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PubMed1986

Neonatal hyperthyroidism in mice has different effects on epidermal growth factor levels in submandibular gland, urine, and blood.

We examined long-term effects of neonatal hyperthyroidism in female mice by measuring the epidermal growth factor levels in the submandibular gland, urine, and serum at the age of 31 days. Hyperthyroxinemia was induced by thyroxine injections (0.4 microgram/g/day) on days 0-6. Littermate controls received the alkaline saline vehicle. The treatment accelerated incisor eruption and eyelid opening. It also retarded growth. The elevation of plasma thyroxine concentration which normally occurs during wk 2 to reach a peak around day 15 was abolished. Submandibular gland epidermal growth factor levels on day 31 were markedly subnormal, indicating maturational delay. In contrast, epidermal growth factor levels were unaffected in urine and supranormal in serum. These differences in response suggest that the regulatory mechanisms governing epidermal growth factor levels in tissues and fluids may acquire thyroid hormone dependence at different stages.

Animals↗
PubMed1984

Red blood cell thyroxine in nonthyroid illness and in heparin-treated patients.

Red blood cell T4 concentrations (RBC T4) were measured in 15 normal subjects, 13 patients with hypo- or hyperthyroidism, and 10 patients with elevated or decreased serum thyroid hormone binding. In each case, RBC T4 was compared with the serum concentration of free T4 measured by equilibrium dialysis ( FT4D ). RBC T4 correlated significantly with FT4D in these subjects (r = 0.90; P less than 0.001). The normal range for RBC T4 was 0.27-0.83 ng/ml. RBC T4 was below the normal range in all 8 patients with hypothyroidism and above the normal range in all 5 patients with hyperthyroidism. It was within the normal range in all 4 subjects with absent or low T4-binding globulin (TBG) and in 5 of the 6 subjects with elevated TBG or familial dysalbuminemic hyperthyroxinemia. The sixth subject (increased TBG) had elevated RBC T4 and FT4D . RBC T4 was similarly measured in 10 patients with severe nonthyroid illness (NTI), 5 of whom had decreased serum concentrations of total T4. RBC T4 was normal in 8 of these patients, elevated in 1, and decreased in 1; in comparison, FT4D was normal in 4, elevated in 5, and decreased in 1. Eight patients receiving continuous iv infusions of heparin were also studied because of previously described similarities in the in vitro thyroid tests of heparin-treated and euthyroid sick patients. FT4D was elevated in 7 of the heparin-treated patients, whereas RBC T4 was elevated in only 2. Furthermore, for any given value of FT4D , RBC T4 was lower in heparin-treated patients than in normal subjects, indicating the presence of an inhibitor of cellular T4 binding in these patients. This putative inhibitor, demonstrated by an elevated FT4D to RBC T4 ratio, was present in 6 of the 8 heparin-treated patients and in 5 of the 10 patients with NTI. The findings of this study support the hypothesis that an inhibitor of cellular T4 binding is present in the serum of some patients with NTI and in most heparin-treated individuals.

Erythrocytes↗
PubMed1984

Comparison of plasma and urinary methods for the direct measurement of the thyroxine to 3,5,3' - triiodothyronine conversion rate in man.

A further development of a new method recently proposed for the direct measurement of the conversion ratio (CR) of T4 to T3 in man is presented. [125I]T4 and [131I]T3 are injected simultaneously, and Sephadex chromatography is performed on urine samples to determine [125I]T3 formed in vivo, while plasma samples are used to measure the injected tracers. CR is calculated with the assumption that urinary [125I]T3 closely reflects [125I]T3 appearing in plasma after the injection of precursor [125I]T4. Four normal subjects and six patients with various thyroid disorders were studied using this method. The experimental data were also analyzed by our previous method based on plasma sampling only and by two recently described methods based on urinary measurements. These comparisons were made in an attempt to ascertain whether there is any systematic difference between the conversion values derived from plasma data and those derived from urinary data. Using plasma data alone, the CR was 28.6 +/- 3.4% (mean +/- SEM) in a group of four normal subjects, 37%, in two untreated hypothyroid patients, 40.2% in one hypothyroid subject receiving T4 treatment, 30.9% in one hyperthyroid patient, 24.9% in one patient with selective hyperthyroxinemia due to amiodarone treatment, and 10.7% in one normal subject after iopanoic acid administration. These values were in excellent agreement with those obtained by the modified procedure described here, in which both urinary and plasma measurements are used. Of the methods using urinary data alone, however, one gave similar results, while the other systematically overestimated the CR, possibly due to delayed excretion of labeled T4 metabolites into the urine. We conclude that 1) the analytical procedure to separate the labeled tracers and metabolites in urine or plasma is critical for the accurate estimation of CR; 2) when an adequate separation procedure is available, plasma and urinary methods for measuring CR yield comparable results; and 3) the plasma method should be used when, in addition to CR, other kinetic (distribution and turnover) parameters of T4 and T3 metabolism are to be estimated.

