SEARCH · Search PubMed

Results for “Hyperthyroidism”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources

PubMed1998

Sustained neonatal hyperthyroidism in the rat affects myelination in the central nervous system.

We have carried out a study of the effects of sustained neonatal hyperthyroidism on myelin and on the oligodendroglial cells, in an effort to obtain further insight into the molecular mechanisms underlying the action of thyroid hormones on the central nervous system (CNS). Expression of the mRNAs of myelin basic protein (MBP) myelin proteolipid protein (PLP), 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNPase), transferrin, and c-Jun was investigated in 10- and 17-day-old normal and hyperthyroid rats, using Northern blot analysis. At 10 days of age, the levels of all the explored mRNAs were markedly higher in the experimental animals. The mRNA of transferrin showed a ninefold increase over control values, suggesting the possibility that this putative trophic factor might act as one of the mediators in the action of thyroid hormones. At 17 days of age on the other hand, the levels of all the mRNAs decreased markedly, reaching values below control, except for c-Jun, which remained higher than in normals. At 70 days of age, hyperthyroid rats showed clear evidence of myelin deficit, in agreement with previous results of our laboratories (Pasquini et al.: J Neurochem 57: Suppl S124, 1991). Immunocytochemistry of 70-day-old rat brain tissue sections showed a substantial reduction in the amount of MBP-reacting structures and a marked decrease in the number of oligodendroglial cells. Although the above-mentioned results could be the consequence, as proposed by Barres et al. (Development 120:1097-1108, 1994) and Baas et al. (Glia 19:324-332, 1997) of a premature arrest in oligodendroglial cell proliferation followed by early differentiation, the persistent high levels of expression of c-Jun, together with the dramatic decrease in the number of oligodendrocytes, suggested the possibility that prolonged hyperthyroidism could activate apoptotic mechanisms in the myelin forming cells. Using propidium iodide-labeled isolated oligodendroglial cells, we found, by flow cytometry, a significant increase in the number of apoptotic/hypo-diploid propidium iodide-positive cells. These results indicate that one of the actions of sustained levels of thyroid hormones in the neonate rat is to increase oligodendroglial cell death by apoptosis.

2',3'-Cyclic-Nucleotide Phosphodiesterases↗

PubMed2004

Antithyroid drug regimen for treating Graves' hyperthyroidism.

BACKGROUND: Antithyroid drugs are widely used in the therapy of hyperthyroidism. There are wide variations in the dose, regimen or duration of treatment used by health professionals. OBJECTIVES: To assess the effects of dose, regimen and duration of antithyroid drug therapy for Graves' hyperthyroidism. SEARCH STRATEGY: We searched the Cochrane Central Register of Controlled Trials (Central), MEDLINE, EMBASE, BIOSIS, CINAHL, HEALTHSTAR, Current Controlled Trials and reference lists. We contacted investigators and hand searched conference abstracts. Most recent search: June 2002. SELECTION CRITERIA: Randomised and quasi-randomised trials of antithyroid medication for Graves' hyperthyroidism were used. DATA COLLECTION AND ANALYSIS: Trial allocation to included, excluded and awaiting assessment categories was made by consensus. Two reviewers independently extracted data and assessed trial quality. Pooling of data for primary outcomes, and select exploratory analyses were undertaken. MAIN RESULTS: Nineteen randomised trials involving 2233 participants were included. Overall the quality of trials as reported was poor; specifically in terms of allocation concealment, assessor blinding and loss to follow-up. Four trials examined the effect of duration of therapy on relapse rates of Graves' hyperthyroidism. In one trial using the Titration regimen, longer duration therapy (18 months) had significantly fewer relapses (37% vs 58%) than six month therapy (Odds ratio (OR) = 0.42, 95% confidence interval (CI) 0.18 to 0.96). In one quasi-randomised trial using the Block-Replace regimen, there was no significant difference between the six and 12 month (relapses rates 41% versus 35%) arms of the study. Extending the duration of therapy to over 18 months was not associated with improved relapse rates (Peto OR = 0.75, 95% CI 0.39 to 1.43). Ten trials examined the effect of Block-Replace versus Titration regime. Relapse rates were similar in both groups at 54% in the Block-Replace group and 58% in the Titration group (Peto OR = 0.83, 95% CI 0.63 to 1.10). Participants reporting rashes (11% versus 5%) and withdrawing due to side effects (16% versus 9%) were significantly higher in the Block-Replace group compared to the Titration group respectively. Three studies considered the addition of thyroxine after initial therapy with antithyroid drugs. There was significant heterogeneity between the studies and the difference between the two groups were not significant (Odds ratio = 0.58, 95% CI 0.05 to 6.21). REVIEWERS' CONCLUSIONS: The evidence (based on three studies) suggests that the optimal duration of antithyroid drug therapy for the Titration regimen is 12 to 18 months. The six month Block-Replace regimen was found to be as effective as the 12 month treatment in one quasi-randomised study. The Titration (low dose) regimen had fewer adverse effects than the Block-Replace (high dose) regimen and was no less effective in trials (based on 10 trials) of equal duration. The incidence of hypothyroidism was not reported and there were no deaths in the study populations.

