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PubMed1990

Differentiating various abnormalities of thyroxin binding to serum proteins by radioelectrophoresis of thyroxin and immunoassay of binding proteins.

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.

Autoantibodies↗
PubMed1988

Amiodarone alters thyroxine transfer and distribution in humans.

Previous studies indicate that increased serum total and free T4 levels may be secondary to a proportionally greater decrease in serum T4 clearance rates than in production rates after short-term amiodarone administration, to increased T4 production rates as well as reduced serum clearance rates in selective hyperthyroxinemia without overt hyperthyroidism following chronic amiodarone administration, and to a relatively greater increase in T4 production rates than in clearance rates in classical hyperthyroidism. To further evaluate amiodarone-induced alterations of T4 metabolism, serum T4 transfer and distribution were evaluated by compartmental analysis of T4 kinetic studies from eight normal subjects receiving short-term amiodarone or an equivalent amount of iodide, five patients with selective hyperthyroxinemia induced by chronic amiodarone therapy (n = 4) or ioxithalamic acid (n = 1), and five with classical hyperthyroidism. The model consisted of rapidly and slowly equilibrating pools exchanging with serum, with all losses occurring from the tissue pools. Short-term amiodarone administration reduced the fractional T4 transfer rates between serum and the rapidly equilibrating pool to 82% of baseline. In selective hyperthyroxinemia the fractional rates of T4 transfer between serum and both extravascular pools were increased sixfold, whereas minimal alterations were present in the hyperthyroid group. The serum equivalent volume of T4 distribution in the slow pool was significantly reduced following short-term amiodarone, whereas serum and rapid pool volumes were reduced in selective hyperthyroxinemia and slow pool volume was increased in hyperthyroidism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Amiodarone-induced hyperthyroidism: assessment of the predictive value of biochemical testing and response to combined therapy using propylthiouracil and potassium perchlorate.

In order to assess the value of thyroid function testing during amiodarone therapy, we reviewed all available tests in 128 patients treated with this drug. Nine patients (7.0%) developed biochemical hyperthyroidism with elevation of both free thyroxine index (FT4I) and free triiodothyronine index (FT3I) and marked suppression of serum thyroid stimulating hormone (TSH) after 1-46 months of therapy; six of these nine patients had clear clinical evidence of thyroid overactivity. Where serial tests were available before development of hyperthyroidism, this complication developed suddenly, despite previously stable normal indices of thyroid function, and could not be predicted by currently-available biochemical tests such as T4, T3, sensitive TSH, thyroglobulin or sex hormone binding globulin (SHBG) assays. Clinical features such as unexplained weight loss, proximal myopathy, exacerbation of arrhythmia, or heat intolerance appear to be the key to prompt diagnosis of this complication. Hyperthyroxinemia without T3 excess was found in 32.8% of patients without progression to true hyperthyroidism. Serum TSH remained detectable by sensitive assay in 17 out of 18 patients with amiodarone-induced euthyroid hyperthyroxinemia and was significantly higher than in patients with equivalent hyperthyroxinemia due to thyroxine therapy. Serial levels of SHBG were higher in patients with true hyperthyroidism than in those with euthyroid hyperthyroxinemia. The effect of combined treatment with propylthiouracil (800 mg/day) and potassium perchlorate (800 mg/day) was evaluated in five of the six clinically hyperthyroid patients. Biochemical euthyroidism was achieved after 7-19 weeks, a response slower than previously reported, indicating that this drug combination does not result uniformly in prompt resolution of amiodarone-induced hyperthyroidism.

Adolescent↗
PubMed1996

Transient elevation of serum thyroid hormone levels following lithium discontinuation.

UNLABELLED: Lithium therapy has been associated with altered thyroid function and even goiter in as many as half of chronically treated patients. We describe the case of a 16-year-old boy who developed transient hyperthyroxinemia after discontinuation of chronic lithium therapy. The lack of clinical hyperthyroidism and the gradual resolution of the biochemical abnormalities in this patient pointed to the benign character of his condition known as "euthyroid hyperthyroxinemia". CONCLUSION: Euthyroid hyperthyroxinemia may be a benign, transient complication of lithium-therapy discontinuation and should be considered in the diagnostic evaluation of lithium-related thyroid abnormalities.

