Abnormally elevated THYROXINE level in the BLOOD.
An inherited autosomal dominant trait characterized by abnormally elevated levels of total serum THYROXINE; (T4) in euthyroid patients with abnormal SERUM ALBUMIN that binds T4 with enhanced affinity. The serum levels of free T4, free T3, and TSH are normal. It is one of several T4 abnormalities produced by non-thyroid disorder. This condition is due to mutations of the ALB gene on CHROMOSOME 4.
The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.
A tetrameric protein, molecular weight between 50,000 and 70,000, consisting of 4 equal chains, and migrating on electrophoresis in 3 fractions more mobile than serum albumin. Its concentration ranges from 7 to 33 per cent in the serum, but levels decrease in liver disease.
Blood proteins that bind to THYROID HORMONES such as THYROXINE and transport them throughout the circulatory system.
A major protein in the BLOOD. It is important in maintaining the colloidal osmotic pressure and transporting large organic molecules.

Structural investigations of a new familial dysalbuminemic hyperthyroxinemia genotype. (1/27)

BACKGROUND: In a previous study, we found that the amino acid substitution R218H in human serum albumin (HSA) was the cause of familial dysalbuminemic hyperthyroxinemia (FDH) in several Caucasian patients. Subsequently the substitution R218P was shown to be the cause of FDH in several members of a Japanese family. This study attempts to resolve discrepancies in the only other study of R218P HSA and identifies two new Japanese R218P FDH patients unrelated to those described previously. METHODS AND RESULTS: Recombinant R218H, R218P, and wild-type HSA were synthesized in yeast, and the affinities of these HSA species for l- and d-thyroxine were determined using fluorescence spectroscopy. The dissociation constants for the binding of wild-type, R218P, and R218H HSA to l-thyroxine were 1.44 x 10(-6), 2.64 x 10(-7), and 2.49 x 10(-7) mol/L, respectively. The circular dichroism spectra of thyroxine bound to R218H and R218P HSA were markedly different, indicating that the structure of the thyroxine/HSA complex is different for either protein. CONCLUSIONS: The K(d) values for l-thyroxine bound to R218P and R218H HSA determined in this study were similar. The extremely high serum total-thyroxine concentrations reported previously for R218P FDH patients (10-fold higher than those reported for R218H FDH patients) are not consistent with the K(d) values determined in this study. Possible explanations for these discrepancies are discussed.  (+info)

A point mutation in the albumin gene in a Chinese patient with familial dysalbuminemic hyperthyroxinemia. (2/27)

Familial dysalbuminemic hyperthyroxinemia (FDH) is an autosomal dominant disorder characterized by euthyroid hyperthyroxinemia. However, FDH has not been reported in Chinese or African patients. Here, we report the first case of FDH in a Chinese patient. A 69-year-old Chinese man was found to have increased serum total T(4) concentrations (198-242nmol/l; normal range 58-148nmol/l) and free T(4) concentrations (>58pmol/l; T(4) analog method, normal range 9-28pmol/l). Serum total T(3) and TSH concentrations were normal. The patient was misdiagnosed as hyperthyroid and was later suspected to have a TSH-producing tumor by the finding of a pituitary microadenoma, which was eventually proven to be a non-functional pituitary 'incidentaloma'. Electrophoretic analysis of the patient's serum proteins demonstrated enhanced albumin binding of [(125)I]T(4). Serum free T(4) concentrations were normal (16-19pmol/l, normal range 9-26pmol/l) when a two-step method was used. Direct sequencing of the albumin gene showed a guanine to adenosine transition in the second nucleotide of codon 218, resulting in a substitution of histidine (CAC) for the normal arginine (CGC) in one of the two alleles in the patient. The point mutation was further confirmed by HphI digestion of exon 7 of the albumin gene. The patient's son was not affected. Our studies demonstrated that the point mutation of the albumin gene in a Chinese patient with FDH was similar to that found in western white families, but differed from that in a Japanese family in whom a guanine to cytosine transition at the same position was found.  (+info)

Abnormal serum free thyroid hormone levels due to heparin administration. (3/27)