Antithyroid Agents↗

PubMed2000

Hyperthyroid heart disease.

The heart is an organ sensitive to the action of thyroid hormone, and measurable changes in cardiac performance are detected with small variations in thyroid hormone serum concentrations. Most patients with hyperthyroidism experience cardiovascular manifestations, and the most serious complications of hyperthyroidism occur as a result of cardiac involvement. Recent studies provide important insights into the molecular pathways that mediate the action of thyroid hormone on the heart and allow a better understanding of the mechanisms that underlie the hemodynamic and clinical manifestations of hyperthyroidism. Several cardiovascular conditions and drugs can interfere with thyroid hormone levels and may pose a difficulty in interpretation of laboratory data in patients with suspected thyroid heart disease. The focus of this report is a review of the current knowledge of thyroid hormone action on the heart and the clinical and hemodynamic laboratory findings as well as therapeutic management of patients with hyperthyroid heart disease.

Atrial Fibrillation↗

PubMed1980

Development of home orientation in hypothyroid and hyperthyroid rat pups.

In order to assess the effects of perinatal hypothyroidism or hyperthyroidism on the development of an integrated behavioral response, we tested hypothyroid, hyperthyroid, and control pups, as well as pups receiving thyroxine replacement therapy, for the development of the home orientation response. Hypothyroidism was induced in the pups by feeding the pregnant or lactating female a diet of .2% propylthiouracil from Day 15 of gestation to Day 22 postpartum. Pups receiving replacement therapy and pups made hyperthyroid were injected daily with thyroxine, starting at birth. The ability of the pups to initiate and maintain locomotion toward the nest was assessed between Days 4 and 22. Hyperthyroid, control, and replacement therapy pups behaved very similarly on the task, showing a peak in the percentage of pups homing between Days 12 and 16. Hypothyroid pups showed a delay in the peak percentage until Day 20, although the percentage of pups was similar to that found in other treatments. An integrated behavioral response can be delayed by hypothyroidism and still emerge apparently intact at a later age.

Animals↗

PubMed2004

Severe hyperthyroidism induces mitochondria-mediated apoptosis in rat liver.

Thyrotoxicosis may be associated with a variety of abnormalities of liver function. The pathogenesis of hepatic dysfunction in thyrotoxicosis is unknown, but has been attributed to mitochondrial dysfunction. We studied the effect of altered thyroid function on the apoptotic index in rat liver. Extensive DNA fragmentation and significantly increased caspase-3 activity (P <.001) and caspase-9 activation (P <.005) were observed in hyperthyroid rat liver; cell death by apoptosis was confirmed. In hyperthyroid rat liver, 60% of mitochondria exhibited disruption of their outer membranes and a decrease in the number of cristae. These findings, along with significant translocation of cytochrome c and second mitochondria-derived activator of caspases to cytosol (P <.005), suggest activation of a mitochondrial-mediated pathway. However, no change in the expression levels of Bcl-2, Bax, and Bcl-x(L) were found in hyperthyroidism. For in vitro experiments, rat liver mitochondria were isolated and purified in sucrose density gradients and were treated with triiodothyronine (T3; 2-8 microM). T3 treatment resulted in an abrupt increase in mitochondrial permeability transition. Using a cell-free apoptosis system, the apoptogenic nature of proteins released from mitochondria was confirmed by observing changes in nuclear morphologic features and DNA fragmentation. Proteins released by 6 microM T3 contained significantly increased amounts of cytochrome c (P <.01) and induced apoptotic changes in 67% of nuclei. In conclusion, using in vivo and in vitro approaches, we provide evidence that excess T3 causes liver dysfunction by inducing apoptosis, as a result of activation of a mitochondria-dependent pathway. Thus, the results of this study provide an explanation for liver dysfunction associated with hyperthyroidism.