Adult↗
PubMed1990

Does a hidden pool of reverse triiodothyronine (rT3) production contribute to total thyroxine (T4) disposal in high T4 states in man.

A hidden pool of rT3 production represents a source of rT3 that is minimally reflected in circulating rT3 levels. To test for the existence of such a source of rT3 production in man, varying doses of the generalized deiodinase inhibitor iopanoic acid (IA) were administered to four hyperthyroxinemic subjects. The doses employed included low-IA (0.5-g load, then 0.5 g/day for 5 days), mid-IA (1.0-g load, then 1.0 g/day for 5 days), and high-IA (3.0-g load, then 3.0 g/day for 5 days). Each patient received 25 microCi [125I]rT3, iv, in the high T4 state and on day 3 of each IA dosing regimen. Serial blood and urine samples were obtained to determine serum rT3 clearance rates and the urinary thyronine metabolite patterns. Although total serum rT3 values were increased by all IA dosages (P less than 0.001), rT3 was lower with high-IA administration (P less than 0.02) than with low- or mid-IA regimens. Low-IA decreased rT3 clearance to 33 +/- 2 L/day (P less than 0.005), while increasing the daily rT3 production to 76 +/- 8 nmol/day (P less than 0.04) compared to the control values (150 +/- 10 L/day and 53 +/- 8 nmol/day, respectively). Mid-IA also reduced rT3 clearance (23 +/- 4 L/day; P less than 0.005) without changing rT3 production (50 +/- 10 nmol/day), while high-IA reduced both rT3 clearance (21 +/- 2 L/day; P less than 0.005) and production (39 +/- 9 nmol/day; P less than 0.04). Intravenously administered tracer rT3 could not be detected in the urine in the high T4 state, but rT3 could not be detected in the urine in the high T4 state, but was prominent after IA administration. It is concluded that a hidden pool of rT3 production exists in vivo in man. Further, low dose IA serves as a selective inhibitor of liver and kidney deiodinase systems, allowing reflection of this hidden rT3 pool in the blood and urine. It would appear that hypertrophy of this hidden pool of rT3 production occurs in high T4 states and may account for the majority of the unrecognized deiodinative metabolites of T4 generated in hyperthyroxinemia.

Adult↗
PubMed2006

Analysis of the factors associated with Tc-99m pertechnetate uptake in thyrotoxicosis and graves' disease.

To determine the factors associated with 20 minute Tc-99m pertechnetate thyroid uptake, we examined all patients in whom thyrotoxicosis was diagnosed at Chiba-Hokusoh Hospital, Nippon Medical School from 2001 April through 2003 March. Patients with thyrotoxicosis diagnosed during this period were 57 with Graves' disease (76%), 11 with transient hyperthyroxinemia (TH)(14.7%), and 7 with subacute thyroiditis (SAT)(9.3%). The uptake of Tc-99m ranged from 0.97% to 40.1% in Graves' disease and from 0.15% to 0.8% in TH. Although TH may include spontaneous resolution of Graves' disease as well as painless thyroiditis, no treatment was necessary for these patients. Uptake in all patients with SAT was less than 0.5%. There were significant correlations between the level of Tc-99m uptake and the levels of free triiodothyronine (fT3), free thyroxine (fT4), thyroid-stimulating hormone (TSH)-binding inhibitory immunoglobulin (TBII), and thyroid stimulating antibody (TSAb) in patients with Graves' disease. Older patients with Graves' disease showed lower uptake than did younger patients. Both Tc-99m pertechnetate uptake and TBII levels, but not fT3, fT4 or TSAb levels, at the beginning of antithyroid drug treatment correlated significantly with the duration of treatment until the daily dose of methimazole reached 5 mg. These data suggest that Tc-99m pertechnetate uptake reflects the severity of Graves' disease and its response to the medical treatment and that antithyroid drug therapy is not necessary when the uptake is less than 0.9%.

Aged↗
PubMed1997

Increased urinary thyroxine sulfate excretion in thyroxine therapy.