Fractionated or unfractionated heparin may produce artefactual elevation in measured concentrations of free thyroid hormones. Although the specific cause is unknown, it may be a consequence of displacement of thyroid hormones from their binding sites by free fatty acids liberated in vitro. We describe four cases of heparin-induced abnormalities in free thyroid hormone measurements where some diagnostic confusion was generated. Increasing physician awareness of this poorly appreciated entity may avert diagnostic confusion and unnecessary investigation.  (+info)

Structural basis of albumin-thyroxine interactions and familial dysalbuminemic hyperthyroxinemia. (4/27)

Human serum albumin (HSA) is the major protein component of blood plasma and serves as a transporter for thyroxine and other hydrophobic compounds such as fatty acids and bilirubin. We report here a structural characterization of HSA-thyroxine interactions. Using crystallographic analyses we have identified four binding sites for thyroxine on HSA distributed in subdomains IIA, IIIA, and IIIB. Mutation of residue R218 within subdomain IIA greatly enhances the affinity for thyroxine and causes the elevated serum thyroxine levels associated with familial dysalbuminemic hyperthyroxinemia (FDH). Structural analysis of two FDH mutants of HSA (R218H and R218P) shows that this effect arises because substitution of R218, which contacts the hormone bound in subdomain IIA, produces localized conformational changes to relax steric restrictions on thyroxine binding at this site. We have also found that, although fatty acid binding competes with thyroxine at all four sites, it induces conformational changes that create a fifth hormone-binding site in the cleft between domains I and III, at least 9 A from R218. These structural observations are consistent with binding data showing that HSA retains a high-affinity site for thyroxine in the presence of excess fatty acid that is insensitive to FDH mutations.  (+info)

A Chinese family with familial dysalbuminaemic hyperthyroxinaemia. (5/27)

We report the results of biochemical and genetic studies in a Chinese family with familial dysalbuminaemic hyperthyroxinaemia. Total thyroxine levels were 1.2 to 1.7 times the upper limit of the reference range and free thyroxine levels were 1.2 to 1.6 times the upper reference limit. Concentrations of thyroid-stimulating hormone (thyrotropin) and free tri-iodothyronine were normal in all family members tested. Overall, thyroid function tests showed high total thyroxine levels in five males and two females over two generations in the family. The diagnosis of familial dysalbuminaemic hyperthyroxinaemia was confirmed by the detection of a guanine to adenine missense mutation in the second nucleotide of codon 218 of the gene encoding human serum albumin, showing that the mutation in this family is the same as that previously found in Caucasian populations.  (+info)

Dysprealbuminemic hyperthyroxinemia in a patient with hyperthyroid graves disease. (6/27)

Rare mutant forms of circulating albumin and prealbumin [transthyretin (TTR)] have increased binding affinity for thyroxine (T4). Patients with these variant plasma proteins, as a result of inherited mutations or as a paraneoplastic phenomenon, typically present with increased serum total T4 and, by some assay methodologies, an increased free T4 as well. Although these individuals are, in fact, euthyroid, nonspecific symptoms may lead to inappropriate treatment for hyperthyroidism. We present a 34-year-old woman in whom a mutant form of TTR with increased T4 binding affinity and coexisting Graves disease was present. Subsequent 131I therapy led to development of postablative hypothyroidism, which was obscured by her higher serum free T4 concentration. Circulating thyroid-binding globulin (TBG), albumin, and TTR concentrations were all within their respective reference limits. A T4-binding protein panel confirmed that TTR-bound T4 was significantly increased, whereas TBG- and albumin-bound T4 was normal, indicating that this patient had euthyroid dysprealbuminemic hyperthyroxinemia, which had been masked by the initial presentation of hyperthyroidism. These findings indicate that hypothyroidism can be masked by coexisting euthyroid dysprealbuminemic hyperthyroxinemia.  (+info)

Prevalence of familial dysalbuminemic hyperthyroxinemia in serum samples received for thyroid testing. (7/27)