Alanine Transaminase↗

PubMed2001

Membrane-Bound and cytosolic forms of heterotrimeric G proteins in young and adult rat myocardium: influence of neonatal hypo- and hyperthyroidism.

Membrane and cytosolic fractions prepared from ventricular myocardium of young (21-day-old) hypo- or hyperthyroid rats and adult (84-day-old) previously hypo- or hyperthyroid rats were analyzed by immunoblotting with specific anti-G-protein antibodies for the relative content of Gs alpha, Gi alpha/Go alpha, Gq alpha/G11 alpha, and G beta. All tested G protein subunits were present not only in myocardial membranes but were at least partially distributed in the cytosol, except for Go alpha2, and G11 alpha. Cytosolic forms of the individual G proteins represented about 5-60% of total cellular amounts of these proteins. The long (Gs alpha-L) isoform of Gs alpha prevailed over the short (Gs alpha-S) isoform in both crude myocardial membranes and cytosol. The Gs alpha-L/Gs alpha-S ratio in membranes as well as in cytosol increased during maturation due to a substantial increase in Gs alpha-L. Interestingly, whereas the amount of membrane-bound Gi alpha/Go alpha and Gq alpha/G11 alpha proteins tend to lower during postnatal development, cytosolic forms of these G proteins mostly rise. Neonatal hypothyroidism reduced the amount of myocardial Gs alpha and increased that of Gi alpha/Go alpha proteins. By contrast, neonatal hyperthyroidism increased expression of Gs alpha and decreased that of Gi alpha and G11 alpha in young myocardium. Changes in G protein content induced by neonatal hypo- and hyperthyroidism in young rat myocardium were restored in adulthood. Alterations in the membrane-cytosol balance of G protein subunits associated with maturation or induced by altered thyroid status indicate physiological importance of cytosolic forms of these proteins in the rat myocardium.

Age Factors↗

PubMed2005

Platysmal myoclonus in subclinical hyperthyroidism.

Hyperthyroidism is associated with various movement disorders, such as chorea and tremors. We report on a young Chinese woman with an unusual presentation of myoclonus, involving both platysmal muscles, in association with subclinical hyperthyroidism. The myoclonus was preceded by symptoms of hyperthyroidism, namely weight loss, menstrual disturbances, and heat intolerance. The movements abated with clonazepam and hyperthyroidism was treated with carbimazole. The myoclonus recurred briefly when she stopped taking clonazepam, but she has since remained well and euthyroid.

Anticonvulsants↗

PubMed2000

Experimental hyperthyroidism causes inactivation of the branched-chain alpha-ketoacid dehydrogenase complex in rat liver.

Hyperthyroidism induced by 3-day treatment of rats with thyroid hormone (T(3); 3,5,3'-triiodothyronine) at 0.1 or 1 mg/kg body wt/day resulted in a reduced activity state (% of enzyme in its active, dephosphorylated state) of the hepatic branched-chain alpha-ketoacid dehydrogenase (BCKDH) complex. One treatment with 0.1 mg T(3)/kg body wt caused a significant effect on the activity state of BCKDH complex after 24 h, indicating that the reduction of the activity state was triggered by the first administration of T(3). Hyperthyroidism also caused a stable increase in BCKDH kinase activity, the enzyme responsible for phosphorylation and inactivation of the BCKDH complex, suggesting that T(3) caused inactivation of the BCKDH complex by induction of its kinase. Western blot analysis also revealed increased amounts of BCKDH kinase protein in response to hyperthyroidism. No change in the plasma levels of branched-chain alpha-keto acids was observed in T(3)-treated rats, arguing against an involvement of these known regulators of BCKDH kinase activity. Inactivation of the hepatic BCKDH complex as a consequence of overexpression of its kinase may save the essential branched-chain amino acids for protein synthesis during hyperthyroidism.

3-Methyl-2-Oxobutanoate Dehydrogenase (Lipoamide)↗

PubMed1999

G proteins, beta-adrenoreceptors and beta-adrenergic responsiveness in immature and adult rat ventricular myocardium: influence of neonatal hypo- and hyperthyroidism.

