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PubMedDate not supplied

[Osteocalcin and hyperthyroidism].

Osteoporosis may be induced by hyperthyroidism through an increase of bone turnover, because bone resorption exceeds formation in this condition. Also therapy with 1-thyroxine, especially by TSH-suppressive doses, may induce a reduction in bone mineral content. Circulating osteocalcin (sBGP) significantly increases both in endogenous and exogenous hyperthyroxinemia and is considered a reliable non invasive marker of bone turnover. In this study an extra-increase of sBGP in hyperthyroid post-menopausal women towards pre-menopausal is reported, the persistence of high sBGP levels in patients affected by any type of hyperthyroidism after four months of therapy and a positive relationship with thyroid hormones (fT4). Therefore monitoring of this serum marker may be suggested also in patient chronically treated with 1-thyroxine to avoid, if possible, overzealous therapy.

Adult↗
PubMed1992

[Thyroid function tests in acute drug intoxication].

It is well known that thyroid function tests may be changed in non-thyroidal illnesses. To understand the influence of acute drug intoxication on thyroid function tests, 31 drug intoxicated patients without previous thyroid disorders and systemic diseases were included in our study. T3, T4, TSH, and resin T3 uptake were checked as soon as they arrived at our emergency service and were compared to that of 58 healthy volunteers. Within 31 patients, 14 were intoxicated by organophosphorous compounds, 6 by sedatives and hypnotics, 3 by strong acid, 2 by paraquet, 2 by rodenticides (warfarin), 2 by lysol and the other 2 were intoxicated by acetaminophen. The mean T3 and TSH levels were significantly lower in the drug intoxicated group. Among the 31 patients, 14 (45.2%) had a low T3, 2 (6.5%) had a low T3 and T4, and 6 (19.3%) had an elevated T4. All of the patients with an elevated T4 were intoxicated by organophosphates. If we divided the 31 patients into 2 subgroups: organophosphate intoxicated group and non-organophosphate intoxicated group, T4 and FT4I were significantly higher in the former group. Thyroid function tests became normal after treatment in 27 patients, discharged in good general condition. T3 and T4 became extremely low in 4 patients before they expired. The present study confirms that acute drug intoxication, like other non-thyroidal illnesses, affects thyroid function tests. Acute organophosphate intoxication may cause transient hyperthyroxinemia.

Acute Disease↗
PubMed1992

Production and functional analysis of normal and variant recombinant human transthyretin proteins.

The most common form of hereditary systemic amyloidosis is familial amyloidotic polyneuropathy associated with single amino acid changes in the plasma protein, transthyretin. In addition, there are two variants of transthyretin (Ser6 and Thr109) not associated with familial amyloidotic polyneuropathy but with familial euthyroid hyperthyroxinemia, also an autosomal dominant disorder. In these autosomal dominant diseases, most affected individuals are heterozygous and therefore have hybrid forms of the tetrameric plasma transthyretin. In order to study the structure/function relationships of homozygous variant transthyretins, normal human transthyretin and five variant transthyretins (Gly6----Ser, Leu58----His, Thr60----Ala, Ile84----Ser, and Ala109----Thr) were produced in Escherichia coli using the expression vector, pCZ11, and site-directed mutagenesis. These recombinant transthyretin (r-TTR) proteins showed the correct size (14 kilodaltons) on sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western analysis and self-associated into tetramers as determined by size exclusion chromatography. Recombinant normal, Ser6, and Ala60 r-TTRs had an affinity for thyroxine indistinguishable from normal human TTR purified from plasma, whereas His58 and Ser84 r-TTRs had significantly reduced affinity. On the other hand, Thr109 r-TTR had a much higher affinity, probably due to its position within the thyroxine-binding pocket. Expression of mutant transthyretins in E. coli provides the opportunity to study structure/function relationships and amyloid-forming capabilities induced by single amino acid substitutions in the transthyretin molecule.

Amino Acid Sequence↗
PubMed2006

Bisalbuminemia from a clinical chemist's viewpoint: a case report and review of the recent literature.

Bisalbuminemia is a rare inherent or acquired abnormality characterized by the occurrence of 2 distinct albumin bands or a single widened albumin band, after electrophoretic screening of blood proteins. Despite the fact that the presence of 2 albumin bands in electrophoresis, representing normal and variant protein, is observed with a frequency of 0.00030.0010 in the average population, its role in various pathological states has not yet been clearly defined. Until now, the only disorders which have been directly linked with the presence of congenital bisalbuminemia are familial dysalbuminemic hyperthyroxinemia (Arg218AEHis and Arg218AE Pro mutations) and hypertriiodothyroninemia (Leu66AEPro mutation), while acquired types of bisalbuminemia have been reported after an overdose of beta-lactam antibiotics and as a consequence of severe pancreatitis. We present a case of bisalbuminemia in an adult man who was referred to our laboratory with a prolonged history of recurrent abdominal pain and review the recent literature in order to better familiarize clinicians as well as laboratory personnel with this entity. The biochemical parameters assessed did not show any alteration which could correlate the protein disorder with any distinct pathology.

