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PubMed1989

Bile acid metabolism in human hyperthyroidism.

Decreased levels of serum cholesterol are a well-recognized finding in hyperthyroidism. Since the conversion to bile acids is an important pathway for the elimination of cholesterol, we studied primary bile acid kinetics in seven hyperthyroid patients before and after medical treatment. Pool sizes, fractional turnover and synthesis rates of cholic acid and chenodeoxycholic acid were determined after oral administration of 50 mg [13C]cholic acid and 50 mg [13C]chenodeoxycholic acid. 13C/12C isotope ratios in serum were measured by capillary gas chromatography/electron impact mass spectrometry. Compared with the euthyroid state, serum cholesterol levels were distinctly lower in hyperthyroidism (150 +/- 33 vs. 261 +/- 51 mg per dl, p less than 0.01). Thyroid hormone excess caused a 34% reduction in cholic acid synthesis (5.8 +/- 2.8 vs. 7.9 +/- 4.2 mu moles per kg per day, p less than 0.02), which was associated with a 47% decrease in cholic acid pool size (11.7 +/- 3.4 vs. 22.0 +/- 5.2 mu moles per kg, p less than 0.01). Chenodeoxycholic acid kinetics exhibited no apparent changes. Thus, total primary bile acid synthesis was diminished by 20% in hyperthyroidism. After normalization of thyroid function, the ratio of cholic acid/chenodeoxycholic acid pool size increased in all patients. This was paralleled by a rise in the ratio of concentrations of cholic acid/chenodeoxycholic acid in serum. The depression of cholic acid synthesis in the presence of unaltered subjects is compatible with an inhibition of hepatic 12 alpha-hydroxylation by thyroid hormone. Furthermore, evidence is provided that, in man, the low serum cholesterol levels found during hyperthyroidism are not caused by an increased conversion of cholesterol to bile acid.

Aged↗
PubMed1983

Reconstitution of heavy chain and light chain 1 in cardiac subfragment-1 from hyperthyroid and euthyroid rabbit hearts.

It is now established that cardiac myosin from hyperthyroid rabbit hearts (TXM) exhibits high Ca2+ ATPase activity. The high Ca2+ ATPase activity of TXM was completely retained in cardiac myosin subfragment-1 (S-1) (1.33 +/- 0.04 mumol Pi/mg per min; euthyroid, 0.51 +/- 0.04). Cardiac S-1 from hyperthyroid and euthyroid rabbits (TXS-1 and NS-1) had the same pattern in SDS-polyacrylamide gel electrophoresis. The possible influence of heavy and light chains of TXM on increasing the ATPase activity was examined by reconstitution in the S-1 preparation. Crosswise reconstitution was performed using cardiac S-1 heavy chain (90,000 daltons) and light chain 1 (LC1) (27,000 daltons) from hyperthyroid and euthyroid hearts. Reconstitution was verified by using radiolabeled LC1. More than 95% of S-1 was recovered with full ATPase activity. When TXS-1 was reconstituted with LC1 from euthyroid hearts, the reconstituted molecule retained high ATPase activity. On the other hand, NS-1 reconstituted with LC1 from hyperthyroid hearts failed to increase the ATPase activity. The ATPase activity of S-1 was determined by the source of the heavy chain. These results suggest that the high Ca2+ ATPase activity of cardiac myosin and S-1 from hyperthyroid animals arises from the molecular alteration of the heavy chain induced by thyroxine administration.

Animals↗
PubMed1996

The influence of hyperthyroidism on beta-adrenoceptor-mediated relaxation of isolated small mesenteric arteries.

