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PubMed1995

Familial dysalbuminemic hyperthyroxinemia in pregnancy.

A 16-year-old pregnant Puerto Rican woman who had been treated for thyrotoxicosis previously was evaluated for goiter, increased total thyroxine (T4) and triiodothyronine (T3) and free T4 estimate, despite a normal thyroid-stimulating hormone (TSH) concentration. These findings are consistent with a TSH-producing pituitary adenoma or the syndrome of generalized thyroid hormone resistance. However, sera from the patient, her mother and subsequently her newborn daughter demonstrated the increased albumin binding of T4 but not T3 that is characteristic of familial dysalbuminemic hyperthyroxinemia (FDH). The free T4 estimate had been elevated artefactually by the increased affinity of FDH albumin for the analog in a one-step assay. The T3 and T4 concentrations were increased by pregnancy and T4 was increased further by FDH. This first report of FDH recognized during pregnancy emphasizes that the effects of pregnancy on thyroid hormone and TSH concentrations complicate the diagnosis of FDH. It is particularly important to distinguish this benign condition from thyrotoxicosis during pregnancy, because inappropriate treatment may affect fetal development.

Adolescent↗
PubMed1994

Induction of hyperthyroxinemia in BALB/C but not in several other strains of mice.

We recently expressed the extracellular domain of the human TSHR (ETSHR) protein using a baculovirus expression system and purified it to homogeneity. The ETSHR specifically binds both TSH and antibodies to TSHR. In the present study, C57BL/6J, SJL/J, BALB/cJ and B10BR.SgSnJ mice were immunized with the recombinant ETSHR or an equivalent amount of control antigen. All strains of mice produced high titers of antibody against the TSHR protein which were capable of blocking the binding of TSH to native TSHR. However, only BALB/cJ mice showed significantly elevated levels of thyroxine in their sera compared to the control mice. Similarly, BALB/cJ mice primed with ETSHR and then challenged with thyroid membranes showed significantly elevated levels of thyroxine. In addition, histopathological examination of thyroid glands from affected mice showed morphological changes characterized by hydropic and subnuclear vacuolar changes and focal scalloping, with no apparent inflammation or glandular destruction. Moreover, mice with elevated thyroxine levels showed increased in vivo thyroidal uptake of 131Iodine. Together, these data suggest that BALB/cJ mice are susceptible to the induction of hyperthyroxinemia.

Animals↗
PubMed1999

Structural investigations of a new familial dysalbuminemic hyperthyroxinemia genotype.

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.

Amino Acid Substitution↗
PubMed1999

[Hyperthyroxinemia and clinical euthyroidism. Report of one case].

The association of hyperthyroxinemia and euthyroidism is frequent and characterized by high plasma thyroxin concentrations, normal TSH values and absence of clinical signs of hyperthyroidism. We report an asymptomatic 28 years old male presenting with a serum total plasma thyroxin of 18.5 micrograms/dl (N 6.1-12.5), a free thyroxin of 2.9 ng/dl (N 0.8-1.4), a TSH of 3.4 microIU/ml (N 0.5-5), and a triiodothyronine of 128 ng/dl (N 80-180). Laboratory assessment did not find high thyroxin binding globulin, albumin or prealbumin concentrations or antithyroxin antibodies. The thyroxin binding capacity of albumin was elevated to 58.2 micrograms/dl (N 11.5-34.1). TSH responded normally to TRH stimulus and was suppressed with exogenous triiodothyronine, which caused an hyperthyroid syndrome. We concluded that this patient had a familial dysalbuminemia.

Adult↗
PubMed1991

Prevalence of familial dysalbuminemic hyperthyroxinemia in serum samples received for thyroid testing.

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.

Female↗
PubMed1990

Elevated thyroxine and free thyroxine in euthyroid patients: familial dysalbuminemic hyperthyroxinemia.

An eleven year old male was evaluated because of persistent elevation of thyroxine levels and elevated thyroxine index calculated as "T7" but normal thyrotropin levels. The findings were demonstrated by thyroxine binding protein electrophoresis to be due to aberrant thyroxine binding to albumin. The abnormality was also documented in the patient's father. This entity, known as familial dysalbuminemic hyperthyroxinemia, is being reported with increasing frequency and should be suspected when elevated total thyroxine and free thyroxine or "T7" levels are associated with a normal thyrotropin level. The case reported is somewhat unusual in that the triiodothyronine affinity of the aberrant protein appears to be more pronounced than usually reported with this syndrome and the corresponding total triiodothyronine level was significantly elevated.

Child↗
PubMed1989

[Familial hyperthyroxinemia with dysalbuminemia: screening of 21,000 patients at the occasion of thyroid evaluation].