Blood Protein Electrophoresis↗
PubMed1991

[Clinical-immunological characteristics of the state of the thyroid gland in children exposed to ionizing radiation because of the Chernobyl AES accident].

Overall 806 children evacuated from the city of Pripyat were examined for the thyroid condition. The children who received a dose of more than 30 rad for the thyroid manifested primary response in the form of euthyroid hyperthyroxinemia, a high risk of the development in future of autoimmune diseases in the lack of hypothyrosis.

Accidents↗
PubMedDate not supplied

[Interrelationship of thyroid and sex functions in males].

The purpose of this experiment was to study on intact and castrated male rats the aftereffects of administration of different androgens for thyroid function as well as the effect of experimental thyrotoxin toxicosis on sex gland incretion and the hormonal status of castrated animals receiving substitution androgenic therapy. The level of hormones was determined by a radioimmunoassay: Castration was shown to be accompanied by suppression of thyroid function, and the administration of androgens activated it. Aromatized testosterone (but not non-aromatized dehydrotestosterone) enhanced thyroxin transformation into T3 and prevented castration-induced estrogenization. Hyperthyroxinemia in castrated animals was accompanied by an increase in progesterone and estradiol concentrations. Hyperestrogenization increased with a parallel administration of androgen. Negative correlation between TSH and sex hormones levels was noted. During thyroxin toxicosis sex hormones served as modulators of hypophyseo-thyroid relationships.

Animals↗
PubMed1989

Binding of labeled thyroxin analog to serum proteins evaluated after radioimmunoassay of free thyroxin.

In ambulatory patients, assay of free thyroxin (FT4) in serum correlates well with thyroid status and with results obtained by equilibrium dialysis. The validity of FT4 results has been questioned mainly in euthyroid patients with altered concentrations of thyroid hormone-binding proteins, as in nonthyroidal illness, hereditary analbuminemia, familial dysalbuminemic hyperthyroxinemia (FDH), and the presence of iodothyronine-binding antibodies. I present here a study of the binding of [125I]T4-derivative to serum proteins in the supernate, which is ordinarily discarded after determination of FT4 by one-step radioimmunoassay with dextran-coated charcoal used to separate the free and bound fractions. The results are expressed as a ratio, with results for a normal serum pool as reference. The average ratio was high in hyperthyroid subjects, 1.26 (SD 0.12, n = 25), and in hypoalbuminemia, 1.20 (SD 0.10, n = 15), and low in FDH, 0.62 (SD 0.11, n = 9), and hypothyroid subjects, 0.90 (SD 0.06, n = 20). In normal individuals it was 0.98 (SD 0.05, n = 30). Determination of the analog-binding rate complements the FT4 result and allows for the recognition of cases with abnormal binding by serum proteins, without recourse to other tests recommended for thyroid-function studies.

Blood Proteins↗
PubMed1989

[The effect of viral hepatitis A on thyroid function in adolescents with thyroid pathology].

In patients with virus hepatitis (VHA) without thyroid pathology, thyroid function decreases but during the recovery, it rapidly restores. In the presence of concomitant thyroid hyperplasia, its function in the acute period of VHA is inhibited to an ever greater degree and remains decreased during convalescence. This circumstance requires the use of replacement hormonal therapy. In cases of concomitant hypothyrosis, the initial level of thyroid hormones diminishes but it does not manifest itself by clinical disease exacerbation. In patients with concomitant toxic goiter, the hormonal status does not undergo any changes in mild forms of VHA, whereas in VHA of medium gravity and grave patterns of VHA, hyperthyroxinemia increases and the course of diffuse toxic goiter is exacerbated. Therefore, the treatment of patients with VHA associated with thyroid pathology should be conducted with regard to thyroid function.

Adolescent↗
PubMed1986

[Ultra-sensitive TSH levels: an aid in the screening for amiodarone-induced thyroid dysfunction].