We investigated the influence of hyperthyroidism on relaxant responses of small mesenteric resistance arteries to beta-adrenoceptor agonists and to compounds stimulating the corresponding second-messenger system. Hyperthyroidism was induced by feeding rats for 28 days with 5 mg/kg L-thyroxine (T4)-containing rat chow. This treatment produced a stable hyperthyroid state, as indicated by several biochemical/metabolic and haemodynamic parameters. Preparations of small mesenteric arteries were mounted in an isometric wire myograph. Subsequently, concentration-effect curves were determined for isoproterenol, noradrenaline and salbutamol as well as for forskolin, dibutyryl-cAMP and theophylline. We also determined concentration-effect curves to the beta-adrenoceptor agonists in the presence of ICI 118,551 and CGP 20712A (i.e., in the presence of a selective beta 2- and beta 1-adrenoceptor antagonist, respectively). Apparent pA2-values were calculated to determine which beta-adrenoceptor subtype causes vasodilation. These experiments indicate that beta-adrenoceptor-mediated vasodilation involves both beta 1- and beta 2-adrenoceptors in mesenteric resistance vessels of both hyperthyroid and control rats. In our experiments hyperthyroidism has a sensitizing influence on vascular responses induced by the beta-adrenoceptor agonist isoproterenol and the selective beta 2-adrenoceptor agonist salbutamol. Sensitization to isoproterenol was abolished in the presence of ICI 118,551, whereas it was emphasized in the presence of CGP 20712A. Although this was not fully supported by the results obtained with noradrenaline, these results indicate that the sensitization to beta-adrenoceptor agonists is probably limited to the beta 2-adrenoceptor/G-protein complex and not associated with alterations of the corresponding second messenger system.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1982

Influence of hyperthyroidism on the kinetics of methimazole, propranolol, metoprolol and atenolol.

The kinetic profiles of oral methimazole 40 mg, propranolol 80 mg, metoprolol 100 mg and atenolol 100 mg were compared in hyperthyroid patients both during the hyper- and euthyroid states. for methimazole, neither the peak concentration (Cmax), the time to reach peak concentration (tmax), the elimination half-life (t 1/2) nor the area under the curve (AUC) value was affected by the hyperthyroid state. For propranolol and metoprolol, which undergo extensive presystemic clearance, the AUC values were lower (p less than 0.02) when the patients were hyperthyroid than when they had become euthyroid, but the t 1/2's were not significantly altered. For atenolol, there were no significant kinetic differences between the hyperthyroid and euthyroid states. The findings are compatible with the assumption that hyperthyroidism does not affect the kinetics of methimazole or atenolol, but that it may enhance presystemic clearance of propranolol and metoprolol.

Administration, Oral↗
PubMed1980

In vivo glucose turnover in hypo- and hyperthyroid starved rat.

The effect of hypo- and hyperthyroidism on glucose turnover in vivo was determined in unanesthetized rats starved for 48 h. Glucose pool and decay rate of specific radioactivity of blood glucose was measured after bolus injection of a mixture of 3H-(2)- and 14C-(U)-glucose under steady state conditions. Compared with euthyroid controls (= 100%), hypothyroidism resulted in a decrease of blood glucose concentration (81%), glucose pool (52%), glucose disappearance rate (39%), and total glucose recycling (12%). In contrast, hyperthyroidism led to an increase of blood glucose concentration (148%), glucose pool (121%), glucose disappearance rate (185%), and total glucose recycling (163%). T 1/2 for glucose was calculated to be 46 min in the hypo-, 34 min in the eu-, and 22 min in the hyperthyroid state. The concentration of circulating glucoregulatory hormones, corticosterone and glucagon were elevated in hyperthyroid rats, while glucagon was diminished in hypothyroid animals. No difference in the level of insulin was found. These data demonstrate that glucose turnover in vivo is a function of the thyroid state being reduced in hypo- and considerably increased in hyperthyroidism.

Animals↗
PubMed1986

Effects of isoproterenol on rubidium transport in slow- and fast-twitch muscles from euthyroid and hyperthyroid rats.

