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PubMed2005

Hyperthyroidism and cerebral venous thrombosis.

The demonstration of an underlying prothrombotic condition in cerebral venous thrombosis (CVT) may have important practical consequences in terms of prevention. Thyrotoxicosis through a hypercoagulable state may be a predisposing factor for CVT. The authors present the cases of 4 patients who developed CVT and hyperthyroidism. At the acute stage, hyperthyroidism was associated with an increase in factor VIII (FVIII). At follow-up, FVIII level remained increased in 2 patients. Hyperthyroidism may have an impact on FVIII level. Accordingly in patients with hyperthyroidism and neurological symptoms, the diagnosis of CVT should be considered and an exhaustive coagulation screening may be appropriate.

Factor VIII↗
PubMed2006

Congenital hyperthyroidism: the fetus as a patient.

Congenital hyperthyroidism is less frequent than congenital hypothyroidism but its impact on growth and development can be as dramatic. The immune form of hyperthyroidism that is transmitted from a mother with Graves' disease to her foetus and then neonate is transient, but cases of persistent congenital hyperthyroidism had also been described, that can now be explained by molecular abnormalities of the thyrotropin receptor. The abundance of published data on the neonatal effects of maternal Graves' disease contrasts with the paucity of information on fetal effects. Recent studies showed that it is of utmost to scrutinize fetal thyroid by expert ultrasonographist and to have a team work with obstetricians and pediatric endocrinologists in pregnant women with Graves' disease. This allowed to accurately determine the fetal thyroid status and to adapt the treatment in the mothers successfully. Fetal hyperthyroidism does exist and needs an appropriate aggressive treatment. Clearly the fetus has become our patient!

Female↗
PubMed2006

Reduced serum acylated ghrelin levels in patients with hyperthyroidism.

BACKGROUND AND OBJECTIVE: Recent studies have revealed that circulating ghrelin levels seem to play a role in energy homeostasis. The effect of hyperthyroidism on ghrelin levels is not fully known. METHODS: Serum levels of ghrelin and its relationship with insulin resistance were evaluated in 48 patients with hyperthyroidism and 43 euthyroid healthy controls. Thyroid hormones, insulin, glucose, ghrelin levels and lipid parameters were measured in all subjects. Insulin sensitivity was determined using the homeostasis model assessment. RESULTS: Serum ghrelin levels were significantly decreased in hyperthyroid patients than in controls (32.5 +/- 23.3 vs. 54.1 +/- 35.5 pg/ml, p < 0.001). Circulating ghrelin levels significantly correlated with age (r = -0.26, p = 0.01), fasting glucose (r = -0.21, p = 0.01), free triiodothyronine (r = -0.18, p = 0.04), free thyroxine (r = -0.23, p = 0.02) and thyroid stimulating hormone (r = 0.21, p = 0.04), but not with blood pressure, body mass index, lipid parameters, insulin and homeostasis model assessment (p > 0.05). Multiple regression analysis revealed glucose level to be the most important predictor of circulating ghrelin level. CONCLUSION: These results indicate that hyperthyroidism has effect on serum ghrelin levels. Further studies are needed for the exact mechanism.

Acylation↗
PubMed1985

Plasma growth hormone response to human growth hormone releasing factor in rats administered with chlorpromazine and antiserum against somatostatin. Effects of hypo- and hyperthyroidism.

The effect of hypo- and hyperthyroidism on the plasma growth hormone (GH) response to synthetic human growth hormone releasing factor (GRF) was determined in conscious, freely moving rats pretreated with chlorpromazine and antiserum against somatostatin. Chlorpromazine plus somatostatin antiserum pretreated rats gave consistent response to GRF which was not observed in untreated rats. Chlorpromazine alone has no effect on GH secretion induced by GRF in rat pituitary monolayer culture. In rats made hypothyroid by thyroidectomy, both basal and peak plasma GH responses to a small (0.25 microgram/kg bw) and a moderate dose of GRF (1 microgram/kg bw) were significantly reduced as compared to controls. In rats made hyperthyroid by the administration of thyroxine, basal and peak plasma GH responses to a small but not to a moderate dose of GRF were significantly reduced as compared to controls. A reduced plasma GH response to a small dose of GRF was observed 8 days after the cessation of thyroxine administration. The pituitary GH reserve was markedly reduced in hypothyroid but not in hyperthyroid rats as compared to their respective controls. These results indicate that plasma GH response to GRF is reduced both in hypo- and hyperthyroidism. The mechanism involved in the phenomenon appears to be different between the two conditions.