The prevalence of familial dysalbuminemic hyperthyroxinemia (FDH), a condition sometimes mistaken for hyperthyroidism, has not been clearly established. I present a study of the prevalence of FDH in serum samples received for thyroid-function tests in a reference laboratory. A prospective study of 15,674 serum samples was carried out over 24 months, of which 13,232 cases were from women (84.42%) and 2442 were from men (15.58%). FDH was diagnosed in 26 cases, 22 in women and four in men. Therefore, the prevalence of FDH in the total number of samples from both sexes was 0.17%, 0.17% in women, and 0.16% in men, which is consistent with a dominant autosomal type of familial transmission. These findings demonstrate that cases of FDH occur frequently; therefore, every laboratory must be prepared to recognize them and thus avoid an incorrect diagnosis of the patient's thyroid function.  (+info)

Differentiating various abnormalities of thyroxin binding to serum proteins by radioelectrophoresis of thyroxin and immunoassay of binding proteins. (8/27)

Using the simple method of protein analysis described here, we could identify thyroxin (T4)-binding-protein abnormalities in euthyroid patients with hyperthyroxinemia or hypothyroxinemia. Serum incubated with [125I]thyroxin was analyzed by agarose gel electrophoresis, with bromphenol blue staining of protein. The relative distribution of radioactive T4 was determined for each binding protein--thyroxin-binding globulin (TBG), transthyretin, albumin, and T4-binding immunoglobulin (when present)--and the mass of T4 bound to each was determined. We also used sensitive immunoassays to quantify TBG, transthyretin, and albumin concentrations, then calculated the mass of T4 (as determined by electrophoresis) bound per unit mass of the respective binding protein. When the concentration of binding proteins was altered (e.g., TBG excess or TBG deficiency), the T4 binding/mass ratio for each protein remained within the expected range; but when the functional affinity of a binding protein was altered--as in dysalbuminemic hyperthyroxinemia and in low-T4 nonthyroidal illness--this ratio was abnormal. This procedure can be used to help identify TBG excess, TBG deficiency, dysalbuminemic hyperthyroxinemia, prealbumin-associated hyperthyroxinemia, variant TBG with reduced affinity for T4, euthyroid sickness, and T4-binding autoantibodies.  (+info)

Hyperthyroxinemia is a condition characterized by an elevated level of thyroxine (T4) in the blood. Thyroxine is a hormone produced by the thyroid gland, and its levels are regulated by another hormone called thyroid-stimulating hormone (TSH). Hyperthyroxinemia can be caused by various factors, including overactive thyroid gland (hyperthyroidism), excessive intake of thyroid hormones, or genetic disorders affecting thyroid hormone metabolism.

It is important to note that hyperthyroxinemia may not always result in symptoms or clinical manifestations of hyperthyroidism, as T4 levels must be converted to the active form of the hormone, triiodothyronine (T3), to exert its effects on various organs and tissues. Therefore, additional tests, such as measuring free T3 and TSH levels, may be necessary to confirm the diagnosis of hyperthyroidism.

Familial Dysalbuminemic Hyperthyroxinemia (FDH) is a benign condition characterized by an elevated level of thyroid hormone T4 (Thyroxine) in the blood, while the patient is clinically euthyroid (not showing symptoms of hyperthyroidism). This is caused by a mutation in the gene for albumin, the most common protein in human serum. The mutated albumin has an increased ability to bind thyroid hormones, leading to an increase in total T4 concentration in the blood. However, the levels of free, active thyroid hormone remain normal.

It is important to note that FDH should be differentiated from other causes of hyperthyroxinemia such as hyperthyroidism or consumption of large amounts of dietary iodine, which can lead to abnormal thyroid function and symptoms associated with hyperthyroidism. In contrast, FDH is not associated with any clinical manifestations of hyperthyroidism and does not require treatment.

Thyroxine (T4) is a type of hormone produced and released by the thyroid gland, a small butterfly-shaped endocrine gland located in the front of your neck. It is one of two major hormones produced by the thyroid gland, with the other being triiodothyronine (T3).

Thyroxine plays a crucial role in regulating various metabolic processes in the body, including growth, development, and energy expenditure. Specifically, T4 helps to control the rate at which your body burns calories for energy, regulates protein, fat, and carbohydrate metabolism, and influences the body's sensitivity to other hormones.