The influence of experimental hyperthyroidism on the catecholamine induced stimulation of rubidium ion transport in the soleus (SOL), a slow-twitch muscle and the extensor digitorum longus (EDL), a fast-twitch skeletal muscle of rats was studied. Thyroxine administration (800 micrograms/kg/day), for ten days induced a rise of ouabain-sensitive 86Rb uptake in SOL muscle, without affecting the ouabain-insensitive uptake, whereas both fractions of 86Rb uptake were increased in EDL muscle from hyperthyroid rats. Isoproterenol (5 mumol/l) caused a two-fold rise in ouabain-sensitive Rb uptake of euthyroid SOL muscle, while in hyperthyroid SOL it could stimulate only the ouabain-insensitive fraction of 86Rb influx. On the other hand, the stimulating action of isoproterenol on euthyroid EDL muscle was due to an enhancement of ouabain-insensitive Rb uptake, but in hyperthyroid EDL it failed to stimulate the ouabain-insensitive transport and caused a marked rise in ouabain-sensitive Rb uptake. The changes in catecholamine mediated transport properties in SOL muscle may be related to fibre type transformation induced by thyroid hormone, although in EDL the changes of catecholamine stimulation are unlikely due to fibre type conversion. Basal and isoproterenol stimulated cAMP levels were significantly reduced in both EDL and SOL muscles from hyperthyroid rats, in contrast with an insignificant decrease in net rubidium uptake caused by isoproterenol at the same concentration.

Animals↗
PubMedDate not supplied

Experimental hyperthyroidism III: Contractile responses to propranolol of the intact heart and of the isolated ventricular myocardium.

The effect of propranolol on cardiac mechanics and haemodynamics was examined on isolated papillary muscle as well as in situ in the closed thorax in euthyroid and hyperthyroid cats. Under propranolol there occurred on isolated papillary muscle significant decreases of muscle contraction, contraction velocity, isometric tension rise velocity and load and velocity values of simultaneously determined force-velocity relations. The 50% decrease of the values found was demonstrable at ca. 5--8 mu/ml for euthyroidal muscles, at 0.3--0.5 mug/ml for hyperthyroidal muscles. Contractility indices determined in situ (dp/dtmax, VCEmax, extrapolated Vmax) showed in hyperthyroidism at equal propranolol concentration a decrease about twice as great as in euthyroidism. The findings, showing a raised responsiveness of the ventricular myocardium in experimental hyperthyroidism to the negative inotropic effect of propranolol are discussed with regard to the therapeutic use of propranolol in hyperthyroidism.

Aged↗
PubMedDate not supplied

Experimental hyperthyroidism I. Hemodynamics and contractility in situ.

The influence of experimental hyperthyroidism (intraperitoneal injection of crystalline L-thyroxine 1 mg/kg/day, 8-18 days) on cardiac mechanics in contractility in situ were studied in 30 hyperthyroid cats and compared with an euthyroid control group (n equals 30). 1. In hyperthyroidism left ventricular weight was considerably increased. Hypertrophy in hyperthyroidism represents a special case of myocardial hypertrophy, associated with an increase of myocardial performance. 2. Heart rate, systolic pressure, cardiac index, external cardiac work and tension time index were increased by 60-180 per cent. 3. Indices of contractility (dp/dtmax, t-dp/dtmax, dp/dtmax/IP) as well as isovolumetric force velocity relationships and VCE-max and Vmax demonstrated a considerable increase of contractility. Maximum rate isovolumetric pressure fall was increased by 120 per cent. Experimental hyperthyroidism is characterized by hypercirculation associated with increases of pressure, volume and velocity factors. The results are discussed with regards to the effects of increased cardiac mechanics on myocardial energy balance.

Animals↗
PubMedDate not supplied

The role of calcium in the enhanced myocardial contractility of the hyperthyroid rat heart.

