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At least 19 recordsLinked to original sources
PubMed1986

Specific methods to identify plasma binding abnormalities in euthyroid hyperthyroxinemia.

Methods to identify the plasma T4-binding abnormalities that can cause euthyroid hyperthyroxinemia were evaluated in patients with excess T4-binding globulin, familial dysalbuminemic hyperthyroxinemia, prealbumin-associated hyperthyroxinemia, and autoantibody binding of T4. Familial dysalbuminemic hyperthyroxinemic serum showed a unique persistence of abnormal [125I]T4 binding when diluted 1:100 in phosphate buffer with added 1000-fold excess of unlabeled T4 (10(-6) M T4). Immunoprecipitation of [125I]T4 by antibody to prealbumin, precipitation of [125I]T4 by polyethylene glycol 6000 19%, and in vitro resin uptake of T3 were specific for prealbumin-associated hyperthyroxinemia, autoantibody binding of T4, and T4-binding globulin excess, respectively. These simple methods facilitate investigation of patients with euthyroid hyperthyroxinemia and will identify individuals and families at risk of misdiagnosis by standard methods. Use of these techniques rules out the known binding abnormalities in hyperthyroxinemic patients and may make the diagnosis of generalized hormone resistance more specific.

Humans↗
PubMed1985

The diagnostic challenge of euthyroid hyperthyroxinemia.

In euthyroid hyperthyroxinemia high levels of thyroxine (T4) may be either transient or persistent, associated with high, normal, or low levels of tri-iodothyronine (T3). Euthyroid hyperthyroxinemia may occur: as a response to abnormal plasma binding (thyroxine binding globulin, albumin, prealbumin, or autoantibodies), because of hormone resistance, after exposure to drugs such as amiodarone, cholecystographic contrast agents, or propranolol, during acute psychiatric illness or stress, and in hyperemesis gravidarum. In some instances the cause of persistent hyperthyroxinemia still remains obscure. No single investigation (including free hormone measurement and the response of thyrotropin to its releasing hormone) can distinguish all of these entities from true hyperthyroidism. Hence, re-evaluation in cases of diagnostic uncertainty should begin with clinical reassessment. Techniques are now available to identify easily some causes of euthyroid hyperthyroxinemia, allowing us to recognise patients and relatives who are at risk of inappropriate treatment. Because measurement of serum T4 remains the key investigation for diagnosis of thyroid dysfunction, it is important to appreciate the full range of conditions that compromise its specificity.

Amiodarone↗
PubMed1990

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

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 nature of this abnormal albumin. Percent T4 bound to albumin was high in FDH, ranging 29-48% (normal range 3-8%), as measured in [125I] T4 loaded serum using a single immunoprecipitation by anti-human albumin antibody. A subject with T4 autoantibody in serum had a lower value. Only a single subject with TBG deficiency had an overlapped value (33%) with that of FDH, but the level of serum T4 could differentiate TBG deficiency from FDH. Isoelectric focusing (IEF) showed a distint albumin band with an isoelectric point of pH 5.05 in all FDH subjects, and this band was not compatible with any of 4 albumin bands seen in normals. These data suggest that only two simple measurements including the level of serum T4 and the single immunoprecipitation for [125I] T4-bound albumin can distinguish FDH from other causes of hyperthyroxinemia.

Adult↗
PubMed1985

Euthyroid hyperthyroxinemia and thyroxine-binding prealbumin excess in islet cell carcinoma.

This manuscript describes euthyroid hyperthyroxinemia secondary to elevated serum T4-binding prealbumin (TBPA) concentrations in a patient with islet cell carcinoma and reports serum TBPA measurements in other patients with islet cell carcinoma. A 73-yr-old man with a 17-yr history of metastatic islet cell carcinoma was found to have hyperthyroxinemia. His total serum T4 concentration was 18.5 micrograms/dl (normal, 5.5-11.5). Eight years previously, his serum T4 concentration was normal. His free T4 concentration, as determined by equilibrium dialysis, was 1.3 ng/dl (normal, 0.9-2.1). Serum T3, TSH, and T4-binding globulin (TBG) concentrations were normal, as was the TSH response to TRH administration. Polyacrylamide gel electrophoresis of the patient's serum in the presence of tracer amounts of [125I]T4 revealed that, compared to normal sera, [125I]T4 binding to TBPA was increased from 30.0 +/- 6.0% (mean +/- SD) to 52.0%. The distribution of [125I]T3 amont albumin, TBG, and TBPA was normal in this electrophoretic procedure. The concentration of TBPA in the patient's serum was 189 mg/dl. In contrast, the mean serum TBPA concentration in normal men was 40 +/- 4 (mean +/- SD) mg/dl, and that in normal women was 18 +/- 4 mg/dl. Sera from the patient's daughter, his brother, 2 sisters, and 2 male paternal cousins contained normal amounts of TBPA, ranging from 34-47 mg/dl in his male relatives and from 26-30 mg/dl in his female relatives. Serum free T4 index determinations in his relatives also were normal. Serum TBPA concentrations were determined in 14 additional patients with islet cell carcinoma. In 1 of these patients, a man with an insulinoma, serum TBPA was elevated (66 mg/dl). This patient's serum T4 level was 7.3 micrograms/dl, and his free T4 index was 7.0. These data and another study suggest that islet cell carcinoma may rarely produce a TBPA-like protein resulting in an elevated serum TBPA concentration. Markedly elevated serum TBPA is associated with euthyroid hyperthyroxinemia.