Serum samples from 21,342 patients undergoing evaluation of thyroid status were screened for familial dysalbuminemic hyperthyroxinemia (FDH) using a specific test based on the measure of charcoal uptake of 125I thyroxine (T4) from serum diluted 1:100 with addition of unlabelled 10(-6) M T4. We found 17 cases of FDH: a higher incidence (8:10,000) than previously reported in the general population (1:10,000). The results of thyroid function tests of patients with FDH are presented: total T4 concentration is increased in only 14 subjects; thyrotropin and free T4 measured by an immunoextraction method are the most useful assays to evaluate the clinical status of these patients.

Humans↗
PubMed1987

Euthyroid hyperthyroxinemia and inappropriate secretion of thyrotropin. Recognition and diagnosis.

Various disease states associated with euthyroid hyperthyroxinemia and inappropriate thyrotropin secretion are becoming increasingly recognized. These diagnoses were established in six (11%) of 57 patients referred for evaluation of elevated free thyroxine index over an 11-month period. Failure to separate these entities from primary thyrotoxicosis may result in unnecessary thyroid ablative therapy and subsequent clinical confusion. Several illustrative patient summaries are presented to outline an approach to this clinical challenge.

Adolescent↗
PubMed1988

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

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 T4 tracer in which thyroxin-binding globulin is denatured in samples by treatment with mild acid at pH less than 3.0. The tracer is bound to the serum albumin and, to a greater extent, to the FDH albumin, because the binding by thyroxin-binding prealbumin is blocked by barbital buffer. The result of the [125I]T4 binding to the albumin is expressed as a T4 binding index, based on results for pooled sera from patients with normal thyroid function as a reference. The mean index in FDH was 4.08 (SD 0.92, n = 5); in hypoalbuminemia, 0.66 (SD 0.18, n = 8); in normal subjects, 1.00 (SD 0.11, n = 20). This albumin-binding index enables the rapid and unequivocal diagnosis of subjects with FDH, without the addition of unlabeled T4.

Charcoal↗
PubMed1994

Elevated thyroxine levels in a euthyroid patient. A search for the cause of euthyroid hyperthyroxinemia.

A clinically euthyroid man with a family history of hyperthyroidism presented for evaluation of an elevated thyroxine (T4) level and an increased free T4 index with a normal thyrotropin (TSH) level. Results of thyroid hormone-binding protein tests confirmed the diagnosis of familial dysalbuminemic hyperthyroxinemia. This disorder should be considered in patients who have a normal serum TSH level, despite an elevated total T4 concentration. Accurate diagnosis is essential to avoid inappropriate treatment. Affected family members also should be identified. No treatment is required, because patients remain euthyroid and maintain a normal free T4 level.

Humans↗
PubMed1984

Familial dysalbuminemic hyperthyroxinemia (FDH): inadequacy of the "analog" methods for assaying free-T4 levels.

Free-T4 levels were determined in familial dysalbuminemic hyperthyroxinemia (FDH) subjects. In agreement with their euthyroid status free-T4 levels were within the normal range when tested by equilibrium dialysis and by the FT4 Immophase method (Corning Medical). However, when using the recently introduced "analog" methods, either Amerlex FT4 or Becton-Dickinson FT4, Free-T4 values were markedly higher than the control values. This discrepancy is probably due to artifactual binding of the labeled analog to the fraction of albumin exhibiting an excessive affinity for T4.

Humans↗
PubMedDate not supplied

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

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 labeled T4 abnormal binding of T4 was detected in the albumin fraction. This binding was sensitive to barbital, and affected T3 to a lesser degree than T4. The excessive binding of T4 to albumin accounts for the normal free-T4 levels in the presence of increased total T4 concentration. Two additional cases of abnormal binding of T4 to albumin were detected in the family of the propositus. The correct evaluation of the thyroid status of these subjects should be important to prevent a misdiagnosis of hyperthyroidism.

Adult↗
PubMed1982

Euthyroid familial hyperthyroxinemia due to abnormal thyroid hormone-binding protein.

A family is described in which three members had an elevated total serum thyroxine level and free thyroxine index. Each affected subject was clinically euthyroid and had a normal pulse wave arrival time (QKd), serum triiodothyronine and free thyroxine levels, and a normal serum thyroxine-binding globulin (TBG) concentration. Electrophoresis of their serum with 125I-labeled thyroxine revealed increased thyroxine binding in the albumin region. In addition, this abnormal protein, like thyroxine-binding globulin, bound 125I-labeled triiodothyronine and 125I-labeled reverse triiodothyronine. However, electrophoresis of serum treated by sialidase (neuraminidase) digestion suggested that this abnormal protein is not an anomalous form of thyroxine-binding globulin "buried" in the albumin area. These cases of euthyroid familial hyperthyroxinemia due to an abnormal thyroid hormone-binding protein show that an elevated serum thyroxine level or free thyroxine index is not always sufficient to confirm the presence of thyrotoxicosis.