The hyperthyroid rat myocardium exhibits enhanced contractility. There is evidence that altered calcium handling by the myocardium may be responsible for this enhanced state. To investigate this, isolated hyperthyroid and euthyroid hearts were perfused in the working mode and exposed to alterations in external calcium concentration. Heart rate was not significantly different in either group of hearts, nor was it altered by the change in calcium. The concentration of calcium needed to elicit half-maximal contractility (dP/dtmax) was lower in the hyperthyroid (0.81 +/- 0.07 mM) than in the euthyroid hearts (1.12 +/- 0.09 mM, p less than 0.05). This increase in calcium sensitivity was unlikely to be at the site of the sarcolemma as verapamil exerted equal negative inotropic effects on both groups of hearts. Dantrolene, which blocks calcium release from the sarcoplasmic reticulum, exerted a significantly greater (p less than 0.01) depression in dP/dtmax after 12 min in the hyperthyroid (50 +/- 7%) than in the euthyroid heart (15 +/- 2%). We conclude from our results that the enhanced contractile state of the hyperthyroid rat heart is likely to involve an altered mechanical response to calcium which is possibly at the level of enhanced calcium release from the sarcoplasmic reticulum.

Animals↗
PubMed1984

The inflammatory response of hyperthyroid and hypothyroid rats. Role of adrenocortical steroids.

The capacity to respond to inflammatory stimuli was tested in hyperthyroid and hypothyroid rats when thyroid defects, induced by hormone administration or thyroparathyroidectomy, respectively, were fully established. Whereas hyperthyroid rats presented consistently depressed inflammatory responses, hypothyroid rats responded in a normal fashion. Decreased reactions to intracutaneously injected histamine and serotonin, inhibited swelling reaction to carrageenin, injected into one of the hind paws, and depressed primary and secondary reactions to adjuvant (heat-killed M. tuberculosis), only occurred in the hyperthyroid group. In addition, only in this group of animals enlargement of the adrenal glands, reduced content of adrenal ascorbic acid, and decreased number of circulating eosinophils, which characterize a circumstance of adrenal cortical hyperactivity, were observed. A spontaneous reversal of the acute inflammatory response of hyperthyroid animals to carrageenin occurred 3-4 days after interruption of hormone administration, and this was coincidental with the return to normal of the previously enlarged adrenal glands. Similarly, specific inhibition of adrenal cortical steroid biosynthesis in hyperthyroid rats with aminoglutethimide, restored the previously depressed response to carrageenin, without interference with the increased levels of seric thyroxin, thus suggesting that the inhibitory effects of thyroid hormones on inflammatory responses are likely to be indirect. It is concluded that an excess of circulating thyroid hormones, but not their deficiency, can impair the development of inflammatory reactions, and that this effect, at least partially, depends on an increased secretion of adrenal corticosteroids.

Adrenal Cortex Hormones↗
PubMed1991

Hyperthyroid dog left ventricle has the same oxygen consumption versus pressure-volume area (PVA) relation as euthyroid dog.

We studied the effects of hyperthyroidism on the relation between O2 consumption (Vo2) and the pressure-volume area (PVA) of the left ventricle (LV) in dogs. PVA is a measure of the total mechanical energy generated per beat of LV. Dogs were treated by daily intramuscular injection of 0.3 or 1.0 mg/kg L-thyroxine over 2-5 weeks. Hyperthyroid dogs had a 40 times higher serum T4, a 40% higher sinus heart rate, and a 35% higher LV Emax (an index of ventricular contractility) than euthyroid dogs. Hyperthyroid dog hearts had linear Vo2-PVA relations like euthyroid dog hearts. The regression line was Vo2 = A x PVA + B, where A was 2.30 (dimensionless) and B was 0.53 J/beat per 100 g LV. B was significantly increased with dobutamine and decreased with propranolol, whereas A was not significantly changed by them. These A and B values were comparable to euthyroid data. Hyperthyroidism did not significantly affect myosin Ca-ATPase activity and V3-type myosin predominance, but increased the speed of the force transient response to length perturbation by 20%-70%, suggesting similar increases in crossbridge cycling rate. We conclude that in spite of accelerated crossbridge cycling rate the Vo2-PVA relation was not altered by hyperthyroidism in dogs.