Thyroid hormones influence a wide range of physiological responses and the heart is considered a major target organ for triiodothyronine action. In the present study we examined closely the presumed relationship between altered thyroid status in the newborn rat and maturation of the regulatory components of the myocardial hormone-sensitive adenylyl cyclase signaling system. Beta -adrenoceptors and the alpha subunits of the stimulatory (Gs) as well as inhibitory (Gi) G proteins were determined in ventricular myocardium of immature (21-day-old) hypo- or hyperthyroid rats and in adult (84-day-old) previously hypo- or hyperthyroid rats. The changes in receptor and G protein levels were correlated with basic parameters of cardiac function and inotropic responsiveness to isoproterenol. All results were compared with those obtained in age-matched controls. Hypothyroidism in immature rats was associated with markedly reduced myocardial beta-adrenoceptor density, lower content of the long isoform (Gsalpha-L) of the stimulatory G protein and increased amounts of Gialpha2 and Gialpha3. These changes were accompanied by substantially diminished sensitivity to the inotropic effect of isoproterenol. On the other hand, no change in beta-adrenoceptor number, an increased level of Gsalpha-L and decreased levels of Gialpha2 were found in hyperthyroid myocardium. Cardiac inotropic responsiveness to isoproterenol in immature hyperthyroid rats was not significantly altered. In adult hearts of previously hyper- or hypothyroid rats, beta-adrenoceptor density was decreased but G protein levels as well as functional response were comparable to those determined in control animals. It may be concluded that physiological level of thyroid hormones is an important modulator of the normal maturation of the beta-adrenergic system in the developing rat ventricular myocardium. In adult rats previously affected by altered thyroid status, the function of their myocardial beta-adrenergic signaling appears to be compensated despite a lower number of the receptors.

Adenylyl Cyclases↗

PubMed2001

Hyperthyroidism increases the risk of ozone-induced lung toxicity in rats.

The risk of lung injury from ozone exposure has been well documented. It is also known that various factors may significantly influence the susceptibility of animals to the toxic effects of ozone. In the present study, we investigated the possibility that hyperthyroidism might be associated with increases in ozone-induced pulmonary toxicity. To create a hyperthyroid condition, mature male Sprague--Dawley rats were given injections of thyroxine (dose range: 0.1 to 1 mg/kg body wt daily for 7 days). Control rats received vehicle injections. The animals were then exposed to air or ozone (dose range: 0.5 to 3 ppm for 3 h). At 18 h postexposure, bronchoalveolar lavage fluid and cells were harvested. In hyperthyroid animals, ozone exposure was associated with three- to sixfold increases in bronchoalveolar lavage fluid lactate dehydrogenase activities and albumin levels as well as the number of polymorphonuclear leukocytes harvested by bronchoalveolar lavage above levels observed in ozone-exposed control rats. Additional results from the present study suggest that these thyroid hormone-linked effects cannot be fully explained by differences in whole-body metabolic rate or changes in the inhaled dose of ozone. These findings indicate that the risk of ozone-induced lung toxicity is substantially increased in a hyperthyroid state and suggest that the susceptibility of the lung to damage from ozone exposure may be significantly influenced by individual thyroid hormone status.

Albumins↗

PubMed1991

Late results of thyroid surgery for hyperthyroidism performed in childhood.

The authors report on the complex follow-up of 60 patients operated on for hyperthyroidism in childhood, on average 13.7 years after surgery. In 16.7% of the patients manifest hypothyroidism, in 45% subclinical hypothyroidism was found; 30% of the patients were euthyroid, and manifest hyperthyroidism recurred in 8.3%. Autonomous adenomas were enucleated in two children and three young adults. Severe disorders in thyroid function developed especially after the surgery of diffuse toxic goiters accompanied by ophthalmopathy. The disorders of humoral and cellular immunity were detected most frequently in recurrent manifest hyperthyroidism. There was no case where ophthalmopathy progressed after the operation. In the offspring of the operated patients the incidence of hyperthyroidism was not increased in childhood. The authors call attention to the importance of postoperative follow-up and hormone treatment.

Adenoma↗

PubMed1992

Mechanism of hyperthyroidism-induced modulation of the L-type Ca2+ current in guinea pig ventricular myocytes.