Although increased thyroxine sulfate (T4S) levels have recently been detected in fetal serum and amniotic fluid, changes in patients in a high thyroxine (T4) state remain unclarified. This study was conducted to determine the changes in T4S in thyroid hormone regulation in women receiving suppressive T4 therapy. With a highly sensitive and specific radioimmunoassay, we measured the serum and urinary concentrations of T4S in 16 premenopausal women with benign nodular goiter before and after three months administration of T4 (3.2 micrograms/kg/day). Serum levels of other thyroid hormones were also measured. Significant increases in mean serum T4 levels post-treatment (11.1 vs. 6.6 micrograms/dL pre-treatment; P < 0.01) were found, although only low T4S levels were detectable in serum both pre- and post-T4 treatment. The mean urinary or creatinine corrected urinary T4S values post-treatment were significantly increased (20 ng/dL or 396 ng/g creatinine vs. 12 ng/dL or 174 ng/g creatinine pre-treatment, P < 0.01). There was a significant correlation between increased creatinine-corrected urine T4S and increased serum free T4. Our results indicate that the sulfation of T4 may be related to the regulation of thyroid hormone metabolism in T4-treated subjects with relative hyperthyroxinemia.

Adult↗
PubMed1981

Clinical study on increased serum thyroxine-binding globulin in cancerous state.

Serum thyroxine-binding globulin (TBG) in 169 patients with various cancers was determined by radioimmunoassay (RIA). Eleven patients showed a high serum TBG level (greater than 35 micrograms/ml). Two of them had been treated with estrogen for prostate cancer. One patient had high serum TBG with serum hepatitis. Another 8 cases had normal liver function and also normal levels serum estrogen. Thus, about 4.7% (8/169) of the cancer patients had high serum TBG and mild hyperthyroxinemia caused by unknown mechanisms. The high TBG level in these patients continued until just before death, or in some cases decreased to normal after removal of cancer tumors by operation. Cancer is occasionally associated with an increase in serum TBG. Although the mechanism is not clear, the increased TBG in the cancerous state in interesting and has significance as a tumor marker.

Adult↗
PubMed1989

Isolated ACTH deficiency associated with transient thyrotoxicosis and hyperprolactinemia.

A 43-year-old woman with isolated ACTH deficiency in association with transient thyrotoxicosis is reported. The initial evaluation revealed that plasma ACTH and cortisol did not respond to corticotropin-releasing hormone (CRH) in the presence of hyperthyroxinemia and hyperprolactinemia. During the replacement therapy with dexamethasone, she developed transient hypothyroxinemia with persistent hyperprolactinemia. Although thyroid open biopsy did not show any evidence of autoimmune thyroiditis or subacute thyroiditis, the data appear to provide other evidence of a possible relationship between acute adrenal insufficiency and transient thyroid dysfunction.

Adrenocorticotropic Hormone↗
PubMed1989

Thyroid function in hyperemesis gravidarum.

Plasma total T4 (TT4), T3 (TT3), free T4 (FT4), free T3 (FT3), thyroxine binding globulin, hCG, and erythrocyte zinc content were measured in 43 women with uncomplicated pregnancy and in 71 patients admitted with hyperemesis gravidarum. Plasma concentration of thyroid hormones in hyperemesis subjects showed wide variability and 32% of subjects had high TT4 (higher than mean +2 SD of normal pregnant subjects), 33% had high FT4, 20% had high TT3, and 20% had high FT3. Red cell zinc content, a tissue marker of thyroid status, in the hyperthyroxinemic subjects was not different from that of normothyroxinemic hyperemesis subjects or of subjects with uncomplicated pregnancy. The elevated TT4 concentration decreased spontaneously in all but two of the hyperemesis subjects to normal pregnant levels. The plasma FT4 concentration at presentation correlated with plasma hCG in hyperemesis gravidarum (partial correlation coefficient r = 0.411, P less than 0.01), but not in normal pregnancy (partial correlation coefficient r = 0.043) after allowing for the effect of gestational age. We conclude that approximately one third of hyperemesis subjects show transient hyperthyroxinemia and suggest that hCG or a molecular variant of hCG may stimulate the thyroid gland.

Adult↗
PubMed1992

Galanin does not affect the growth hormone-releasing hormone-stimulated growth hormone secretion in patients with hyperthyroidism.