Adenoma, Islet Cell↗
PubMed1986

[Hyperthyroxinemia without hyperthyroidism].

The various causes of persisting hyperthyroxinemia without hyperthyroidism are discussed after short case histories of an infant with hyperthyroxinemia due to TBG excess, discovered by newborn screening for congenital hypothyroidism and a girl with peripheral resistance to thyroid hormones disclosed by investigation of a small goiter. The differentiation of these various causes by thyroid function-tests is indicated. Though the anomalies leading to euthyroid hyperthyroxinemia are usually harmless their timely recognition, also in other members of the family, will prevent erroneous diagnosis and treatment of hyperthyroidism.

Child↗
PubMed1991

Heterogeneity of serum prolactin in patients with menstrual disorder in conjunction with hyperthyroxinemia.

Since the secretion of PRL is regulated by the hypothalamic-pituitary axis, an increase in large molecular size PRL in the serum is most likely due to secretion by the pituitary itself. The present study was performed to investigate the possible occurrence of PRL heterogeneity in 128 subjects with menstrual disorder in conjunction with hyperthyroxinemia (88 with untreated Graves' disease, 40 with subacute thyroiditis) and 50 age- and sex-matched healthy controls. All 128 patients in this study were suffering from amenorrhea or oligomenorrhea at the time of their initial visit. PRL heterogeneity was found in the sera of 5 of 88 (5.7%) patients with untreated Graves' disease, in 2 of 40 (5.0%) patients with subacute thyroiditis, but in none of the normal controls. PRL heterogeneity remained essentially unchanged in patients with Graves' disease over 6 months of treatment; however, in patients with subacute thyroiditis, either big-big PRL or big PRL decreased significantly along with a corresponding increase in little PRL associated with recovery from the illness within 6 months. The menstrual disorders in all patients were restored to normal after restoration to a euthyroid state. The underlying cause of the occurrence of PRL heterogeneity in patients with menstrual disorder in conjunction with hyperthyroxinemia is not known.

Adolescent↗
PubMed1987

Familial dysalbuminemic hyperthyroxinemia associated with primary thyroid disease.

This study describes a family with intrinsic thyroid disease in addition to familial dysalbuminemic hyperthyroxinemia, a syndrome associated with euthyroidism and increased binding of thyroxine to serum albumin. The simultaneous occurrence of thyroid disease and elevated serum thyroxine concentrations due to familial dysalbuminemic hyperthyroxinemia may confound the diagnosis of the two concurrent disorders and the subsequent therapy of the thyroid disease.

Adult↗
PubMed1989

Euthyroid hyperthyroxinemia due to familial excess of thyroxine-binding globulin.

The correct diagnosis of benign hyperthyroxinemia in this patient and his family members will spare them the unnecessary testing and treatment for thyrotoxicosis that has befallen some such patients. Results of the usual blood tests for assessment of thyroid function, such as T4, T3, and thyrotropin determinations, were not uniformly diagnostic, and were potentially misleading. An increased T4 level, a nonsuppressed TSH level, normal levels of FT4 and FT4D, and a low level of T3RU were clues that led to a request for specific measurement of serum TBG levels in multiple family members; family testing was essential for the diagnosis of euthyroid hyperthyroxinemia due to familial hepatic overproduction of TBG.

Adult↗
PubMed1987

Familial dysalbuminemic hyperthyroxinemia.