Animals↗
PubMed1984

Lipid composition of liver mitochondria and microsomes in hyperthyroid rats.

Triiodothyronine-induced alteration of the lipid pattern in rat-liver mitochondria and microsomes has been investigated. In mitochondria, a 25% total cholesterol decrease and a 14% phospholipid increase have been detected. In these hyperthyroid rat liver organelles, a strong decrease in the total cholesterol/phospholipid molar ratio occurs. On the contrary, in microsomes from the same animals, a decrease of about 23% has been measured for both total cholesterol and phospholipids; hence, in this fraction, the total cholesterol/phospholipid molar ratio is unaffected by hyperthyroidism. The liver mitochondrial phospholipid composition, unlike the microsomal composition, is altered significantly in hyperthyroid rats; a 7.4% phosphatidylcholine decrease is accompanied by a similar additive percentage increase of both phosphatidylethanolamine and cardiolipin. In regard to total phospholipid fatty acid composition in liver microsomes from hyperthyroid rats, no variation has been observed compared with the control rats, whereas in mitochondria from the same animals, a meaningful linoleic acid decrease with a similar arachidonic acid increase has been found. In addition to fatty acid alteration, the separated mitochondrial phospholipid classes also exhibit some increase in stearic acid. Among phospholipids, cardiolipin changes the most of the esterified fatty acids in hyperthyroid rat liver. In this compound, a strong increase in the percentage of both palmitic and stearic acid and a 32.4% decrease of linoleic acid have been found.

Animals↗
PubMedDate not supplied

Influence of exogenous ATP on blood sugar, serum insulin and serum free fatty acids in short-term experimental hyperthyroid dogs and in euthyroid controls.

We studied the influence of ATP administration on blood sugar (BS), serum immunoreactive insulin (IRI) and serum free fatty acid (FFA) responses to glucose-induced hyperglycemia in short-term experimental hyperthyroid (STEH) dogs and in euthyroid controls. Hyperthyroidism was induced by a 10-day s.c. treatment with 100 micrograms/kg body weight 1-thyroxine. Glucose challenge was performed by i.v. infusion (700 mg/kg body weight as a priming dose, followed by 20 mg/kg body weight/min for 60 min). ATP (1 mg/kg body weight/min) was infused for 100 min 40 min before and 60 min during glucose administration). Glucose-induced hyperglycemia was more prolonged in the hyperthyroid group. ATP treatment did not affect the BS profile of controls but raised that of STEH animals. In the normal controls the insulinemic response to hyperglycemia was enhanced during ATP infusion. By contrast, in the STEH dogs insulin levels during glucose infusion was lower than in controls and did not significantly increase when ATP was added. ATP infusion induced a significant elevation of serum FFA, which was more pronounced in hyperthyroid animals with a greater fall during glucose administration and a marked increase during the period of recovery from hyperglycemia. In conclusion, we postulate that short-term hyperthyroidism in dogs may inhibit adenylate cyclase function in pancreatic B-cells and chiefly stimulate the action of cAMP-phosphodiesterase activity, thereby affecting insulin secretion.

Adenosine Triphosphate↗
PubMedDate not supplied

Severe acute renal failure due to tubulointerstitial nephritis, pancreatitis, and hyperthyroidism in a patient during rifampicin therapy.

It is well known that rifampicin can cause nephrotoxicity. Rifampicin-related pancreatitis and hyperthyroidism are rarely reported in the same patient in the presence of tubulointerstitial nephritis. Reported herein is the medical management of a patient with hemolytic anemia, acute renal failure, pancreatitis, and hyperthyroidism during with rifampicin therapy. A 50-year-old man was admitted to the hospital owing to abdominal colic and acute renal failure. He was treated with 2 courses of tetracycline-rifampicin for brucellosis 3 weeks and 4 months prior to admission. Physical examination showed blood pressure of 130/70 mm Hg, pulmonary crackles, and edema. Laboratory findings are detailed in the case report. Findings of abdominal ultrasonography suggested edematose pancreatitis and thyroid ultrasonography showed several solid nodules. Renal biopsy showed tubulointerstitial nephritis. Although rifampicin-related tubulointerstitial nephritis and acute renal failure are not uncommon during rifampicin therapy, the convergence of hyperthyroidism, pancreatitis, tubulointerstitial nephritis, and acute renal failure rarely presents in the same patient. Although pancreatitis, tubulointerstitial nephritis, and acute renal failure were ameliorated with corticoid therapy within 2 months, hyperthyroidism continued and required antithyroid therapy. In conclusion, rifampicin may trigger hyperthyroidism in patients with goiter.