Patients with hyperthyroidism have reduced spontaneous and stimulated growth hormone (GH) secretion. The aim of our study was to evaluate the effects of galanin, a novel neuropeptide which stimulates GH secretion in man, on the GH response to GHRH in patients with hyperthyroidism. Eight untreated hyperthyroid patients with Graves' disease (6F, 2M, aged 25-50 years) and six healthy volunteers (3F, 3M, aged 27-76 years) underwent from -10 to 30 min in random order: (i) porcine galanin, iv, 500 micrograms in 100 ml saline; or (ii) saline, iv, 100 ml. A bolus of human GHRH(1-29)NH2, 100 micrograms, was injected iv at 0 min. Hyperthyroid patients showed blunted GH peaks after GHRH+saline (10.2 +/- 2.5 micrograms/l) compared to normal subjects (20.7 +/- 4.8 micrograms/l, p < 0.05). GH peaks after GHRH+galanin were also significantly lower in hyperthyroid subjects (12.5 +/- 3 micrograms/l) compared to normal subjects (43.8 +/- 6 micrograms/l, p < 0.05). That galanin is not able to reverse the blunted GH response to GHRH in hyperthyroidism suggests that hyperthyroxinemia may either increase the somatostatin release by the hypothalamus or directly affect the pituitary GH secretory capacity.

Adult↗
PubMed1997

Simultaneous xenotransplantation of human Graves' thyroid tissue and autologous bone marrow cells in severe combined immunodeficient mice: successful reconstitution of human Graves' hyperthyroidism.

Human thyroid xenografts and the autologous bone marrow (BM) cells from five patients with Graves' disease (GD) were simultaneously xenografted into severe combined immunodeficient (SCID) mice to study the role of BM cells for the perpetuation of human GD autoimmunity and hyperthyroidism. All SCID mice engrafted with thyroid tissue (TH) alone, TH + autologous peripheral blood mononuclear cells, and TH + autologous BM cells produced similar amounts of human IgG; however, the production in TH + BM-engrafted mice peaked later than that of mice without BM. Production of thyroperoxidase antibody and thyroglobulin antibody in TH + BM-bearing SCID mice peaked in later weeks after xenografting than in those without BM. Moreover, human Graves' hyperthyroidism was actually reconstituted in TH + BM-transplanted mice; this was confirmed by (A) significantly higher levels and longer periods of secreting thyroid-stimulating antibody than those in mice without BM engraftment. (B) persistent hyperthyroxinemia up to the end of the experiment. (C) extremely high radioidine uptake of the xenografted thyroid tissue, and (D) histological findings of the maintenance of hyperplastic change of the xenografted thyroid epithelial cells. Human BM stem cells (CD34) were identified only in mice with TH + BM xenografts when analyzed by immunohistochemistry. In conclusion, (A) we have developed an animal model for human hyperthyroid GD by simultaneous xenotransplantation of GD thyroid tissue plus autologous BM cells into SCID mice, and (B) BM cells have a crucial role for perpetuating human GD autoimmunity and hyperthyroidism in this system.

Adult↗
PubMed2005

Sympatho-vagal control of heart rate variability in patients treated with suppressive doses of L-thyroxine for thyroid cancer.

OBJECTIVE: This study aimed to analyze the autonomic control of heart rate variability (HRV) in subjects receiving chronic l-thyroxine (l-T4) treatment after total thyroidectomy and (131)I therapy for differentiated thyroid carcinoma. METHODS: Blood pressure (BP) and sympatho-vagal activity (evaluated by power spectral analysis (PSA) of time-domain parameters of HRV) were studied in clinostatism and after orthostatism in 24 healthy controls, and in 12 patients taking l-T4 (125-200 mug/day) to maintain serum TSH levels at <0.01 muIU/ml. The study of HRV by PSA is a non-invasive method of analyzing sympatho-vagal control of HRV by quantifying high-frequency (HF) (0.15-0.4 Hz) and low-frequency (LF) (0.04-0.15 Hz) powers. RESULTS: Patients on L-T4 treatment had undetectable TSH levels, serum free T4 (fT4) above the normal range or at the upper limit in one case, and normal free tri-iodothyronine (fT3) levels. Heart rate and R-R intervals were not different in the two groups, both in clinostatism and in ortostatism. Systolic and mean BP were higher in patients than in controls and were inversely correlated with actual serum fT4 levels. During clinostatism, thyroid patients showed significantly lower LF power (P = 0.035), LF/(LF + HF) (P = 0.008) and LF/HF (P = 0.01) than controls. When patients moved from lying to standing, there was a significantly different decrease in orthostatic LF power (P = 0.001), LF/(LF + HF) (P = 0.044) and LF/HF (P = 0.047) versus controls. CONCLUSIONS: Changes in autonomic control of HRV, characterized by decreased sympathetic activity and impaired sympatho-vagal balance with preserved vagal tone, are detectable in patients with hyperthyroxinemia due to suppressive l-T4 therapy and increased systolic and mean, but not diastolic, BP.