The positive inotropic effects of thyroid hormone in the heart, increased force and velocity of contraction have been mostly attributed to modulation of myosin ATPase isoenzymes (V1, V2 and V3), and sarcoplasmic reticulum Ca2+ pumping activity. In addition, we have suggested that the effects on ventricular contraction result from a thyroid hormone-induced increase in L-type Ca2+ current (ICa,L). Due to the central role of ICa,L in excitation-contraction coupling, we studied mechanisms whereby thyroid hormone augments this current. Since thyroid hormone modulates adenylate cyclase activity in various tissues, we tested the hypothesis that the hormone activates adenylate cyclase, leading to increased cyclic adenosine monophosphate (cAMP) levels, protein kinase A activation, Ca2+ channel phosphorylation and increased ICa,L. We therefore stimulated or inhibited different sites along the "adenylate cyclase cascade", and measured ICa,L and isometric twitch in ventricular myocytes and papillary muscles from euthyroid and hyperthyroid guinea pigs. Our major findings were as follows. In euthyroid myocytes, 0.1 microM isoproterenol (Iso) increased ICa,L (at VM = 0 mV) from -7.04 +/- 0.72 to -22.26 +/- 1.88 pA/pF, P < 0.05, while in hyperthyroid myocytes (ICa,L = -21.48 +/- 2.94 pA/pF), Iso was ineffective. In euthyroid myocytes, intracellular application of cAMP (50 microM) was as potent as Iso, but ineffective in hyperthyroid myocytes. In hyperthyroid myocytes, a protein kinase A inhibitor (2 microM) lowered ICa,L from -26.82 +/- 1.54 to -10.17 +/- 1.70 pApF (P < 0.05), but had no effect in euthyroid myocytes.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗

PubMed1982

Prolactin response to thyrotropin-releasing hormone in children with Turner's syndrome and hyperthyroidism.

Plasma prolactin (PRL) response to synthetic thyrotropin-releasing hormone (TRH) was studied in 26 prepubertal and 19 pubertal children with constitutional short stature, 7 patients with Turner's syndrome and 10 patients with hyperthyroidism. The mean basal concentrations of plasma PRL did not differ among groups. In prepubertal children PRL responses to TRH were comparable in both sexes, while pubertal children plasma PRL levels after TRH in females were significantly higher (P less than 0.05) than those in age-matched males. Plasma PRL levels after TRH in patients with Turner's syndrome were significantly higher (P less than 0.05) than those in age-matched males, but were not significantly different from those in age-matched females. Plasma PRL response to TRH was markedly suppressed in patients with hyperthyroidism before treatment, but it returned to normal after treatment when patients became euthyroid. A significant correlation (P less than 0.05) between peak concentrations of plasma PRL and TRH stimulation and plasma T3 but not T4 levels was observed. These data suggest that a sex difference in TRH-stimulated PRL secretion appears around puberty and that plasma PRL response to TRH is suppressed in children with hyperthyroidism. The magnitude of plasma PRL response to TRH is closely correlated with the severity of hyperthyroidism when judged by plasma T3 but not T4 concentrations.

Adolescent↗

PubMed1987

Pharmacokinetics of theophylline in hyperthyroid and hypothyroid patients with chronic obstructive pulmonary disease.

The pharmacokinetics of theophylline was investigated in five hyperthyroid, five hypothyroid, and five euthyroid patients, all with chronic obstructive pulmonary disease. Wide individual variability was found in theophylline kinetics, but the rate of elimination of theophylline was significantly higher in hyperthyroid, and lower in hypothyroid patients than in the euthyroid patients (kel = 0.155, 0.060 and 0.107 h-1, respectively). The values for clearance and volume of distribution were not consistently changed compared with those in the euthyroid group, although all the parameters except AUC were significantly different in hyperthyroid and hypothyroid patients. There was a positive correlation between both thyroxine and triiodothyronine serum concentrations and total body clearance of theophylline (r = 0.795 and r = 0.791, respectively). It is concluded that in spite of the wide interindividual variability and the relatively small differences in the pharmacokinetics of theophylline in thyroid dysfunction compared with the euthyroid status, these differences have to be considered in certain clinical situations, as they may require changes in the therapeutic regimen for administration of theophylline in hyperthyroid or hypothyroid patients.

Adult↗

PubMed1977

Force-velocity relations of the portal vein of hyperthyroid rats.