Animals↗
PubMed1994

Vascular reactivity to vasoconstrictors in aorta and renal vasculature of hyperthyroid and hypothyroid rats.

Vascular reactivity to vasoconstrictors in relation to altered thyroid function was studied in two preparations: aortic strips and the isolated perfused kidney. To assess whether the possible alterations in vascular reactivity were restricted to a specific agonist or whether they involved the contractile system, receptor-mediated and nonspecific smooth muscle stimulants were used. Male Wistar rats were divided into three groups: control, hyperthyroid and hypothyroid rats. Aortic strips from hypothyroid rats were less sensitive to phenylephrine and KCl when the data were expressed in absolute values or as percentages of the maximum responses. Sensitivity and reactivity in strips from hyperthyroid rats were similar to those observed in control strips. Renal vasculature obtained from hypothyroid rats also showed a markedly reduced sensitivity to phenylephrine, with normal maximal responses. The response to vasopressin at 3-10(-11) mol/l was also decreased, as was the reactivity to barium chloride. In contrast, renal vasculature of hyperthyroid rats showed markedly enhanced reactivity to all agonists: the concentration-response curves were characterized by a similar threshold and a greater maximal response. These results demonstrate that hypothyroidism is accompanied by a marked decrease in sensitivity to vasoconstrictors in large arteries as well as in resistance vessels. This decrease may be secondary to a generalized alteration in the contractile system of vascular smooth muscle cells and may play a role in the decreased blood pressure in these animals. In contrast, isolated perfused kidneys of hyperthyroid rats showed increased vascular reactivity to vasoconstrictors, which may play a role in the maintenance of elevated blood pressure in these animals.

Animals↗
PubMed1985

Distal renal tubular acidosis and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism. Report of 1 case without nephrocalcinosis.

In a 33-year-old woman concurrence of a complete distal renal tubular acidosis (RTA) and lymphocytic thyroiditis with spontaneously resolving hyperthyroidism was observed. Until recently, the rare association of RTA and hyperthyroidism had been thought to be governed by nephrocalcinosis, via hypercalcemia and hypercalciuria. However, in this case, nephrocalcinosis was not present, but there were histological signs of renal interstitial mononuclear cell infiltration, and the RTA persisted despite the resolution of the hyperthyroidism. This observation supports the idea that immunological mechanisms may relate RTA and hyperthyroidism when the latter has an autoimmune origin.

Acidosis, Renal Tubular↗
PubMed1969

Anaerobic performance and metabolism of the hyperthyroid heart.

Anaerobically periused hearts from rats with experimentally induced hyperthyroidism exhibited accelerated deterioration of pacemaker activity and ventricular performance. The diminished anaerobic performance of hyperthyroid hearts was associated with decreased adenosine triphosphate (ATP) levels and a reduced rate of anaerobic glycolysis as reflected in decreased lactic acid production during 30 min of anoxic perfusion.Studies on whole heart homogenates demonstrated inhibition at the phosphofructokinase (PFK) step of the glycolytic pathway. Such inhibition was not demonstrated in the hyperthyroid heart cytosol. It is postulated that an inhibitor of PFK which resides dominantly in the particulate fraction is probably responsible for the diminished anaerobic glycolysis and performance of the hyperthyroid heart.

Adenosine Triphosphate↗
PubMed1974

Triiodothyronine and thyroxine in hyperthyroidism. Comparison of the acute changes during therapy with antithyroid agents.