Adult↗
PubMed1987

Application of an immunoradiometric assay for thyrotrophin in evaluation of thyroidal and nonthyroidal disease states.

We evaluated an immunoradiometric assay for serum TSH (IRMA-TSH) and compared it with established indices of thyroid function in 208 patients with either frank thyroid disease, conditions of abnormal thyroxine protein binding, or conditions which are known to produce discordant thyroid results, viz. pregnancy or estrogen treatment and nonthyroidal illness (NTI). As expected, a wide scatter of TSH results was found in treated thyroid disease: 53 patients (53%) from both groups (initially hypo- or hyperthyroid) had TSH values less than 0.5 mU/l, but only one was considered to be clinically mildly toxic. All the pregnant, estrogen-treated and abnormal thyroxine protein-binding patients had TSH results within the reference range 0.5-6.0 mU/l, except one familial dysalbuminemic hyperthyroxinemia (FDH) patient (T4 level, 178 nmol/l) lost to follow-up with a TSH level of 8.5 mU/l, and one euthyroid, low-TBG patient being treated inappropriately with thyroxine, with a TSH level less than 0.5 mU/l. All the untreated thyrotoxic patients and 15 (26.3%) of the NTI patients had TSH results of 0.5 mU/l or lower. Because of this high incidence of low TSH levels in euthyroid NTI, we cannot recommend this IRMA-TSH as the initial test of thyroid function.

Estrogens↗
PubMed1994

Prevalence of abnormal thyroid function tests in connective tissue disease.

The prevalence of thyroid function tests' abnormalities in 170 patients with various connective tissue diseases (CTD) was examined and compared to a group of 100 age- and sex-matched controls. The overall prevalence of diagnosed thyroid disease was 3.5%. Categorizing the patients into 5 "functional groups" by the concurrent thyroid function test/results showed normal thyroid function tests in 14%, isolated elevated TSH levels with normal T4 and T3 levels in 4% and findings consistent with the laboratory diagnosis of primary hypothyroidism in 3%. The "euthyroid sick syndrome" was evidenced in 54% and elevated T4 levels and/or increased or normal T3 values with normal TSH in 25%. Antimicrosomal antibodies were noted in 12 patients (7%), with the highest incidence in systemic lupus erythromatosus patients (10%). patients with mixed connective tissue disease had significantly (p < 0.0005) higher frequency of hypothyroidism, whereas patients with systemic vasculities had higher frequency of hyperthyroxinemia. In conclusion, CTD patients frequently have abnormal results of one or more of thyroid function tests. Hypothyroidism and hyperthyroidism should be considered when evaluating symptoms and signs in CTD and a significant subset of CTD patients appears to be predisposed to the development of hyperthyroidism.

Adolescent↗
PubMed1995

Commonly asked questions about thyroid function.

Thyroid function abnormalities in asymptomatic outpatients are common. When a patient is found to have an abnormality in thyrotropin (thyroid-stimulating hormone) or free or total thyroxine (T4), a review of the patient's medications and a careful neck examination will usually provide the explanation. Further diagnostic laboratory studies should include additional tests of T4 or thyrotropin. Determining the presence of antimicrosomal antibodies is useful for further assessment of "subclinical" hypothyroidism, and measures of protein binding (T4-binding capacity or T4-binding protein electrophoresis) help confirm a suspected congenital or acquired abnormality of T4 binding. Recognition of euthyroid hypothyroxinemia and hyperthyroxinemia is important in order to avoid intervention with inappropriate treatment. Management of subclinical hypothyroidism and hyperthyroidism necessitates clinical judgment about the patient's symptom profile and risks for long-standing or progressive thyroid dysfunction.

Humans↗
PubMed2002

Surgery-induced thyroiditis: fact or fiction?

Neck surgery carries a risk that the patient will develop postoperative thyroiditis as a result of the surgical procedure. Surgery-induced thyroiditis can manifest in a mild form as serum hyperthyroxinemia or in a more severe form as clinical hyperthyroidism. We describe a case of surgery-induced thyroiditis and review the very limited literature on this subject.