Adolescent↗
PubMed1997

Abnormal thyroid function tests in infants with congenital hypothyroidism: the influence of soy-based formula.

OBJECTIVE: To assess the etiology of hyperthyroxinemia or hyperthyrotropinemia in infants with congenital hypothyroidism who are on replacement therapy with L-thyroxine. METHODS: These infants were treated with recommended doses of L-thyroxine following the diagnosis of congenital hypothyroidism. Because of hyperthyroxinemia (2 patients) and hyperthyrotropinemia (1 patient), medication compliance and dietary practice (formula type, age of introduction, and discontinuation or change of the formula) were assessed. Clinical evaluation was also performed. RESULTS: Elevated thyroxine level in 2 infants was associated with discontinuation of soy formula 4 weeks previously; reduction of L-thyroxine dose normalized serum levels in both of these infants. In the third infant, who received soy formula from 1 week of age, TSH remained elevated despite incremental L-thyroxine doses of 19 micrograms/kg/day; discontinuation of soy formula was followed by normalization of the TSH in 3 weeks and helped attain a subsequent decrement of L-thyroxine dose to 8.6 micrograms/kg/day. Neither the hyperthyroxinemia nor hyperthyrotropinemia in these infants was associated with any adverse behavioral-developmental consequence. CONCLUSION: When initiating soy-formula feeding in infants with congenital hypothyroidism, the L-thyroxine dose should be increased because of significant reduction in intestinal absorption: conversely, when soy feeding is discontinued, the L-thyroxine dose should be decreased.

Congenital Hypothyroidism↗
PubMed1995

Long-term effects of thyroid hormone on lymphocyte subsets in spleens and thymuses of mice.

We examined the effects of the long-term administration to mice of thyroid hormone or propylthiouracil (PTU) on lymphocyte subsets in spleens, and thymuses to clarify whether hyperthyroxinemia itself causes the changes in lymphocyte subsets, such as the marked increase in CD5+ B cells and decrease in natural killer (NK) cells, observed in hyperthyroid Graves' disease. Both the number and proportion of splenic NK (Thy-1+ asialo GM1+) cells were increased in hyperthyroxinemic mice treated with thyroxine (T4) for both short and long terms (8 and 32 weeks, respectively), those of splenic and thymic T (CD5+ sIgM-) cells and CD5-B cells were increased only in hypothyroxinemic mice treated with PTU for 32 weeks, compared with those in euthyroid mice. These data indicate that 1) long-term hyperthyroxinemia increases splenic and thymic T cells and splenic NK cells, but not CD5+ B cells, in mice, 2) long-term hypothyroxinemia induced by PTU treatment increases splenic B cells and CD5- B cells, and 3) hyperthyroxinemia itself does not cause the changes in CD5+ B cells and NK cells, which are observed in hyperthyroid Graves' disease, in mice.

Animals↗
PubMed2003

Follow-up of newborns with elevated screening T4 concentrations.

OBJECTIVE: To determine the type and incidence of hyperthyroxinemic disorders detected by follow-up of infants with elevated screening total T4 (TT4) values. STUDY DESIGN: Infants born in Oregon with a screening TT4 measurement >3 SD above the mean were offered enrollment. Serum TT4, free T4, total T3, free T3, and thyroid-stimulating hormone concentrations were measured in study infants and their mothers. RESULTS: Over a 20-month period, 101 infants (51 boys) and their mothers enrolled in the study (of 241 eligible infants), from a total screening population of 80,884; 17 infants were identified with persistent hyperthyroxinemia (TT4 >16 microg/dL). Ten had thyroxine-binding globulin excess (1:8088), 5 had evidence for increased T4 binding but not thyroxine-binding globulin excess (1:16,177), and 2 had findings compatible with thyroid hormone resistance (1:40,442); the other 84 infants had transient hyperthyroxinemia. Sequence analysis revealed a point mutation in the thyroid hormone receptor-beta gene in one infant with thyroid hormone resistance; no mutation was identified in the other infant. CONCLUSIONS: Although neonatal Graves' disease occurs in approximately 1 in 25,000 newborn infants, we did not detect any case among 80,884 infants, most likely because their mothers were receiving antithyroid drugs. Although the other hyperthyroxinemic disorders in the aggregate occur frequently (1:4758) and may benefit from detection, in general they do not require treatment.