In 66 untreated patients with hyperthyroidism, serum triiodothyronine (T(3)) and thyroxine (T(4)) concentrations were measured by immunoassay. The mean T(3) level was 478+/-28 ng/100 ml (all values mean+/-SEM) and the T(4) was 20.6+/-0.6 mug/100 ml. The serum T(4)/T(3) ratio by weight was 48+/-2 as opposed to a value of 71+/-3 in euthyroid adults. There was a significant inverse correlation of the T(4)/T(3) ratios with serum T(3) (r=0.77; P<0.01) but not with serum T(4)(r=0.21). These results suggested that relative overproduction of T(3) is consistently present in patients with hyperthyroidism. To examine the acute effects of various antithyroid agents on serum T(3) and T(4) concentrations, iodide, propylthiouracil (PTU), and methylmercaptoimidazole (MMI) were given alone to mine patients, and serial T(3) and T(4) measurements were made. There was an acute decrease in serum T(3) over the first 5 days in the three iodide and three PTU-treated patients which was greater than that seen in the MMI group. This suggested that PTU and MMI had different effects on T(3) production. To compare the effects of PTU and MMI under conditions in which thyroidal hormone release was minimized, these drugs were given in combination with iodide. The mean daily dosage of PTU was 827 (n=11) and of MMI was 88 (n=8). In the PTU+iodide group, the initial serum T(3) concentration was 586+/-61 ng/100 ml and decreased significantly to 326+/-41 on day 1 and to 248+/-21 on days 2 and 3, respectively, and did not change further on days 4 and 5. In the MMI + iodide group, basal serum T(3) was 645+/-90 ng/100 ml and decreased to 568+/-81, 452+/-73, and 344+/-51 on days 1, 2, and 3, respectively, and did not change thereafter. While the initial T(3) concentrations in serum were not different in the PTU and MMI groups, the T(3) concentrations in the PTU patients were significantly lower on days 1 and 2 and during the apparent plateau period on days 3-5. Serum T(4) concentrations decreased gradually in both groups, from 23.9+/-2.0 mug/100 ml, initially, to 17.5+/-1.6 on day 5 in the PTU group and from 22.0+/-2.6 to 14.6+/-2.0 in the MMI-treated patients. The T(4) values were not significantly different at any time. These changes resulted in increases in the serum T(4)/T(3) ratios in both groups, but these ratios were substantially higher in the patients treated with PTU + iodide. The initial serum T(4)/T(3) ratio was 43+/-3 and increased to 74+/-7 and 88+/-7 on days 1 and 2 in the PTU group, reaching a plateau value of 91+/-7 during days 3-5. Comparable values for MMI-treated patients were 35+/-2, 42+/-3, 52+/-6, and 54+/-3 during the plateau period. Previous investigations have shown that PTU inhibits T(4) deiodination in hyperthyroid patients and decreases T(3) production from T(4) in animals. The greater acute decrease in serum T(3) and the higher serum T(4)/T(3) ratios in the PTU-treated patients seems best explained by an inhibition of peripheral T(3) production by this agent. This conclusion is further supported by a direct relationship between the T(4)/T(3) ratio on days 3-5 and the dose of PTU administered. These results further suggest that both thyroidal and extrathyroidal pathways contribute substantially to the apparent overproduction of T(3) in hyperthyroidism.

Antithyroid Agents↗
PubMed1991

Mechanisms of impaired exercise capacity in short duration experimental hyperthyroidism.

To investigate the mechanism of reduced exercise tolerance in hyperthyroidism, we characterized cardiovascular function and determinants of skeletal muscle metabolism in 18 healthy subjects aged 26 +/- 1 yr (mean +/- SE) before and after 2 wk of daily ingestion of 100 micrograms of triiodothyronine (T3). Resting oxygen uptake, heart rate, and cardiac output increased and heart rate and cardiac output at the same submaximal exercise intensity were higher in the hyperthyroid state (P less than 0.05). However, maximal oxygen uptake decreased after T3 administration (3.08 +/- 0.17 vs. 2.94 +/- 0.19 l/min; P less than 0.001) despite increased heart rate and cardiac output at maximal exercise (P less than 0.05). Plasma lactic acid concentration at an equivalent submaximal exercise intensity was elevated 25% (P less than 0.01) and the arteriovenous oxygen difference at maximal effort was reduced (P less than 0.05) in the hyperthyroid state. These effects were associated with a 21-37% decline in activities of oxidative (P less than 0.001) and glycolytic (P less than 0.05) enzymes in skeletal muscle and a 15% decrease in type IIA muscle fiber cross-sectional area (P less than 0.05). Lean body mass was reduced (P less than 0.001) and the rates of whole body leucine oxidation and protein breakdown were enhanced (P less than 0.05). Thus, exercise tolerance is impaired in short duration hyperthyroidism because of decreased skeletal muscle mass and oxidative capacity related to accelerated protein catabolism but cardiac pump function is not reduced.