A family with familial dysalbuminemic hyperthyroxinemia is described. The syndrome is inherited as an autosomal dominant trait and is characterized by marked elevation of serum thyroxine, due to increased binding of thyroxine to albumin, whereas serum triiodothyronine is normal. Serum free thyroxine is normal when measured with ultrafiltration or equilibrium dialysis, but artefactually high when measured with an analogue assay. The importance of the condition, which is harmless, lies in the misinterpretation of values with subsequent erroneous treatment of thyrotoxicosis. By using an ultrasensitive TSH method it is possible to discriminate between euthyroid and hyperthyroid patients and thereby to avoid incorrect diagnosis in subjects with euthyroid hyperthyroxinemia.

Adolescent↗
PubMed1991

Hyperthyroxinemia in major affective disorders.

Ninety-nine patients fulfilling DSM-III criteria for primary major affective disorder, either bipolar or unipolar, were studied. A 12% prevalence of elevated thyroxine levels was found. Three of the 12 hyperthyroxinemia patients also had elevated free thyroxine index. No statistically significant difference in response to antidepressant treatment was observed between the hyperthyroxinemia group and the normal serum thyroxine group.

Adult↗
PubMed1987

Hyperthyroxinemia due to the coexistence of two raised affinity thyroxine-binding proteins (albumin and prealbumin) in one family.

The T4-binding proteins of a euthyroid subject with persistent hyperthyroxinemia (T4, greater than 20 micrograms/dl) were present in normal concentrations. Abnormal transport of both T4 and rT3 was demonstrated by reverse flow paper electrophoresis; excess T4 was bound to albumin and prealbumin, while increased binding of rT3 was confined to prealbumin. The three T4-binding proteins in the serum of the subject were isolated by affinity chromatography and characterized. Equilibrium dialysis experiments demonstrated a 20-fold increase in affinity of the albumin for T4 (Ka, 5.1 X 10(6) M-1) and a 4-fold increase in affinity of prealbumin for T4 (Ka, 3.0 X 10(8) M-1); T4-binding globulin affinity was normal. Nine other members of the family were also studied. Two sisters of the propositus have both the abnormal albumin and the variant prealbumin, while a brother has normal T4-binding proteins. The mother has the abnormal albumin alone. The father, his sister, and one of his three brothers have the variant prealbumin only. Despite the presence of the variant prealbumin in some of the paternal relatives of the propositus, their total iodothyronine concentrations were within the normal ranges; the condition may, therefore, often go undetected. The characteristics of the albumin found in the affected members of this kindred are those we have defined for familial dysalbuminemic hyperthyroxinemia type I, which is inherited as an autosomal dominant trait. The pattern of inheritance of the variant prealbumin is also consistent with a dominant mode with strong penetrance. The presence of two separately inherited abnormal T4 transport proteins in the same family suggests that both conditions may be more common than has been thought.

Adolescent↗
PubMed1990

Transient prealbumin-associated hyperthyroxinemia in TSH-producing pituitary adenoma.

This case report describes a 38-year-old male who was hospitalized for further clarification of clinically mild hyperthyroidism. His increased total hormone levels, the elevated free thyroid hormones and the elevated basal TSH with blunted response to TRH strongly suggested a pituitary adenoma with inappropriate TSH incretion. Transmission computed tomography showed an intrasellar expansion, 16 mm in diameter. The neoplastic TSH production was confirmed by an elevated alpha-subunit and a raised molar alpha-sub/TSH ratio. However, T4 distribution on prealbumin (PA, TTR), albumin (A) and thyroxine binding globulin (TBG) showed a clearly increased binding to PA (39%), indicating additional prealbumin-associated hyperthyroxinemia. The absolute values of PA, A and TBG were within the normal range. After removal of the TSH-producing adenoma, basal TSH, the free thyroid hormones and T4 binding to prealbumin returned to normal. Therefore, the prealbumin-associated hyperthyroxinemia had to be interpreted as a transitory phenomenon related to secondary hyperthyroidism (T4 shift from thyroxine binding globulin to prealbumin) rather than a genetically conditioned anomaly of protein binding.

Adenoma↗
PubMed1989

Hyperthyroxinemia in patients receiving thyroid replacement therapy.