Female↗
PubMed2000

Thyroid function and psychiatric morbidity in patients with manic disorder receiving lithium therapy.

Euthyroid hyperthyroxinemia as a result of a transient increase in thyroid-stimulating hormone (TSH) levels may contribute to the development of manic disorder. Lithium has a potent short-term antithyroidal effect that may account for its antimanic action. The thyroid function and psychiatric morbidity of 46 adult patients with manic disorder were assessed prospectively before and 1 and 6 months after lithium treatment. At baseline, the free thyroxine level (FT4, 16.23 +/- 3.11 pmol/L) was at the high end of the normal range, whereas the free triiodothyronine (FT3, 4.24 +/- 0.65 pmol/L) and TSH (1.47 +/- 0.73 mIU/L) levels were within the normal range. All patients were clinically euthyroid, but five of them (11%) had elevated FT4 levels. Baseline FT3 and FT4 levels were positively correlated with past psychiatric morbidity. The FT4 level at baseline and after 1 month of treatment was positively correlated with scores on the Brief Psychiatric Rating Scale (p < 0.02) and negatively correlated with scores on the Global Assessment Scale (p < 0.005). During the first month of treatment, the reduction of FT3 and FT4 levels was significantly correlated with a decrease in psychiatric symptoms. By 6 months, the FT3 level was no longer significantly different from that at the baseline, but FT4 levels remained significantly lower. The TSH level increased progressively from baseline to 6 months. Multilevel models showed that FT4 and serum lithium levels were positively and negatively associated with psychiatric symptoms, respectively. The findings of the study lend support to the notion that euthyroid hyperthyroxinemia contributes to acute mania and suggest that lithium's short-term antimanic action may be mediated by its antithyroid effect.

Adult↗
PubMed1987

Suppression of peripheral blood natural killer cell activity by excess thyroid hormone.

Natural killer (NK) cells were assessed in patients with hyperthyroxinemia due to Graves' disease or treatment with thyroxine (T4). Cytolytic activity was measured with 51Cr-labeled K562 tumor cells and NK enumeration was by flow cytometry using NKH-1 monoclonal antibody to identify the relevant surface marker. Activity was uniformly decreased in association with hyperthyroxinemia, regardless of the underlying pathology; however, there was no reduction in the number of NKH-1+ cells. NK activity was enhanced by addition of interleukin 2 (IL-2) in both control and patients' cells although the value in the latter instance failed to reach the basal control level. Production of IL-2 by lymphocytes from hyperthyroxinemic subjects, in response to phytohemagglutinin, was also reduced. Since NK cells are thought to act as a defense against viral infections and some malignancies and may play a role in autoregulation of the immune system, this effect of T4 may have significant biological implications.

Cell Line↗
PubMed1991

[Evaluating thyroid gland function in patients with protein anomalies].