Adult↗
PubMed1992

Non-beta-adrenergic-mediated peripheral circulatory hyperkinesia in hyperthyroidism.

Systolic time intervals and brachial circulation, evaluated by pulsed Doppler in terms of arterial diameter, blood velocity and flow, and vascular resistance, were studied in 12 hyperthyroid patients and in 12 normal controls. In patients, arterial circulation was studied before and during mechanical exclusion of the hand, and hemodynamic measurements were repeated after beta-blocker treatment and after obtainment of euthyroid state. Compared with controls, patients had higher heart rate (P < 0.001), lower systolic time intervals (P < 0.05, P < 0.01), and higher blood velocity (P < 0.05). Beta blockade decreased heart rate (P < 0.05, P < 0.001) but did not change systolic time intervals and arterial circulation. Euthyroid state decreased heart rate (P < 0.01), preejection period (P < 0.01), and blood velocity (P < 0.01) and flow (P < 0.05). The decreases in velocity and flow before hand exclusion when euthyroid state was obtained were correlated with hyperthyroid values of velocity and flow respectively (r = 0.85, r = 0.90, P < 0.01, P < 0.001). Vascular resistance during hand exclusion was correlated negatively with serum T3 level during hyperthyroid and euthyroid states. Thus, thyroid hormones but not beta-adrenoreceptors participate in the peripheral hyperkinesia of hyperthyroidism.

Adrenergic beta-Antagonists↗
PubMed1978

Plasma 25-hydroxyvitamin D and alkaline phosphatase isoenzymes in hyperthyroidism.

Plasma 25-hydroxyvitamin D (25-OHD) values in 22 hyperthyroid patients did not differ significantly from those of controls matched for age, sex, and the time of year that plasma samples were taken. In the hyperthyroid group, plasma alkaline phosphatase was significantly higher than in controls, and an increase in bone type alkaline phosphatase occurred in 50%. In the 18 female hyperthyroid patients the plasma gamma-glutamyl transferase was significantly increased compared with controls. Mean values for plasma albumin, alanine transferase, and calcium showed no significant difference between hyperthyroid and control patients.

Alkaline Phosphatase↗
PubMedDate not supplied

Hyperthyroidism and concurrent thyroid cancer.

AIMS AND BACKGROUND: The aim of this study was to analyze the frequency of coexisting hyperthyroidism and thyroid malignancy in endemic goiter areas and review the current literature on the subject. METHODS: During the period January 1984 to June 1998, 1853 patients were examined for hyperthyroidism at the Spedali Civili Hospital of Brescia, Italy; 512 (27.6%) subjects underwent surgery. Of these patients 108 (21%) had Graves' disease, 251 (49%) multinodular toxic goiter (MTG) and 153 (30%) uninodular toxic goiter (UTG). RESULTS: Malignancy was found in 24 (4.7%) patients: 19 females and 5 males with a mean age of 52.2 years (range, 21-76 years). The frequency of cancer in Graves' disease was 6.4%, 5 females and 2 males; in MTG 3.9%, 2 females and 8 males, and in UTG 4.4%, 7 females and 1 male. CONCLUSIONS: Our data confirm previous reports on the frequency of thyroid cancer in hyperthyroidism. This association is more relevant than previously suspected. The frequent coexistence of hyperthyroidism and neoplasia, demonstrated by our study and the most recent literature, underlines the importance of studying and excluding the possibility of neoplastic degeneration by means of a systematic approach.

Adult↗
PubMedDate not supplied

[Is there a relationship between hyperemesis gravidarum and hyperthyroidism?].