Amiodarone modifies thyroid hormone secretion and hypothyroidism occurs in some cases. The latter diagnosis is often difficult and is of particular importance in these patients as it may have serious consequences for the heart. Early diagnosis is therefore essential but difficult because of the induced hyperthyroxinemia with maintenance of euthyroidism and a hypotriiodothyronemia. The diagnostic performance of an ultrasensitive method of measuring TSH (TSH-U), capable of distinguishing hyper and euthyroidism were compared with standard thyroid function tests and TSH stimulation with TRH in 50 patients treated with amiodarone. Only 6 of the 14 patients with hyperthyroxinaemia had TSH-U values in the hyperthyroid range: only one of these patients had an increased triiodothyronine. In 2 cases the THS-U was low but the T4L was normal. In 4 patients, increased TSH-U allowed diagnosis of latent or patent hypothyroidism. There was a close correlation between results of the TRH stimulation test and those of the TSH-U in all cases. This test may therefore be used as an initial screening test for thyroid dysfunction in patients on amiodarone and is simple, reliable and relatively cheap to perform. It makes it unnecessary to measure all thyroid hormonal parameters and the TRH test simultaneously.

Amiodarone↗
PubMed1987

Hyperthyroxinemic mice have reduced natural killer cell activity. Evidence for a defective trigger mechanism.

Natural killer (NK) activity of peripheral blood lymphocytes from hyperthyroxinemic patients (Graves' disease or thyroxine (T4)-treated) is severely depressed. In order to study the relationship of thyroid hormone to NK activity, a model for hyperthyroxinemia was induced in mice by addition of T4 to the drinking water. Control mice were hypothyroid (fed propylthiouracil) or normal. Serum T4 levels were elevated (within 2 wk) in mice fed thyroid hormone. Six weeks after initiation of the diets, in vitro NK activity was undetectable in the peripheral blood, spleen, or lung mononuclear cell populations harvested from hyperthyroxinemic mice. Control mice had NK activity within the normal range. Spleen cells from mice fed thyroid hormone and control mice were tested for their ability to release lytic factors (natural killer cytotoxic factors). Lymphoid cells were incubated for 20 hr with unlabeled Yac-1 cells. Supernatants were tested for their capacity to lyse 51Cr-labeled Yac-1 cells in a 20-hr chromium release assay. Unlike controls, supernatants from hyperthyroxinemic spleen cells incubated with Yac-1 targets were unable to lyse 51Cr-Yac-1 cells. The NK cells from the mice fed T4 synthesized lytic factors because nonspecific stimuli, such as 12-O-tetradecanoyl phorbol-13-acetate and the calcium ionophore A23187, induced release of lytic factors capable of lysing Yac-1 targets into the media. These data support the hypothesis that excess thyroid hormone interferes with the triggering mechanism used by NK targets to cause release of lytic molecules from NK cells.

Animals↗
PubMed1987

Serum sex hormone-binding globulin in amiodarone-treated patients. A marker for tissue thyrotoxicosis.

The lodinated antiarrhythmic drug amiodarone frequently causes an elevation of the serum thyroxine (T4) level in patients who remain clinically euthyroid. Less frequently, true iodine-induced hyperthyroidism may occur. The clinical and laboratory distinction between these two conditions is often difficult. Since the serum sex hormone-binding globulin (SHBG) concentration is elevated in hyperthyroidism, this study was carried out to evaluate the serum SHBG concentration as a possible marker of hyperthyroidism in patients receiving amiodarone. Patients treated with amiodarone were divided into three groups: clinically euthyroid with normal serum T4 and triiodothyronine (T3) concentrations, clinically euthyroid with elevated serum T4 and normal T3 concentrations, and clinically hyperthyroid with elevated serum T4 and T3 concentrations. The mean serum SHBG concentration was significantly elevated in amiodarone-induced hyperthyroid patients, while it was normal in euthyroid patients treated with amiodarone who had normal or elevated serum T4 concentrations. The results suggest that the hyperthyroxinemia induced by amiodarone is not associated with excess thyroid hormone action in the liver unless the serum T3 concentration is also elevated.

Aged↗
PubMed1986

Amiodarone therapy effects on childhood thyroid function.

Thyroid function was systematically evaluated in 15 consecutive children (mean age 13.7 years, range 0.5 to 19.5 years) before and serially during treatment with amiodarone (Cordarone), a potent antiarrhythmic agent. Amiodarone is known to affect thyroid homeostasis by competitive inhibition of 5'-monodeiodinase, which converts L-thyroxine (T4) to triiodothyronine (T3) and reverse T3 (rT3) to 3,3'-diodothyronine (T2), and also by the direct effects of its high iodine content (37% by weight). Clinical and/or biochemical evidence of hypothyroidism occurred in three patients, two of whom required treatment with L-thyroxine. An additional patient had persistent hyperthyroxinemia but no clinical evidence of hyperthyroidism. Results from the patients who remained euthyroid showed characteristic alterations in serum thyroid function tests. These included significant increases in serum T4, rT3, basal thyroid-stimulating hormone and thyroid-stimulating hormone response to thyrotropin-releasing hormone testing. These changes were considered to be compensatory adjustments by the pituitary-thyroid axis to competitive inhibition of 5'-monodeiodinase by the amiodarone. Routine screening of thyroid function is needed to allow early detection of hypothyroidism when these compensations fail to occur.