T4 is produced by combining iodine and tyrosine, an amino acid found in many foods. Once produced, T4 circulates in the bloodstream and gets converted into its active form, T3, in various tissues throughout the body. Thyroxine has a longer half-life than T3, which means it remains active in the body for a more extended period.

Abnormal levels of thyroxine can lead to various medical conditions, such as hypothyroidism (underactive thyroid) or hyperthyroidism (overactive thyroid). These conditions can cause a range of symptoms, including weight gain or loss, fatigue, mood changes, and changes in heart rate and blood pressure.

Prealbumin, also known as transthyretin, is a protein produced primarily in the liver and circulates in the blood. It plays a role in transporting thyroid hormones and vitamin A throughout the body. Prealbumin levels are often used as an indicator of nutritional status and liver function. Low prealbumin levels may suggest malnutrition or inflammation, while increased levels can be seen in certain conditions like hyperthyroidism. It is important to note that prealbumin levels should be interpreted in conjunction with other clinical findings and laboratory tests for a more accurate assessment of a patient's health status.

Thyroxine-binding proteins (TBPs) are specialized transport proteins in the blood that bind and carry thyroid hormones, primarily Thyroxine (T4), but also Triiodothyronine (T3) to a lesser extent. The majority of T4 and T3 in the blood are bound to these proteins, while only a small fraction (0.03% of T4 and 0.3% of T3) remains unbound or free, which is the biologically active form that can enter cells and tissues to exert its physiological effects.

There are three main types of thyroxine-binding proteins:

1. Thyroxine-binding globulin (TBG): This is the major thyroid hormone transport protein, synthesized in the liver and accounting for approximately 70-80% of T4 and T3 binding. TBG has a high affinity but low capacity for thyroid hormones.
2. Transthyretin (TTR), also known as prealbumin: This protein accounts for around 10-20% of T4 and T3 binding. It has a lower affinity but higher capacity for thyroid hormones compared to TBG.
3. Albumin: This is the most abundant protein in the blood and binds approximately 15-20% of T4 and a smaller fraction of T3. Although albumin has a low affinity for thyroid hormones, its high concentration allows it to contribute significantly to their transport.

The binding of thyroid hormones to these proteins helps maintain stable levels in the blood and ensures a steady supply to tissues. Additionally, TBPs protect thyroid hormones from degradation and rapid clearance by the kidneys, thereby extending their half-life in the circulation.

Serum albumin is the most abundant protein in human blood plasma, synthesized by the liver. It plays a crucial role in maintaining the oncotic pressure or colloid osmotic pressure of blood, which helps to regulate the fluid balance between the intravascular and extravascular spaces.

Serum albumin has a molecular weight of around 66 kDa and is composed of a single polypeptide chain. It contains several binding sites for various endogenous and exogenous substances, such as bilirubin, fatty acids, hormones, and drugs, facilitating their transport throughout the body. Additionally, albumin possesses antioxidant properties, protecting against oxidative damage.

Albumin levels in the blood are often used as a clinical indicator of liver function, nutritional status, and overall health. Low serum albumin levels may suggest liver disease, malnutrition, inflammation, or kidney dysfunction.