UNLABELLED: This retrospective study evaluates the incidence and degree of thyroidal stimulation in patients with hyperemesis, and the correlation between thyroid function, the hCG level and the severity of the hyperemesis gravidarum. The role of antithyroidea is discussed in patients with a gestational hyperthyroidism. The degree of thyroid stimulation on the outcome of the pregnancy was studied. At admission hCG, TSH, FT4, FT3, TSI, anti-TPO and anti-Tg were determined. The severity of the hyperemesis gravidarum was evaluated by the degree of ketonuria, % weight loss, and the electrolytes and the liver function disorders. An ultrasound to confirm the gestational age and to exclude a multiple pregnancy or a trophoblastic disease was carried out. RESULTS: In a period of 1 January '91 to 31 January '94, 48 hyperemesis gravidarumpatients were admitted at the maternity. 22.9% of the hyperemesispatients had thyroid stimulation; 4 patients had a decreased TSH and an increased FT4 (group 2) and 7 patients had a decreased TSH, an increased FT4 and FT3 (group 3). The age of the mother, the parity and the gestational age at admission are comparable, and do not differ from the patients without thyroid disorders (group 1). Parameters, determining the severity of hyperemesis gravidarum, are not significantly different in the 3 groups. Treatment with antithyroidea in the group with proven hyperthyroidism (decreased TSH, increased FT4 and FT3) does not only lead to normalisation of the thyroid tests, but also to an improvement of the symptomatology. The gestational age at delivery and the birthweight of the babies are comparable in the 3 groups. CONCLUSION: In patients admitted with hyperemesis gravidarum, we found 23% of the women to present a thyroid stimulation. This hyperthyroidism differs from the auto-immune hyperthyroidism, i.e. the patients have no thyroid antibodies, no classic clinical signs of thyrothoxicosis. Probably, the absolute hCG concentration and its biological activity plays a crucial role in the thyroid stimulation. This degree of thyroid stimulation has no influence on the severity of the hyperemesis gravidarum, neither on the outcome of the pregnancy.

Adult↗
PubMed2004

The metabolic and cardiovascular effects of hyperthyroidism are largely independent of beta-adrenergic stimulation.

Hyperthyroidism and states of adrenergic hyperactivity have many common clinical features, suggesting similar pathogenic mechanisms of action. The widespread use of beta-adrenergic receptor (betaAR) antagonists (beta-blockers) to treat hyperthyroidism has led to the belief that the physiological consequences of thyroid hormone (TH) excess are mediated in part via catecholamine signaling through betaARs. To test this hypothesis, we compared the response to TH excess in mice lacking the three known betaARs (beta-less) vs. wild-type (WT) mice. Although beta-less mice had a lower heart rate at baseline in comparison to WT mice, the metabolic and cardiovascular responses to hyperthyroidism were equivalent in both WT and beta-less mice. These data indicate that the metabolic and cardiovascular effects of TH excess are largely independent of betaARs. These findings suggest that the efficacy of clinical treatment of hyperthyroidism with beta-blockers is due to antagonism of sympathetic signaling, and that this process functions independently of TH action.

Adrenergic beta-Agonists↗
PubMed2006

Probing the genetic basis for thyrotropin receptor antibodies and hyperthyroidism in immunized CXB recombinant inbred mice.

Immunization with adenovirus encoding the TSH receptor (TSHR) or its A-subunit induces Graves' hyperthyroidism in BALB/c and BALB/c x C57BL/6 offspring but not C57BL/6 mice. High-resolution genetic maps are available for 13 recombinant inbred CXB strains generated from BALB/c x C57BL/6 progeny by repeated brother x sister matings to establish fully inbred lines. CXB strains were studied before and after A-subunit adenovirus immunization for TSHR antibodies (TBI, inhibition of TSH binding), serum T4, and thyroid histology. All strains developed TBI activity (at variable levels), six strains became hyperthyroid, and one was overtly thyrotoxic. No low TBI responders became hyperthyroid, but high TBI did not predict hyperthyroidism. Preimmunization T4 levels varied in different CXB strains and was unrelated to subsequent T4 elevation. Linkage analysis indicated that different chromosomes were involved in generating TSHR antibodies and serum T4 before and after immunization. TBI activity was linked in part with major histocompatibility (MHC) genes on chromosome 17 (Chr 17) but induced Graves' disease involved non-MHC genes (Chr 19 and 10). The Chr 10 locus is close to the Trhde gene that encodes TSH-releasing hormone degrading enzyme. Expression of Trhde is controlled by thyroid hormones and linkage with a thyroid function-related gene is intriguing. Our data, the first genome scan in murine Graves' disease, provides insight into the role of MHC and non-MHC genes in human and murine Graves' disease. Finally, our study demonstrates the potential of recombinant inbred mice for discriminating between immune-response genes and thyroid function susceptibility genes in Graves' disease.

Adenoviridae↗
PubMed1979

The hypothalamic-pituitary-gonadal axis during hyperthyroidism in the rat.