Acute Kidney Injury↗
PubMed2002

Blood coagulation and fibrinolysis in patients with hyperthyroidism.

Several papers concerning abnormalities of blood coagulation and fibrinolysis during hyperthyroidism, have been published. Increased von Willebrand Factor (vWF) activity and high fibrinogen levels have been reported. However, there is controversy concerning the presence of a hypercoagulable state in hyperthyroidism. We investigated various hemostatic parameters in 41 hyperthyroid patients and compared them to 20 euthyroid controls. Prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, factors V, VII, VIII, IX and X activities, vWF, antithrombin III (AT III), protein C, protein S, tissue plasminogen activator (t-PA) and tissue plasminogen activator inhibitor-1 (PAI-1), as well as common lipid variables, were measured. The relationships between serum thyroid hormones and these hemostatic parameters were examined. Compared with control subjects, fibrinogen, factor IX, vWF, AT III and PAI-1 were significantly increased in patients (p<0.05, p<0.0001, p<0.05, p<0.01 and p<0.0001; respectively), whereas factor X and t-PA were decreased (p<0.05). We showed that free T4 (FT3) levels were correlated with factor VIII activity (r=0.35, p<0.05). FT4, FT3 and TSH did not correlate with fibrinogen, vWF, AT III, t-PA, or PAI-1. AT III was inversely correlated with factor VII activity (r=-0.48, p<0.01). Protein C and S were correlated with vWF levels (r=0.58, p<0.0001; r=0.55, p<0.0001, respectively). Protein C was inversely correlated with t-PA (r=-0.39, p<0.01). There was a negative correlation between triglycerides, LDL-C and F X (r=-0.45, p<0.05; r=-64, p<0.01, respectively). Mean platelet volume (MPV) was correlated with anti-thyroid peroxidase (TPO) antibodies (in Graves'disease) and F IX activity (r=0.57, p<0.05 and r=0.39, p<0.05; respectively). We found important differences in the coagulatory /fibrinolytic parameters between the hyperthyroid patients and healthy controls. Hyperthyroid patients may experience vascular endothelial dysfunction and decreased fibrinolytic activity in blood. This endothelial activation may represent a situation with a higher thromboembolic potential.

Adenoma↗
PubMed2004

Relationship between management of hyperthyroidism and course of the ophthalmopathy.

The relationship between treatment for hyperthyroidism and course of Graves' ophthalmopathy (GO) has been and still is a matter of debate. Literature often presents conflicting data, due to several influencing factors, such as selection bias, nonrandomized and uncontrolled or retrospective features of many studies, nonstandardized evaluation of ocular changes. However, it seems clear that neither antithyroid drug treatment nor thyroidectomy affect the natural course of GO, while radioiodine therapy may cause, in about 15% of cases, GO progression. The latter is more likely in patients who smoke, have pre-existing GO and more severe hyperthyroidism, or whose post-radioiodine hypothyroidism is not promptly corrected by L-thyroxine. GO progression after radioiodine therapy can be prevented by concomitantly treating patients with glucocorticoids, thus making radioiodine therapy a safe procedure also in GO patients. The presence of GO should not, therefore, influence the choice of treatment for hyperthyroidism. Should antithyroid drug treatment or thyroidectomy be selected for patients with mild ophthalmopathy, no treatment for GO is necessary, while a short course of moderate doses of glucocorticoids is advised if radioiodine therapy is chosen. In patients with severe GO, treatment of hyperthyroidism and management of GO proceed independently of each other, and either definitive (radioiodine or thyroidectomy) or conservative (antithyroid drugs) treatment for hyperthyroidism can be selected while treating GO. The authors' preference goes to the former, because it depletes intrathyroidal autoreactive T lymphocytes and removes thyroid antigens, which are likely to be involved in the pathogenesis of autoimmune reactions of the ophthalmopathy.