Aged↗
PubMed1975

Experimental studies on the annual cycles of thyroid and adrenocortical functions in relation to the reproductive cycle of drakes.

The annual variations in the basal plasma contents of testosterone, thyroxine and corticosterone have been measured in Peking drakes living outdoors, in Southern France. 10 The plasma testosterone titer underwent a more than 20-fold increase during the vernal reproductive period (March-April). In early June the circulating testosterone fell to near autumnal values, and the testosterone MCR was augmented. These were the first manifestations of the cessation of the vernal reproductive period. 20 The plasma thyroxine levels were minimal in autumn, moderately augmented (40%) in winter (January-March), but exhibited a 3-fold increase in early June. The resulting steep (13-fold) increase of the plasma thyroxine/testosterone ratio preceded the onset of the post-nuptial moult. 30 Modifications of testosterone secretion and clearance rate similar to those occurring in June were initiated in spring by i.m. injections of thyroxine at a dosage (1 mg/d) that induced June-July thyroxine plasma levels. On the other hand, an experimentally induced steep decrease of testosterone (castration) induced enhanced plasma thyroxine concentrations similar to the June values, while an induced (10 mg/d testosterone i.m.) hypertestosteronemia corresponding to the reproductive period depressed the plasma thyroxine levels. Strong reciprocal negative interactions between testis and thyroid might therefore afford a partial explanation of the peculiar thyroxine/testosterone imbalance that occurred in June immediately prior to the moult. 40 Cold-exposed "short-day" (December) ducks exhibited a marked increase in plasma thyroxine levels, while exposure of December ducks to "long days" (18L-6D) at 25 degrees C depressed the thyroxine titers. The inhibitory effect of "long days" on the blood level of thyroxine was further evident in castrated ducks. Exposure of "short day" ducks (December) to a combined treatment by "long days" (18L-6D) and cold (4 degrees C) produced an endocrine picture similar to the January-March pattern, i.e. highly increased testosterone plasma levels, but unaffected testosterone MCR, together with a moderate increase in plasma thyroxine concentration. 50 Corticosterone plasma concentrations increased during the reproductive season, as a result of a seasonally augmented binding-capacity of the CBG. Exogenous testosterone (10 mg/d) which induced spring-like circulating levels of male hormones, caused a similar increase in CBG-bound and total corticosterone levels. 60 In June the MCR of both corticosterone and aldosterone were elevated (as was the testosterone MCR). Similarly enhanced MCR of both corticosteroids were brought on in spring by an exogenous thyroxine treatment, leading to a June-like state of hyperthyroxinemia.

Adrenal Cortex↗
PubMedDate not supplied

[Thyroxine (T4) and tri-iodothyronine (T3) determinations: techniques and value in the assessment of thyroid function].

Hormonal production of the thyroid gland is constituted of thyroxine or T4 (80%) and triiodothyronine or T3 (20%). In the circulation, whole T4 originates from thyroid secretion but most of T3 (80%) is produced extrathyroidally from T4 deiodination. Conversion of T4 to T3 may be influenced by various conditions and circulating T3 is a less reliable reflection of thyroid hormone production than T4. In serum most of T4 and T3 is bound to binding proteins and only 0.02% of T4 and 0.3% of T3 is free. Because of their higher diagnostic performance, free T4 (FT4) and free T3 (FT3) measurements have superseded total (free + bound) hormone determination. Total hormone measurements remain useful for research studies or in case of severe hyperthyroidism. Equilibrium dialysis/RIA is considered as the reference method for free hormone measurements. Routine clinical laboratories use automated direct two-step or one-step immunoassays with a high molecular weight ligand or labelled antibody. Free hormone measurement remains technically demanding, especially in sera from severe non-thyroid ill patients with low serum thyroxine binding capacity. Interference from anti-thyroid hormone antibodies and familial dysalbuminemic hyperthyroxinemia depends on the assay method, but is now less marked and less frequently detected. To be able to correctly interpret the results of an assay, it is necessary to assess its performance in biologically and clinically well-characterised serum samples. FT4, and FT3 measurements, if FT4 is normal and hyperthyroidism suspected, are used to confirm and assess the level of hypo and hyperthyroidism (overt or subclinical). When the thyroidal status is unstable (first months of a thyroid treatment, altered L-T4 dose, subacute thyroiditis) or when the hypothalamic-pituitary function is disturbed (central hypothyroidism), TSH determination is diagnostically misleading and only free hormone measurements are reliable for thyroid function assessment.

Humans↗