Child↗
PubMed1982

Hyperthyroxinemia in patients treated with high-dose propranolol.

Six patients with hyperthyroxinemia (five men and one woman) were evaluated for possible hyperthyroidism. All were taking large daily doses of propranolol--480 +/- 155 (+/- SE) mg--for treatment of angina pectoris. The patients had no clinical evidence of hyperthyroidism, although three had small goiters. Further evaluation of the patients revealed elevated serum free thyroxine levels and/or free thyroxine index, low-normal serum triiodothyronine levels, and elevated serum reverse triiodothyronine levels in all six. The thyroid-stimulating hormone response to thyrotropin-releasing hormone was normal in two patients, subnormal in three patients, and absent in one patient. One patient was restudied while receiving low-dose propranolol (80 mg a day), with normalization of all thyroid functional parameters. The data suggest that the abnormalities seen in patients taking high doses of propranolol were due to drug-induced blockade of iodothyronine deiodination. Signs and symptoms of hyperthyroidism are lacking in patients taking large doses of propranolol. If such a patient is discovered to have an elevated serum thyroxine level, a more complete evaluation of thyroid function is necessary before the diagnosis of thyrotoxicosis can be made. The thyrotropin-releasing hormone test may be of particular value in this circumstance.

Aged↗
PubMed1985

Reversible hyperthyrotropinemia, hyperthyroxinemia, and hyperprolactinemia due to adrenal insufficiency.

This 55-year-old woman presented with primary adrenal insufficiency that led to multiple endocrine gland dysfunctions. Despite symptoms suggestive of hypothyroidism, she had mildly elevated serum thyroid hormone levels associated with elevated thyrotropin levels, hyperprolactinemia, and mild hypercalcemia. These abnormalities corrected with corticosteroid replacement but could be reproduced, in part, when the corticosteroids were temporarily withdrawn. The findings in this patient suggest that physiologic concentrations of glucocorticoids modulate prolactin secretion and the pituitary-thyroid axis. Adrenal insufficiency should be considered in the differential diagnosis of hyperprolactinemia and hyperthyrotropinemia with or without associated hyperthyroxinemia.

Adrenal Insufficiency↗
PubMed1986

Modulation of thyroid parameters by exogenous thyroxine in familial dysalbuminemic hyperthyroxinemia.

A patient with familial dysalbuminemic hyperthyroxinemia (FDH) was given graded doses of exogenous thyroxine (0.2 mg/d for 2 weeks; 0.4 mg/d for 2 weeks; 0.6 mg/d for 2 weeks) to study modulation of various thyroid parameters. The plasma concentration of the serum transport proteins, thyroxine binding globulin (TBG), sex hormone binding globulin (SHBG), and cortisol binding globulin (CBG) as well as serum thyroxine (T4), triiodothyronine (T3), absolute free thyroxine (FT4), and serum protein binding of T4 tracer were measured. At the end of T4 treatment, T4 and T3 were increased by 151% and 78%, respectively. The FT4 increased (157%), while the percent dialyzable free T4 fraction (DFT4) showed no significant change. SHBG, a protein sensitive to thyroid hormone (TH) action, increased 148% (from 0.23 to 0.57 micrograms/dL) after treatment but this concentration was still in the normal range; TBG and CBG decreased by about 16%. Analysis of the electrophoretic 125I-T4 distribution pattern in serum during T4 treatment showed essentially no change in TBG-bound T4 (percent tracer carriage X total T4), while there was a progressive increase in albumin-bound T4 (341% increase over pretreatment value) and a lesser increase in prealbumin (TBPA)-bound T4 (187%). These observations describing alterations in TH action, serum T4-protein binding, and the failure of percent DFT4 to increase with elevation in serum total T4 are of clinical significance in evaluating thyroid function parameters in FDH patients undergoing TH treatment.

Adult↗
PubMed1993

Effect of short-term hyperthyroxinemia on vitamin D metabolism in congenital hypothyroidism.

The circulating concentrations of vitamin D metabolites were measured in nine children (four to ten years of age) with congenital hypothyroidism on L-thyroxine therapy, before and after a short term increase (33%) in dosage. The concentrations of 25-hydroxyvitamin D and 24,25-dihydroxyvitamin D were not altered, but the concentration of 1,25 dihydroxyvitamin D was significantly higher in the serum of the children after three weeks of hyperthyroxinemia. This was associated with an increase in urinary calcium excretion. The increases in serum concentration of 1,25 dihydroxyvitamin D cannot be explained by differences in serum levels of calcium, phosphorus or parathyroid hormone. These findings differ from data obtained in adults.

25-Hydroxyvitamin D 2↗