Antithyroid Agents↗
PubMed2006

Endothelial dysfunction in subjects with subclinical hyperthyroidism.

Numerous clinical and experimental reports suggest that a high von Willebrand factor (vWf) level reflects endothelial damage or endothelial dysfunction. The present study was designed to evaluate vWf in subclinical hyperthyroidic subjects compared with euthyroidic subjects. We selected 20 subclinical hyperthyroidic subjects and 20 euthyroidic control subjects matched for age, gender and body mass index. The level of vWf was significantly higher in the subclinical hyperthyroidic group than in the euthyroidic group (42.9+/-9.6 vs 37.6+/-6.4%, p=0.026). In conclusion, our results suggest that subjects with subclinical hyperthyroidism tend to have an endothelial dysfunction. Endothelial dysfunction could contribute to increasing the cardiovascular risk in subclinical hyperthyroidism.

Adult↗
PubMed1998

Role of colestipol in the treatment of hyperthyroidism.

The enterohepatic circulation of thyroxine (T4) and triiodothyronine (T3) is higher in thyrotoxicosis. Bile-salt sequestrants bind iodothyronines and thereby increase their fecal excretion. We, therefore, evaluated the effect of colestipol-hydrochloride administration on clinical and biochemical indices of patients with hyperthyroidism. In a prospective, controlled trial, ninety-two adult volunteers with Graves' disease, toxic autonomous nodule or toxic multinodular goiter were randomly assigned into the following treatment protocols: Group 1, 30 mg of methimazole (MMI) and 20 g of colestipol-hydrochloride (COL) daily; Group 2, 30 mg of MMI daily; and Group 3, 15 mg of MMI 20 g of COL daily. The patients were further classified into Group A, severe hyperthyroidism (baseline levels of total T3 (TT3) > or =5 nmol/l) and Group B, mild to moderate thyrotoxicosis (baseline levels of TT-3<5 nmol/l). Crook's clinical index, serum free T4 (FT4), TT3 and thyroid stimulating hormone (TSH) levels were determined before (WO), following one week (W1) and two weeks (W2) of treatment. Serum TT3 level decreased (mean+/-SE) at W1 by 40.8+/-2.6% of WO in Group1 and by 29.2+/-2.4% in Group 2 (p<0.001), and down further to 47.8+/-3.0% at W2 in Group 1, and 40.6+/-2.8% in Group 2 (p=0.01). Serum FT4 level decreased (mean+/-SE) from WO to W1 by 31.7+/-2.7% in Group 1 and by 16.2+/-3.1% in Group 2 (p=0.005), and down to 49.1+/-2.8% of WO at W2 in Group 1 and to 38.7+/-3.5% in Group 2 (p=0.07). In sub groups B COL was not effective in reducing thyroid hormone levels nor in ameliorating the clinical status of the patients. However, in Group A3 COL lowered FT4 (p=0.001) and TT3 (p=0.05) levels as compared to group A2. At W2 the clinical hyperthyroidism score improved faster in Group A1 (p<0.001) and Group A3 (p=0.012) as compared to the control Group A2. In conclusion, COL is an effective and well tolerated adjunctive agent in the treatment of hyperthyroidism. Its main effect is in severe cases of thyrotoxicosis, and in the first phase of treatment. As adjunctive COL treatment in hyperthyroidism allows reducing MMI dosage it may decrease the rate of dose dependent MMI side effects.

Adult↗