AN), an antimetabolite in the synthesis of pyridine nucleotides. Formation of 14CO2 from glucose labeled either in the C-1 or C-6 position was studied to estimate the pentose phosphate shunt activity. A dose of 6-AN markedly reduced oxidation of [1-14C]glucose but did not affect that of [6-14C]glucose induced by TSH. Concomitantly there was a marked decrease in thyroidal endocytotic response to TSH. These inhibitions by 6-AN were completely abolished by the pretreatment with nicotinamide. Methylene blue, which oxidizes NADPH and thus stimulates activity of the pentose shunt, significantly depressed thyroidal endocytosis in response to TSH in vitro. These inhibitions of colloid droplet formation by 6-AN or methylene blue were not manifested against dibutyryl cyclic AMP stimulation. Furthermore, a dose of 6-AN, which seems to inhibit only the pentose phosphate shunt, markedly depressed TSH-induced formation of cyclic amp. These findings suggest that the pentose phosphate shunt might play an important role in triggering TSH stimulation of thyroid hormone secretion by supplying NADPH, and further, that NADPH dependency in thyroid hormone secretion is at a site prior to the generation of cyclic AMP.

6-Aminonicotinamide

Simple, rapid thyroid function testing with 99mTc-pertechnetate thyroid uptake ratio and neck/thigh ratio.

To avoid the technical difficulties and errors inherent in the measurement of early thyroid uptake of 99mTcO4-,techniques which are independent of absolute uptake, neck extrathyroidal background and dose standards were evaluated in a series of 108 patients. After intravenous injection of 2 mCi 99mTcO4-, radioactivity was recorded over the neck and thigh. Thyroid uptake ratios were calculated as the ratios of activity over the neck at two times. A neck/thigh ratio was calculated from the recorded activities at 15 min after injection. Examination of these parameters showed that a combination of the 15 min neck/thigh ratio and the 10'/2' thyroid uptake ratio best served to discriminate thyroid function: 92% of hyperthyroid cases were correctly identified by a neck/thigh ratio above 4.7 and 95% of hypothyroid cases were identified by the combination of a neck/thigh ratio below 3 and a 10'/2' thyroid uptake ratio below 1. Correct classification of euthyroidism was 84% but with the exclusion of patients previously treated with 131I, this rose to 91%. The accuracy of the 99mTc procedure is comparable to that of the standard 24 hr 131I uptake run concurrently in this series and duplicates the accuracy of computer assisted determinations of absolute thyroid 99mTcO4- uptakes. The procedure provides a convenient method for the evaluation of thyroid function as an accompaniment to 99mTcO4- thyroid imaging.

Humans

Thyroid function in early sub-acute thyroiditis.

A 53-year-old woman with an early form of de Quervain's disease involving both thyroid lobes was found to have her thyroid uptake of iodine suppressed, although the serum thyroid hormone concentrations were normal while the administration of TRH resulted in significant increase in the serum TSH concentrations. After administration of TSH the thyroid reserve was found to below. The diagnosis of sub-acute thyroiditis was confirmed on biopsy. The above data seem to indicate that the suppression of the thyroid uptake in the early stage of de Quervain's disease may be directly caused by the inflammatory condition of the gland, rather than, as is usually the case, by the excess of thyroid hormones and, consequently, by the suppression of pituitary TSH secretion.

Female

Fibrotubular Tumors of the Thyroid: An Emerging Thyroid Neoplasm Characterized by Distinctive Morphology and Recurrent OCLN::PRKCI Gene Fusions Spanning the Adenoma-Carcinoma Spectrum.

The histopathologic and genomic landscape of thyroid tumors is well characterized, although new genetic alterations and tumor types are being described. We present 2 cases of thyroid tumors originating from follicular cells that had highly unusual and distinct morphologic features and carried an OCLN::PRKCI gene fusion. These tumors were well circumscribed, encapsulated, and composed of irregularly shaped tubular and follicular structures surrounded by layers of distinct fibrocollagenous basement membrane material positive for type IV collagen and laminin; they showed no definitive nuclear features of papillary carcinoma. Importantly, whereas one of the tumors had no invasive growth, the other demonstrated tumor capsule invasion, compatible with the adenoma-carcinoma spectrum seen in thyroid follicular and oncocytic tumors. Gene expression profiles of these tumors differed from those of common types of papillary thyroid carcinoma. The unusual and reproducible histopathologic characteristics and unique molecular profiles of these tumors support their designation as a distinct type of thyroid neoplasm that exists in noninvasive and invasive forms and, therefore, can be designated as fibrotubular adenoma and carcinoma. Recognition of this distinct entity is important for improving diagnostic accuracy and avoiding overtreatment of this likely indolent type of thyroid neoplasia.

Humans

Thyroid hormones homeostasis and TSH in autonomic thyroid nodule.