Adolescent↗
PubMed1985

Comprehensive study of a thyroxin-analog-based assay for free thyroxin ("Amerlex FT4").

The basic theory of thyroxin-analog-based radioimmunoassays for free thyroxin has been extended to evaluate definitively the effects arising from residual binding of the tracer analog to serum proteins. Using experimentally determined binding constants and computer simulation techniques, we studied the effects of thyroxin-analog binding to serum proteins on results of Amerlex FT4 radioimmunoassay, using this improved mathematical model. Results from computer-simulation studies were compared both directly with in vitro experimental results and indirectly with clinical studies. Agreement was good among all three approaches. The relatively weak binding of analog to thyroxin-binding globulin and prealbumin does not significantly perturb Amerlex FT4 assay results. Binding of the analog by albumin has a small but quantifiable effect on assay results, amounting to an intrinsic bias of 0.08 pmol of free thyroxin per liter per gram of albumin per liter for euthyroid serum samples. This bias is unlikely to be important for most clinical laboratory samples, but it may be significant when one is interpreting results for those rare patients with genetic albumin abnormalities such as analbuminemia or familial dysalbuminemic hyperthyroxinemia. Massively increased concentrations of nonesterified fatty acids (e.g., after treatment with heparin) will lead to a spurious increase in free thyroxin in this and most other techniques, including equilibrium dialysis.

Computers↗
PubMed1977

[Influence of vitamin A deficiency on thyroxinemia in the rat].

During the 9 post-weaning weeks there is not in the vitamin A-deficient Rats the regular decrease of the thyroxinemia which occurs in the control Rats. So the vitamin A-deficient Rats studied in plateau of weight have a total thyroxinemia greater than that of control Rats (+71%). It is possible to speculate that numerous symptoms of the deficiency are the result of this hyperthyroxinemia.

Animals↗
PubMed1977

Hyperthyroidism from thyroid metastasis of pancreatic adenocarcinoma.

A nontender goiter rapidly developed in a 54-year-old patient with suspected disseminated carcinoma. Thyroid function tests showed increased thyroxine, triiodothyronine resin uptake, free thyroxine index, and free thyroxine. Radioactive iodine uptake by the gland was near zero, and thyroid-stimulating hormone (TSH) was undetectable. Histologic examination of the thyroid before and after death showed invasion and disruption of the thyroid follicles by adenocarcinoma (pancreatic primary). Release of thyroglobulin by follicular disruption probably resulted in hyperthyroxinemia and suppression of TSH and radioactive iodine uptake, as occurs in subacute thyroiditis.

Adenocarcinoma↗
PubMed1978

Complete heart block with hyperthyroidism.

Thyrotoxicosis developed in a patient while receiving thyroid hormone therapy for clinical hypothyroidism. The development of second-degree heart block of Mobitz type 1 variety was followed by third- and then first-degree heart block. We conclude that the varying degrees of heart block were secondary to hyperthyroxinemia caused by Graves' disease and exogenous thyroid hormone.

Adult↗
PubMed1981

[Misinterpretation of thyroid function caused by alteration in thyroxine binding globulin concentration (author's transl)].

Two children with undiagnosed TBG alteration were incorrectly treated for hyperthyroidism and hypothroidism, respectively. The first child exhibited hyperthyroxinemia and hypertriiodothyroninemia caused by an increase of TBG. The unoccupied binding sites of serum for thyroid hormones measured by T3-uptake were elevated as usually seen in hypothyroidism. In contrast thyroxine and triiodothyronine were extremely low in the serum of the second patient due to inherited TBG deficiency. T3-uptake was decreased to a value normally found in hyperthyroidism. The paradoxical results of T3-uptake and thyroxine levels indicated changes of concentrations of thyronine binding proteins. The quantitative determination of TBG established the correct diagnosis of TBG elevation and TBG deficiency, respectively.

Child↗
PubMed1984

Effect of amiodarone on thyroid hormone economy.

Serum thyroxine (T4), triiodothyronine (T3), resin uptake of T3 (RT3U), thyroid stimulating hormone (TSH) and TSH response to thyrotropin releasing hormone (TRH) were measured in 92 patients treated with amiodarone for up to 4 years. Two patients developed thyrotoxicosis, while euthyroid hyperthyroxinemia occurred in 29 (32%). Hypothyroidism was diagnosed in 11 patients (12%), and a further 11 had tests consistent with a "failing thyroid." Of 39 patients with normal values of T4, 15 had abnormal responses to TRH. Of the 92 patients, 24 were tested before administration of amiodarone and then sequentially; alterations in thyroid function were frequent within the first 3 months. A scheme is proposed for early recognition of disturbed thyroid function due to amiodarone.

Adult↗