Types include: Familial dysalbuminemic hyperthyroxinemia Familial euthyroid hyperthyroxinemia Thyroid hormone resistance ... Hyperthyroxinemia is a thyroid disease where the serum levels of thyroxine are higher than expected. Thyroxine or ... syndrome "four/000051350" at Dorland's Medical Dictionary "four/000051350" at Dorland's Medical Dictionary "Hyperthyroxinemia ...
... is a type of hyperthyroxinemia associated with mutations in the human serum albumin ... March 1982). "Familial dysalbuminemic hyperthyroxinemia: a syndrome that can be confused with thyrotoxicosis". New England ... May 2003). "Structural basis of albumin-thyroxine interactions and familial dysalbuminemic hyperthyroxinemia". Proceedings of ...
Spratt, DI; Pont, A; Miller, MB; McDougall, IR; Bayer, MF; McLaughlin, WT (July 1982). "Hyperthyroxinemia in patients with ...
Invalid if other proteins or immunoglobulins compete with TBG, including familial dysalbuminemic hyperthyroxinemia Feingold, K ...
... hyperthyroxinemia, familial dysalbuminemic MeSH C19.874.410.500 - thyroid hormone resistance syndrome MeSH C19.874.482.281 - ...
... most accurately termed hyperthyroxinemia) can occur for a number of other reasons: Inflammation of the thyroid is called ...
Types include: Familial dysalbuminemic hyperthyroxinemia Familial euthyroid hyperthyroxinemia Thyroid hormone resistance ... Hyperthyroxinemia is a thyroid disease where the serum levels of thyroxine are higher than expected. Thyroxine or ... syndrome "four/000051350" at Dorlands Medical Dictionary "four/000051350" at Dorlands Medical Dictionary "Hyperthyroxinemia ...
Euthyroid hyperthyroxinemia is defined as a condition in which the serum total thyroxine (T4) and triiodothyronine (T3) ... encoded search term (Euthyroid Hyperthyroxinemia) and Euthyroid Hyperthyroxinemia What to Read Next on Medscape ... Euthyroid Hyperthyroxinemia Medication. Updated: Feb 01, 2018 * Author: Justyna Bart, MD, PhD; Chief Editor: George T Griffing ... Euthyroid hyperthyroxinemia due to familial excess of thyroxine-binding globulin. South Med J. 1989 Mar. 82(3):368-71. [QxMD ...
Transthyretin mutations in hyperthyroxinemia and amyloid diseases M J Saraiva. Hum Mutat. 2001 Jun. ... Thyroxine-binding proteins--familial euthyroid hyperthyroxinemia due to point mutations of transthyretin]. Hishinuma A, ... Among these are mutations responsible for hyperthyroxinemia, presenting high affinity for thyroxine (a TTR ligand). Compound ...
Hyperthyroxinemia (n = 86). −4.8 (−9.1 to −0.5) a −4.5 (−8.8 to −0.1) a −4.7 (−9.1 to −0.4) a −0.5 (−3.9 to 3.0). −0.2 (−3.6 to ... Hyperthyroxinemia (n = 35). −1.3 (−3.9 to 1.4). −1.3 (−3.9 to 1.4). −1.3 (−4.0 to 1.3). 1.2 (−2.9 to 5.2). 1.2 (−2.8 to 5.2). ... Hyperthyroxinemia (n = 33). −0.9 (−3.8 to 2.0). −0.5 (−3.5 to 2.4). −0.6 (−3.5 to 2.4). −1.1 (−5.5 to 3.3). −0.7 (−5.1 to 3.7) ... Hyperthyroxinemia (n = 68). −1.1 (−3.1 to 0.8). −1.0 (−3.0 to 0.9). −1.1 (−3.0 to 0.9). −0.2 (−3.2 to 2.7). 0.0 (−3.0, 3.0). ...
Factitious hyperthyroidism is higher-than-normal thyroid hormone levels in the blood and symptoms that suggest hyperthyroidism. It occurs from taking too much thyroid hormone medicine.
neonatal hyperthyroxinemia. *neurodevelopmental abnormalities independent of thyroid function, including speech delay and ...
Reversible hyperthyrotropinemia, hyperthyroxinemia and hyperprolactinemia due to adrenal insufficiency. Am J Med 1985;79:271- ...
Immunologic and biochemical factors in hyperemesis gravidarum with or without hyperthyroxinemia. Gynecol Obstet Invest. 1999. ...
Hyperthyroxinemia in trophoblastic disease].. Cano C; MacGregor C; Zárate A; Ruiz JE; Salazar LM. Rev Invest Clin; 1983; 35(3): ...
Euthyroid familial hyperthyroxinemia due to abnormal thyroid hormone-binding protein. Am J Med 73:283-289. 6287840. . Crossref ...