The rat, an animal without testosterone-estrogen-binding-globulin, was treated with L-T4 to the point of hyperthyroidism in order to study the hypothalamic-pituitary-testicular axis during this condition. Hyperthyroidism led to a significant decline in serum FSH, a fall in serum LH which was not satistically significant, and no change in serum levels of testosterone or estradiol. Testes of hyperthyroid rats produced significantly more testosterone during in vitro incubations than did the testes of control animals. We conclude that hyperthyroidism in the rat leads to a fall in FSH levels either via direct pituitary suppression or via accelerated FSH metabolism. In addition, in vitro studies suggest that excess thyroid hormone may stimulate intratesticular 17 beta-hydroxysteroid dehydrogenase.

Animals↗
PubMed1984

The contribution of local thyroxine monodeiodination to intracellular 3,5, 3'-triiodothyronine in several tissues of hyperthyroid rats at isotopic equilibrium.

The local conversion of T4 as a source of intracellular T3 in several organs of both hypothyroid and euthyroid rats has recently been recognized to be an important phenomenon. In the present study the source and quantity of T3 in various peripheral tissues of hyperthyroid rats were investigated. Athyreotic rats received a continuous iv infusion of 3.5 micrograms T4/100 g BW X day over a prolonged period in order to attain hyperthyroid conditions. At the same time, the animals also received a continuous iv infusion of [125I]T4 and [131I]T3 until isotopic equilibrium was achieved. After the animals were bled and perfused, the source and quantity of T3 in various tissue homogenates and subcellular preparations of liver, kidney, and the anterior pituitary gland were analyzed. In spite of the elevated plasma T3 and T4 levels, the concentration of T3 in the cerebral cortex and cerebellum was within the normal range. The contribution of T3 derived from local T4 to T3 conversion [Lc T3(T4)] was rather low in both parts of the brain (cerebral cortex, 26%; cerebellum, 15%) when compared with values previously determined for euthyroid rats (cerebral cortex, 67%; cerebellum, 50%). It is concluded that in the cerebral cortex and cerebellum of hyperthyroid rats normal T3 concentrations were maintained by a compensatory decrease in the degree of Lc T3(T4). Whereas previous studies revealed that Lc T3(T4) contributes significantly to the T3 in the pituitary glands of both hypothyroid and euthyroid rats, this was not the case for the hyperthyroid animals; virtually all T3 was derived from plasma. The elevated plasma T3 levels caused an increased T3 content in both the homogenate and the nuclear fraction, leading to plasma TSH levels which were below the detection limit. It was found that the T3 in muscle was derived exclusively from plasma. Both the liver and kidney showed high concentrations of T3. Whereas Lc T3(T4) was the main source of T3 in the liver, it contributed only a minor fraction of the total T3 content in the kidney. In the liver Lc T3(T4) accounted for 50-53% of the T3 content in the mitochondrial and cytosolic fractions and about 64% in the microsomal fraction. In the kidney there was a small, but significant, amount of Lc T3(T4) in these subcellular fractions. In contrast, in the hepatic nuclei only 13% of the T3 was attributable to Lc T3(T4), whereas no Lc T3(T4) could be detected in the renal nuclei.

Animals↗
PubMed1987

Protein degradation in skeletal muscle during experimental hyperthyroidism in rats and the effect of beta-blocking agents.

beta-Blocking agents are increasingly used in the management of hyperthyroid patients. The effect of this treatment on increased muscle protein breakdown in the hyperthyroid state is not known. In the present study, experimental hyperthyroidism was induced in rats by daily ip injections of T3 (100 micrograms/100 g BW) during a 10-day period. Control animals received corresponding volumes of solvent. In groups of rats the selective beta-1-blocking agent metoprolol or the nonselective beta-blocker propranolol was infused by miniosmotic pumps implanted sc on the backs of the animals. Protein degradation was measured in incubated intact soleus and extensor digitorum longus muscles by determining tyrosine release into the incubation medium. The protein degradation rate in incubated extensor digitorum longus and soleus muscles was increased by 50-60% during T3 treatment. Metoprolol or propranolol did not influence muscle protein breakdown in either T3-treated or control animals. The results suggest that T3-induced increased muscle proteolysis is not mediated by beta-receptors, and muscle weakness and wasting in hyperthyroidism might not be affected by beta-blockers.

Adrenergic beta-Antagonists↗