The euthyroid hyperthyroxinemia (EHT) is characterized on the one hand by a normal basal THS or TRH-TSH response but also by high plasma values of total thyroxine (TT4) on the other. However if only TT4 is assessed, "hyperthyroidism" may be diagnosed erroneously. EHT may be caused by an increase of specific thyroxine binding proteins which may be hereditary (permanent) or acquired (transient). The most frequent disturbance is due to an estrogen induced increase of thyroxine binding globulin (TBG) in the course of pregnancy, anticonceptive drugs or estrogen treatment. The albumin associated HT (FDH syndrome), first reported in 1979, has autosomal dominant traits. 144 patients with FDH syndrome were observed during the period between 1984 and 1990, i.e. 7% (1986) of all hyperthyroid patients explored. Family screening is required to prevent unjustified treatment. Additionally existing disturbances of thyroid function as well as other protein binding anomalies may both cause problems in differential diagnosis. Prealbumin associated hyperthyroxinemia (PAAH), first published in 1982, may be due to an inherited increase in affinity, but may also be the consequence of a true elevation of prealbumin plasma concentration in the course of an islet cell cancer; both conditions are extremely rare. Nearly as rare are patients with plasma autoantibodies directed against T4 and/or T3 (5 cases); yet, a reverse T3 autoantibody could be observed in merely 1 case. By means of our modified radio-thyroxine-agarosegel-iceelectrophoresis all such protein anomalies may be diagnosed and differentiated in 1 procedure. Moreover, all other types of EHT must be taken into consideration by differential diagnosis.

Blood Protein Disorders↗
PubMed1988

Direct determination of free thyroxin in undiluted serum by equilibrium dialysis/radioimmunoassay.

We have designed a re-usable dialysis cell and a complex dialysis buffer, with which undiluted serum samples can be dialyzed with minimal changes in their serum matrix. Dialysate thyroxin (free T4) is then measured by a sensitive RIA for T4. The range of reportability was 2-128 ng/L, the normal range was 8-27 ng/L, and the interassay CV was 7%. Free T4 concentrations in various disorders were as follows: hyperthyroidism, 32-478 ng/L; in both excess thyroxin-binding globulin (TBG) and familial dysalbuminemic hyperthyroxinemia, 9-27 ng/L; primary hypothyroidism, less than 2-7 ng/L; central hypothyroidism, 4-6 ng/L; severe TBG deficiency, 9-25 ng/L; hypothyroxinemias of nonthyroidal illness, 8-35 ng/L. With this free-T4 assay, which is adaptable to clinical laboratory use, one can differentiate hyperthyroidism from the major euthyroid hyperthyroxinemias and hypothyroidism from the major euthyroid hypothyroxinemias.

Adult↗
PubMedDate not supplied

Excessive thyroid hormone replacement therapy.

BACKGROUND: Excessive thyroid hormone replacement carries the potential for serious long-term metabolic complications (e.g., accelerated osteoporosis). The increased bioavailability of commercially available products, along with improved laboratory assays for measuring thyrotropin (TSH), has led to an increased chance of actual or detected iatrogenic hyperthyroxinemia. The purpose of this study was to determine the frequency of excessive prescribing and to examine the impact of changes in potency of replacement thyroid hormone formulations and sensitivity of thyroid function tests on its incidence. METHODS: A retrospective chart review was done of patients requiring thyroid hormone replacement therapy treated at a university-based, family medicine residency training program. The following information was extracted from each chart: specific thyroid medication (including dose and date of onset of therapy) and thyroid laboratory tests results (including serum thyroxine [T4] and TSH). This information from two different time periods (1975 to 1981 and 1982 to 1989) was compared using one-way analysis of variance. RESULTS: Serum T4 levels were not significantly different between the two time periods, 1975 to 1981 and 1982 to 1989 (8.06 +/- 2.93 micrograms/dl versus 9.0 +/- 03.69 micrograms/dl; NS), despite significant changes in TS serum levels (23.6 +/- 38.9 mIU/mL versus 7.44 +/- 18.7 mIU/ml; P = 0.009) and levothyroxine dosage (184 +/- 59.6 micrograms/d versus 145 +/- 64.1 micrograms/d; P = 0.002). Significantly more patients had low (supersuppressed) TSH levels between 1982 and 1990 than between 1975 and 1981 (33 percent versus 10 percent; P = 0.02.) CONCLUSIONS: Excessive thyroid hormone replacement with iatrogenic hyperthyroxinemia is a common occurrence. Clinicians need to be aware of this problem and implement measures (e.g., periodic monitoring of TSH) to minimize the occurrence of overdosing and the potential for long-term complications.

Adult↗