Thirty patients with autonomic thyroid nodules were studied. Thyroid scintigram, iodine uptake at 2 and 24 hrs, PBI, total thyroxine, serum T3(RIA), basal TSH and 30 minutes after TRH administration were performed. A lack of concordance was found between the clinical signs and the laboratory data. According to the data obtained the patients were grouped into 3 categories: having 1) autonomic thyroid nodules with normal PBI, T4t, T3 values and absent or diminished TSH response to TRH; 2) autonomic thyroid nodules with increased T3 secretion and no response to TRH despite a normal T4 and iodine uptake, 3) hyperfunctional autonomic nodules in which PBI, T4t, T3 and iodine uptake are increased. TSH response to TRH is the most sensitive test for hyperthyroidism, more sensitive than the circulating thyroid hormones assay, and best fitted for adequate therapeutic management. Serum triiodothyronine was found to be increased in 95% of the patients. Thus, there is a T3 thyreotoxicosis in most of the autonomic nodules. TRH test and serum T3 assay being essential elements in starting the treatment, they have to be included among the tests used in autonomic thyroid nodules investigation.

Adenoma

Thyroid-stimulating hormone and cyclic adenosine 3',5'-monophosphate in the regulation of thyroid gland function.

The initial step in TSH action reflects binding of the hormone to specific receptor sites on the plasma membrane. Such binding has been studied using plasma membranes, homogenates, isolated thyroid cells grown in culture, and thyroid slices. 3-H- and iodinated TSH preparations have been used; the latter have been prepared using both chloramine-T and lactoperoxidase. Some of the discrepancies reported in the literature might reflect the different thyroid and hormone preparations and the variable incubation conditions which have been used. In general, good correlation exists between binding of TSH and activation of adenylate cyclase in thyroid plasma membranes. Data is reviewed related to activation of protein kinase in intact thyroid cells by TSH. Although there is impressive evidence for cyclic AMP mediation of effects of TSH on the thyroid, some data that are inconsistent with this concept are considered, especially in relationship to 32-P incorporation into phospholipid. The role of cyclic GMP in thyroid function is discussed.

Adenylyl Cyclases

[Ultrasound for differentiated carcinoma of the thyroid, autonomous adenoma and thyroiditis (author's transl)].

The article deals with a number of thyroid abnormalities which produce similar sonographic patterns, characterised by a paucity of echos of low amplitude. It concerns three more or less circumscribed changes (differentiated carcinoma of the thyroid, autonomous adenoma and focal thyroiditis) and two diffuse thyroid conditions (sub-acute and lymphocytic diffuse thyroiditis, hyperthyroidism). Carcinoma of the thyroid is of particular interest. The distinguishing features and differential diagnosis are discussed.

Diagnosis, Differential

Thyroid-stimulating hormone regulation of ornithine decarboxylase activity in the thyroid.

TSH (1.0 U im) caused a 22-fold increase in thyroidal ornithine decarboxylase activity (ODC) 6 hours after administration in intact rats. Hypophysectomized rats treated with 1 U TSH showed a 5-fold increase in thyroid ODC activity. This stimulation appeared to be specific for TSH since hormones known to induce ODC activity in other target tissues, such as ACTH or LH, showed no significant stimulation. DIBUTYRYL CYCLIC AMP and aminopylline caused a 12-fold increase in ODC activity 5 hours after administration. Prostaglandins have also been implicated in the TSH-induced stimulation of cyclic AMP. Indomethacin (1.0 mg/100 g body wt, ip), an inhibitor of prostaglandin synthesis, was administered 3 hours before TSH with a resulting 30% diminution (P less than .001) in ODC activity compared with the administration of TSH alone. To rule out the possibility that the increase in ODC activity with TSH might be due to increased thyroid hormone secretion, ODC activity was evaluated 6 hours after triiodothyronine administration (60 mug/100 g body wt), and no significant increase in thyroid ODC activity was found. Stimulation of ODC activity was 90% inhibited by the intraperitoneal administration of actinomycin D (80 mug/100 g body wt) or cycloheximide (400 mug/100 g body wt) given simultaneously with TSH. These results indicated that TSH specifically stimulated thyroid ODC activity, which may be important for the growth-promoting action of the hormone on the thyroid gland. This action may be mediated by cAMP and prostaglandins and may require new protein synthesis.

Adrenocorticotropic Hormone

Alteration of thyroidal responsiveness to TSH under the influence of circulating thyroid hormone: short feed-back regulatory effect.

In order to examine the hypothesis that the thyroidal responsiveness to TSH is under the influence of thyroid hormone, following the T3 injection to the mice, serum T3 concentrations and the response of thyroid tissue to a fixed dose of TSH in terms of intracellular colloid droplet formation was studied. The colloid droplets induced by TSH was significantly reduced when serum T3 was decreasing, while it was significantly increased when serum T3 was increasing. This results demonstrate for the first time the existence of short feed-back loop regulating intra-thyroidal function by circulating T3. To delineate the possible mechanism of action of T3, the thyroid gland of mouse whose serum T3 concentration was elevated by injecting 50 mug T3, was incubated with TSH in vitro. TSH-induced cyclic AMP generation was not inhibited at all but colloid droplet formation was significantly inhibited in the thyroid tissue of the animal whose serum T3 concentration was enormously high. Thus, it was demonstrated that the site at which T3 affects is beyond cylcic AMP generation but prior to endocytosis, being consistent with our previous results.

Animals