Stryker TD, Molitch ME: Reversible hyperthyrotropinemia, hyperthyroxinemia, and hyperprolactinemia due to adrenal insufficiency ...
Reference ranges for total thyroxine (TT4) are as follows: In newborns up to age 14 days: 11.8-22.
Abnormalities of serum TH binding proteins leading to euthyroid hyperthyroxinemia or hypotriiodothyronemia. --Genetic ...
Structural Basis of Albumin-Thyroxine Interactions and Familial Dysalbuminemic Hyperthyroxinemia. Petitpas, I., Petersen, C.E ...
Induction of hyperthyroxinemia in BALB/C but not in several other strains of mice. Wagle NM, Dallas JS, Seetharamaiah GS, Fan ...
Familial euthyroid hyperthyroxinemia is caused by benign variants in TTR, including p.Gly26Ser, p.Ala129Thr, p.Ala129Val, and p ... Transthyretin mutations in hyperthyroxinemia and amyloid diseases. Hum Mutat. 2001;17:493-503. [PubMed: 11385707] ...
Hyperthyroxinemia 1 0 Note: The number of publications displayed in this table will differ from the number displayed in the ...
... neonatal hyperthyroxinemia, neurodevelopmental abnormalities independent of thyroid function, including speech delay and ...
Hyperthyroxinemia - Preferred Concept UI. M0010872. Scope note. Abnormally elevated THYROXINE level in the BLOOD. ...
Hyperthyroxinemia [C19.874.410] * Hyperthyroxinemia, Familial Dysalbuminemic [C19.874.410.249] * Thyroid Hormone Resistance ... Hyperthyroxinemia Preferred Concept UI. M0010872. Scope Note. Abnormally elevated THYROXINE level in the BLOOD.. Terms. ... Hyperthyroxinemia Preferred Term Term UI T020957. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1987). ... Hyperthyroxinemia. Tree Number(s). C19.874.410. Unique ID. D006981. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/D006981 ...
Hyperthyroxinemia [C19.874.410] * Hyperthyroxinemia, Familial Dysalbuminemic [C19.874.410.249] * Thyroid Hormone Resistance ... Hyperthyroxinemia Preferred Concept UI. M0010872. Scope Note. Abnormally elevated THYROXINE level in the BLOOD.. Terms. ... Hyperthyroxinemia Preferred Term Term UI T020957. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1987). ... Hyperthyroxinemia. Tree Number(s). C19.874.410. Unique ID. D006981. RDF Unique Identifier. http://id.nlm.nih.gov/mesh/D006981 ...
Dysprealbuminemic euthyroidal hyperthyroxinemia (disorder). Code System Preferred Concept Name. Dysprealbuminemic euthyroidal ...
... hyperthyroxinemia,noun,E0400406,thyroxinemia,noun,E0572195,yes hyper,hypertonic,adj,E0032835,tonic,adj,E0061326,yes hyper, ...
C3009 Endocrine System Disorder C118467 Pediatric Endocrine Terminology C131850 Hyperthyroxinemia Hyperthyroxinemia Supranormal ... C131813 Familial Dysalbuminemic Hyperthyroidism Familial Dysalbuminemic Hyperthyroxinemia Familial Dysalbuminemic ...
neonatal hyperthyroxinemia. * neurodevelopmental abnormalities independent of thyroid function, including speech delay and ...
Euthyroid hyperthyroxinemia ditandai peningkatan kadar thyroxine total (T4) dan triiodothyronine total (T3), namun thyroid ... Penyebab lainnya adalah genetik (familial dysalbuminemic hyperthyroxinemia), hepatitis, 5-fluorouracil (5-FU), perphenazine, ...
Reference ranges for total thyroxine (TT4) are as follows: In newborns up to age 14 days: 11.8-22.
Reference ranges for total thyroxine (TT4) are as follows: In newborns up to age 14 days: 11.8-22.
  • An identical missense mutation in the albumin gene results in familial dysalbuminemic hyperthyroxinemia in 8 unrelated families. (uchicago.edu)
  • Clinical characteristics of familial dysalbuminemic hyperthyroxinemia in Chinese patients and comparison of free thyroxine in three immunoassay methods. (cdc.gov)
  • Euthyroid hyperthyroxinemia is defined as a condition in which the serum total thyroxine (T4) and triiodothyronine (T3) concentrations are increased, but the thyroid-stimulating hormone (TSH) concentration is normal and there are no clinical signs or symptoms of thyroid dysfunction. (medscape.com)