The effect of thyroxine on the elementary process of contraction of vascular smooth muscle was tested on 38 hyperthyroid and in 38 control rats. Hyperthyroidism was induced by i.p. injections of triiodthyronine or 1-htyroxine for 2 weeks. By means of afterloaded isotonic contractions of the tetanized portal vein force velocity relations were calculated. There was a slight increase in both the extrapolated velocity of shortening at zero load [from 0.93 +/- 0.04 ML/s (control rats) to 1.03 +/- 0.04 ML/s (hyperthyroid rats; P less than 0.05)], and the peak force generation (from 14.8 +/- 0.4 mN to 16.1 +/- 0.4 mN; P less than 0.005). The maximum of mechanical power development at a distinct extent of afterload was augmented from 1.35 +/- 0.06 muW/ML to 1.68 +/- 0.06 muW/ML (P less than 0.005). The influence of thyroxine on the elementary process of contraction in vascular smooth muscle is discussed in connection with the much stronger effect of hyperthyroidism on cardiac muscle contraction.

Animals↗

PubMed1982

Thyroid-stimulating hormone (TSH) receptor antibodies and antibodies stimulating adenyl cyclase in relatives from two families with a high prevalence of Graves' hyperthyroidism: a ten-year follow-up study.

Thyroid-stimulating hormone (TSH) receptor antibodies and antibodies stimulating adenyl cyclase were measured in 47 relatives of patients with Graves' hyperthyroidism from two families with a high prevalence of the disease, in whom bioassays for the long-acting thyroid stimulator (LATS) had been performed 10 years earlier. Tests were also carried out in six propositi from the two families and age- and sex-matched normal subjects from six families. There had been no new cases of hyperthyroidism since the first study, although one subject was clinically and biochemically hyperthyroid at the time of study and two more were biochemically borderline hyperthyroid but clinically euthyroid. Levels of serum T4 thyrotropin, and percentage T3 resin uptake and free thyroxine indices were similar for relatives and normal subjects, although the mean serum T3 level for relatives was significantly greater than that for the normal subjects. Antibodies were not detected by either assay in any relative. Significant titers of antithyroglobulin antibodies were demonstrated in 4 of 44 relatives but in none of 46 normals tested, while thyroid cytoplasmic antibodies were detected in 8 of 44 relatives and 3 of 45 normals. The mean serum IgG for Graves' relatives was significantly greater than that for the normals, although the mean IgM and IgA levels for the two groups were not significantly different.

Adenylyl Cyclases↗

PubMed1990

Psychopathological and neuropsychological symptoms in patients with subclinical and remitted hyperthyroidism.

To investigate relationships between hyperthyroidism and behavior, 45 formerly hyperthyroid patients (now euthyroid) and 51 control subjects were investigated by (a) a semi-structured psychiatric examination, (b) self-rating scales to assess mood states and personality, and (c) neuropsychological tests. Patients with "subclinical" or "remitted" hyperthyroidism showed more abnormalities than the controls in all dimensions investigated. Forty-three percent of patients (10% of controls) complained of "seriously reduced" well-being with feelings of fear, hostility, and inability to concentrate. While a fearful-agitated syndrome dominated in the initial phase of the illness, a mainly depressive syndrome was characteristic after a longer period of remission. More than 25% of the patients (2% of controls) showed "markedly impaired" neuropsychological functioning. Patients with a relapse within 2.5 years exhibited the most abnormal results. Even after a longer period of hormonal remission, there was no complete psychopathological and neuropsychological normalization. A thorough follow-up of hyperthyroid patients is recommended.

Adenoma↗

PubMed1981

[T3-hyperthyroidism under the aspects of secretion and peripheral production of thyroid hormones (author's transl)].

In contrast to T4/T3-hyperthyroidism, where T4, T3, and r-T3 serum concentrations (SC) are elevated, in T3-hyperthyroidism the T3-SC alone is increased, whereas T4-SC is normal and r-T3 may be decreased. Endogenous labelling of T4 with 131I is increased in T3-hyperthyroidism similarly as in T4/T3-hyperthyroidism, clearly reflecting an increased thyroidal formation of T4 in T3-hyperthyroidism. The contradiction of a normal SC to T4 in the presence of enhanced thyroidal formation of T4 may be explained by increased peripheral T4-deiodination. Since in T3-hyperthyroidism T3-SC are elevated whereas r-T3-SC are decreased, there is good evidence for a shift in T4 conversion.

Humans↗