hyperthyroxinemia/ألبيومين

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Hyperthyroxinemia associated with high thyroxine binding to albumin in euthyroid subjects.

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Hyperthyroxinemia, and a high free-T4 index (calculated from T4 levels and T3 Resin uptake), was observed in an euthyroid boy. Thyroxine-binding globulin and prealbumin levels were normal. Direct assay of free-T4 yielded a normal value. Upon electrophoretic separation of a serum sample enriched with

A point mutation in the albumin gene in a Chinese patient with familial dysalbuminemic hyperthyroxinemia.

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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

A Chinese Family with Familial Dysalbuminemic Hyperthyroxinemia (FDH) due to R242H Mutation on Human Albumin Gene: Reevaluating the Role of FDH in Patients with Asymptomatic Hyperthyroxinemia.

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Familial dysalbuminemic hyperthyroxinemia (FDH) has now become an established cause for spurious asymptomatic hyperthyroxinemia. Several different codon mutations on albumin gene had been identified. We here provided an established but rarely reported heterozygous mutation based on

A novel missense mutation in codon 218 of the albumin gene in a distinct phenotype of familial dysalbuminemic hyperthyroxinemia in a Japanese kindred.

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Familial dysalbuminemic hyperthyroxinemia (FDH) is the most common cause of inherited euthyroid hyperthyroxinemia in Caucasians. To our knowledge, no such documentation on Asians exists. Six of 8 members of a 3-generation Japanese family were found by us to carry the FDH phenotype. Serum total T4

Familial dysalbuminemic hyperthyroxinemia in a Swiss family caused by a mutant albumin (R218P) shows an apparent discrepancy between serum concentration and affinity for thyroxine.

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Familial dysalbuminemic hyperthyroxinemia (FDH), is the most common cause of inherited increase in serum total T4 (TT4) in the Caucasian population. It is caused by a mutation (R218H) in the human serum albumin (HSA) gene, resulting in 10-fold higher affinity for T4 and, in heterozygous affected

Diagnosis of familial dysalbuminemic hyperthyroxinemia and investigation of the nature of the variant albumin.

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A variant albumin with abnormally increased thyroxine-binding affinities has been identified, and termed as familial dysalbuminemic hyperthyroxinemia (FDH). The aims of this study are to seek for a method of diagnosis to distinguish FDH from other causes of hyperthyroxinemia and to investigate the

A novel albumin gene mutation (R222I) in familial dysalbuminemic hyperthyroxinemia.

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BACKGROUND Familial dysalbuminemic hyperthyroxinemia, characterized by abnormal circulating albumin with increased T4 affinity, causes artefactual elevation of free T4 concentrations in euthyroid individuals. OBJECTIVE Four unrelated index cases with discordant thyroid function tests in different

Identification of a human serum albumin species associated with familial dysalbuminemic hyperthyroxinemia.

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Familial dysalbuminemic hyperthyroxinemia (FDH) is a form of euthyroid hyperthyroxinemia that is due to an increased affinity of serum albumin for T4. Unlike the many physiologically neutral alloalbumins that have been identified by serum electrophoresis, FDH variants have not been reproducibly

Thyroxin binding by human serum albumin after denaturation of the thyroxin-binding globulin in familial dysalbuminemic hyperthyroxinemia.

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Abnormal binding of thyroxin (T4) to serum albumin of subjects with familial dysalbuminemic hyperthyroxinemia (FDH) is generally demonstrated by the T4-loaded charcoal uptake test, with T4 added in excess (0.1 mmol/L) to accentuate T4 binding to albumin in FDH. I describe a binding study involving

Detection of albumin binding abnormalities in sera of patients with familial dysalbuminaemic hyperthyroxinaemia using isoelectric focusing.

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Definitive diagnosis of familial dysalbuminaemic hyperthyroxinaemia (FDH) requires finding a high concentration of [125I]T4 bound to albumin. We used isoelectric focusing (IEF) in agarose gels to study the sera of three members of a family with FDH and compared the distribution of [125I]T4 obtained

A novel mutation in the Albumin gene (R218S) causing familial dysalbuminemic hyperthyroxinemia in a family of Bangladeshi extraction.

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BACKGROUND Familial dysalbuminemic hyperthyroxinemia (FDH) is a common cause of euthyroid hyperthyroxinemia. Clinical recognition of FDH is crucial for preventing unnecessary therapy in clinically euthyroid patients with abnormal thyroid function tests. Our goal was to identify the cause of abnormal

Can the type of variant albumin in familial dysalbuminemic hyperthyroxinemia be determined by measuring iodothyronines in serum?

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A recent report documented the existence of three putative types of variant albumin in dysalbuminemic hyperthyroxinemia (DH) and suggested that measurement of the total concentration of three iodothyronines (T4, T3 and rT3) in serum of affected subjects could aid in their differentiation. In the

Familial Dysalbuminemic Hyperthyroxinemia in a Japanese Man Caused by a Point Albumin Gene Mutation (R218P).

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الدخول التسجيل فى الموقع

Familial dysalbuminemic hyperthyroxinemia (FDH) is a familial autosomal dominant disease caused by mutation in the albumin gene that produces a condition of euthyroid hyperthyroxinemia. In patients with FDH, serum-free thyroxine (FT4) and free triiodothyronine (FT3) concentrations as measured by

An identical missense mutation in the albumin gene results in familial dysalbuminemic hyperthyroxinemia in 8 unrelated families.

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Familial dysalbuminemic hyperthyroxinemia (FDH) is the most common form of inherited increase of serum thyroxine in Caucasians. It is the result of increased thyroxine-binding to serum proteins and is inherited as a dominant trait. The entire coding region of the albumin gene of a subject with FDH

Fluorescence investigations of albumin from patients with familial dysalbuminemic hyperthyroxinemia.

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Familial dysalbuminemic hyperthyroxinemia (FDH) is an autosomal dominant syndrome in which clinically euthyroid patients have elevated total thyroxine levels. These high serum thyroxine levels are traceable to altered binding of thyroxine to the patient's albumin. Albumin from FDH patients and

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