  • In the past, euthyroid hyperthyroxinemia was a diagnostic challenge and many patients were inappropriately treated for thyroid disease. (medscape.com)
  • In these circumstances, euthyroid hyperthyroxinemia frequently remains undetected with no harm to the patients. (medscape.com)
  • [ 1 ] This should always alert the physician to search for one of the causes of euthyroid hyperthyroxinemia. (medscape.com)
  • [ 9 ] Euthyroid hyperthyroxinemia has been described in association with substitution of alanine in codon 109 with valine or threonine. (medscape.com)
  • Lithium-induced euthyroid hyperthyroxinemia, described as an elevation in serum thyroid hormone levels without clinical manifestations of thyrotoxicosis, 7 has not been reported to our knowledge. (psychiatrist.com)
  • Stratakis and Chrousos 8 described a case of transient euthyroid hyperthyroxinemia associated with discontinuation of chronic lithium treatment. (psychiatrist.com)
  • We report a patient who developed transient euthyroid hyperthyroxinemia within a few weeks of initiation of lithium therapy. (psychiatrist.com)
  • To our knowledge, this is the first reported case of lithium-induced transient euthyroid hyperthyroxinemia. (psychiatrist.com)
  • Although the role of lithium in thyroid hormone synthesis and release has been extensively investigated and reviewed, 9 how it may induce euthyroid hyperthyroxinemia is unclear. (psychiatrist.com)
  • Dttrh Is also known as hyperthyroxinemia, dysprealbuminemic, euthryroidal hyperthyroxinemia 2, dystransthyretinemic euthyroidal hyperthyroxinemia. (mendelian.co)
  • Hyperthyroxinemia is a thyroid disease where the serum levels of thyroxine are higher than expected. (wikipedia.org)
  • The various causes of hyperthyroxinemia in patients who are euthyroid are listed in Etiology . (medscape.com)
  • The specific features of thyrotoxicosis and euthyroid hyperthyroxinemia developed due to the use of cordarone]. (medscape.com)
  • Lithium-induced transient euthyroid hyperthyroxinemia: a case report. (medscape.com)
  • A point mutation in transthyretin increases affinity for thyroxine and produces euthyroid hyperthyroxinemia. (medscape.com)
  • Thyroxine-binding proteins--familial euthyroid hyperthyroxinemia due to point mutations of transthyretin]. (medscape.com)
  • Tucker WS Jr. Euthyroid hyperthyroxinemia due to familial excess of thyroxine-binding globulin. (medscape.com)
  • Hyperprealbuminemia, euthyroid hyperthyroxinemia, Zollinger-Ellison-like syndrome and hypercorticism in a pancreatic endocrine tumour. (medscape.com)
  • Maternal thyroid function was classified into 7 categories: euthyroid, overt/subclinical hyperthyroidism, overt/subclinical hypothyroidism, hyperthyroxinemia, and hypothyroxinemia. (medscape.com)
  • Abnormalities of serum TH binding proteins leading to euthyroid hyperthyroxinemia or hypotriiodothyronemia. (nih.gov)
  • A new family with hyperthyroxinemia caused by transthyretin Val109 misdiagnosed as thyrotoxicosis and resistance to thyroid hormone--a clinical research center study. (medscape.com)
  • The potential effects of maternal thyroid dysfunction (subclinical hypothyroidism and hyperthyroidism, and hyperthyroxinemia/hypothyroxinemia) in pregnancy on offspring neuropsychological development remain inconclusive. (medscape.com)
  • Hyperthyroxinemia is a thyroid disease where the serum levels of thyroxine are higher than expected. (wikipedia.org)
  • Kvetny J, Poulsen H. Transient hyperthyroxinemia in newborns from women with autoimmune thyroid disease and raised levels of thyroid peroxidase antibodies. (medscape.com)
  • Mattman A, DeMarco ML, Wong S , Holmes DT, Lee J. Grave clinicopathologic correlation: a case of hyperthyroxinemia. (ubc.ca)