Eleven patients, with a history of hypothyroidism, who had hyperthyroxinemia and an elevated free thyroxine index but normal serum triiodothyronine concentrations on levothyroxine replacement underwent levothyroxine dose reduction at three-month intervals until the free thyroxine index fell into the normal range. All were clinically euthyroid throughout. Normalization of the thyrotropin response to thyrotropin-releasing hormone occurred concomitantly, indicating correction of subtle hyperthyroidism. The mean thyroxine dose decreased from 161 micrograms/d (2.06 micrograms/kg) to 120 micrograms/d (1.51 micrograms/kg). The resting heart rate fell in eight of 11 patients (P less than .02). The left ventricular ejection fraction decreased in eight of 11 patients, although the decrease was not statistically significant. Considering the sensitivity of pituitary, cardiac, and bone tissue to even a small excess of thyroxine over time, hyperthyroxinemia associated with an elevated free thyroxine index should be corrected even in patients taking levothyroxine replacement who are clinically euthyroid and whose serum triiodothyronine concentrations are within normal limits.

Adult↗
PubMed1988

Detection of protein binding abnormalities in euthyroid hyperthyroxinemia.

This is a procedure for rapidly identifying the three common abnormalities in binding of thyroxin by protein. After incubation with [125I]thyroxin, serum proteins are separated by electrophoresis on agarose gel and binding of thyroxin to the various protein fractions is determined after autoradiography. Quantitatively abnormal binding to albumin or prealbumin and thyroxin autoantibodies is easily demonstrated by this technique. Normally, less than 6% is bound to albumin, and no binding by prealbumin is detected. In dysalbuminemic hyperthyroxinemia, about 30% of the serum thyroxin is bound to albumin; in prealbumin-associated hyperthyroxinemia, 7% is bound to prealbumin. With this procedure these protein-binding abnormalities can be simply identified, and it may be useful when results of a thyroxin assay are not consistent with results of a sensitive thyrotropin assay or the patient's clinical examination.

Autoantibodies↗
PubMed1987

Thyrotropin hyperresponsiveness to TRH despite hyperthyroxinemia in amiodarone-treated subjects.

Pituitary responsiveness to TRH was assessed prospectively over 24 weeks, in 15 patients receiving 300 mg amiodarone a day. All developed significant hyperthyroxinemia (both total and free), and marked elevations in reverse T3 compared to pretreatment levels. Although basal TSH levels were unchanged in all of them, TSH increased by greater than 50% when compared to pretreatment responses, in eight patients, while they remained unchanged (+/- 15%) in the remaining seven. All eight with exaggerated responses also showed significant reductions (P less than .001) in plasma levels of total and free T3, whereas in the seven who did not show any increase in TSH responses, T3 levels were unchanged. The increase in TSH response to TRH was strongly correlated (r = -.82, P less than .001) with T3 levels. Total and free T4 levels were equally elevated in both groups. These observations indicate that amiodarone effectively blocks the suppressive effect of hyperthyroxinemia on TSH secretion, and that T3 is the mediator of thyroid feedback control in amiodarone treated patients.

Amiodarone↗
PubMed1985

Familial euthyroid hyperthyroxinemia secondary to pituitary and peripheral resistance to thyroid hormones.

Among 18 family members, representing four generations studied, a familial form of euthyroid hyperthyroxinemia was found in 6. The increased serum total thyroxine value in all hyperthyroxinemic subjects could not be explained by abnormalities in binding proteins. Five of the six patients had a goiter, and all had increased concentrations of triiodothyronine and free thyroxine without symptoms or signs of hyperthyroidism. Basal serum levels of thyroid-stimulating hormone (thyrotropin) were normal in all six; in the four who were tested, these levels responded normally to thyrotropin-releasing hormone (TRH). The normal suppression of basal and TRH-stimulated thyrotropin increase after administration of triiodothyronine did not occur. These patients seem to have resistance of peripheral and pituitary tissues to the actions of thyroid hormones. Family studies revealed that the disorder appeared as a new sporadic mutation and was consistent with an autosomal-dominant mode of inheritance. This disorder, an important example of euthyroid hyperthyroxinemia, should not be confused with Graves' disease.

Adolescent↗
PubMed1985

Euthyroid hyperthyroxinemia and rapid cycling affective disorder: case report.

A 32-year-old woman with rapid cycling bipolar illness had numerous clinical problems throughout 19 affective episodes and six hospital admissions within 34 months. Persistent hyperthyroxinemia, always associated with manic episodes, led to a diagnostic work-up that ruled out a primary thyroid dysfunction and pointed to oral contraceptives, appetite suppressants, and psychiatric illness as likely causes of elevated T4 values. The contention that an underlying thyroid hypofunction is the basis of rapid cycling is questioned. The extent to which a bipolar disorder increases T4 levels and the role of euthyroid hyperthyroxinemia in the pathogenesis of rapid cycling are discussed.

Adult↗