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PubMed1981

Turnover and splanchnic metabolism of free fatty acids in hyperthyroid patients.

The arterial concentration and turnover rate and the splanchnic exchange of FFA were examined after an overnight fast in a group of 11 female patients with clinical and laboratory evidence of hyperthyroidism. [14C]oleic acid was infused intravenously and the hepatic venous catheter technique was used. As compared with healthy control individuals, the arterial concentrations of FFA and oleic acid were elevated by 30--40% in the hyperthyroid group. Both the turnover rate and the fractional turnover of oleic acid were significantly increased. The turnover rate correlated directly with arterial concentration of oleic acid in both the control and the patient group but the slope was steeper in the patients. The splanchnic uptake of oleic acid was three times higher than in the control group. The augmented uptake was a consequence of elevated arterial concentrations and increased hepatic plasma flow, whereas fractional splanchnic uptake remained unchanged. Ketone body production was four- to fivefold greater in the patients and could be largely accounted for by increased splanchnic FFA uptake. In six patients studied after treatment resulting in a return to normal thyroid function, a significant reduction was observed in arterial FFA, estimated hepatic blood flow, oleic acid turnover, and ketone body production. It is concluded that hyperthyroidism is characterized by increased turnover and splanchnic uptake of FFA and augmented ketogenesis. These findings can be explained on the basis of elevated arterial FFA concentrations and increased blood flow, particularly to the splanchnic bed.

Adult↗
PubMed1985

Substrate cycling between gluconeogenesis and glycolysis in euthyroid, hypothyroid, and hyperthyroid man.

Substrate, or futile cycles, have been hypothesized to be under hormonal control, and important in metabolic regulation and thermogenesis. To define the role of thyroid hormones in the regulation of substrate cycling in glycolysis and gluconeogenesis, we measured rates of cycling in normal (n = 4), hypothyroid (n = 5), and hyperthyroid (n = 5) subjects employing a stable isotope turnover technique. Glucose labeled with deuterium at different positions (2-D1-, 3-D1-, and 6,6-D2-glucose) was given as a primed-constant infusion in tracer doses, and arterialized plasma samples were obtained and analyzed by gas-chromatography mass-spectrometry for the steady state enrichment of glucose that was labeled at the various positions. The rate of appearance (Ra) was then calculated for each isotopic tracer. The difference between the Ra determined by 2-D1-glucose (Ra2) and the Ra determined by 3-D1-glucose (Ra3) represents the substrate cycling rate (SCR) between glucose and glucose-6-phosphate. The difference between the Ra determined by 3-D1-glucose (Ra3) and the Ra determined by 6,6-D2-glucose (Ra6) represents the SCR between fructose-6-phosphate and fructose-1,6-diphosphate. The difference between Ra2 and Ra6 represents the combined SCR of both cycles. In normal subjects (serum thyroxine [T4] = 8.4 +/- 1.2 microgram/dl (all expressions, mean +/- SD), n = 4), the rates of appearance for Ra2, Ra3, and Ra6 were 3.23 +/- 0.56, 2.64 +/- 0.50, and 2.00 +/- 0.27 mg/kg X min, respectively, whereas those in the hypothyroid subjects (T4 = 1.0 +/- 0.8 microgram/dl; n = 5) were 1.77 +/- 0.56 (P less than 0.01), 1.52, 1.57 +/- 0.31 (P less than 0.05) mg/kg X min, respectively. Conversely, the rates of appearance for Ra2 and Ra6 in the hyperthyroid subjects (T4 = 23.9 +/- 3.6 micrograms/dl) were 3.94 +/- 0.43 (P less than 0.05) and 2.54 +/- 0.22 (P less than 0.02), respectively, compared with the normal subjects. On the basis of these data, we noted that the normal subjects had a combined SCR of 1.23 +/- 0.35 mg/kg X min. In contrast, the hypothyroid patients had a significantly decreased combined SCR, 0.20 +/- 0.54 mg/kg X min (P less than 0.02). The hyperthyroid patients had a combined SCR of 1.39 +/- 0.23 mg/kg X min (P less than NS). To determine whether these cycles responded to thyroid hormone treatment, these same hypothyroid subjects were acutely treated for 1 wk with parenteral 50 micrograms/d sodium L-triiodothyronine and chronically with 100-150 micrograms/d L-thyroxine. After 7 d, their mean oxygen consumption rate and carbon dioxide production rate increased significantly from 102+/-13 micromol/kg.min, to 147+/-34 micromol/kg.min (P<0.05), and from 76+/-13 micromol/kg.min to 111+/-19 micromol/kg.min (P<0.05), respectively. The combined SCR (Ra(2)--Ra(6) remained unchanged at 0.07+/-0.37 mg/kg.min. However, after 6 mo of oral L-thyroxine therapy (T(4)=9.5+/-1.4 microgram/kl) the treated hypothyroid patients had increased their combined SCR (Ra(2)--Ra(6)) to 0.86 +/-0.23 mg/kg.min (P<0.02), a value not significantly different from the combined SCR of normal subjects. We conclude that substrate cycling between glucose and glucose-6-phosphate and between fructose-6-phosphate and fructose-1,6-diphosphate occurs in man and is affected by thyroid hormone. Substrate cycles may represent a mechanism by which thyroid hormone alters the sensitivity of certain reactions to metabolic signals.

Adult↗
PubMed1997

Congenital hyperthyroidism caused by a solitary toxic adenoma harboring a novel somatic mutation (serine281-->isoleucine) in the extracellular domain of the thyrotropin receptor.

Activating somatic mutations in the thyrotropin (TSH) receptor have been identified as a cause of hyperfunctioning thyroid adenomas, and germline mutations have been found in familial nonautoimmune hyperthyroidism and sporadic congenital hyperthyroidism. All mutations reported to date have been located in the transmembrane domain. We now report an example of an activating mutation in the extracellular, TSH-binding domain, found in a male infant with congenital hyperthyroidism due to a toxic adenoma. The pregnancy was remarkable for fetal tachycardia. Scintigraphic studies demonstrated a large nodule in the right lobe, and a hemithyroidectomy was performed at the age of 2 yr. Direct sequencing of the TSH receptor gene revealed a mutation in one allele resulting in a substitution of serine281 by isoleucine (Ser281--> Ile) in the extracellular domain. The mutation was restricted to the adenomatous tissue. Expression of the Ser281--> Ile mutation in vitro revealed an increase in basal cAMP levels. Affinity for TSH was increased by the mutation. These findings demonstrate that activating mutations can also occur in the extracellular domain of the TSH receptor, and support a model in which the extracellular domain serves to restrain receptor function in the absence of TSH or antibody-induced conformational changes.

Adenoma↗
PubMed1981

Hyperthyroidism and propylthiouracil-induced agranulocytosis during chronic lithium carbonate therapy.

The authors describe the case of a 49-year-old woman who developed a goiter, mild symptoms of hyperthyroidism, and grossly elevated thyroid function tests after 2 years of treatment with lithium carbonate. Thyroid microsomal autoantibodies were also present. She was retreated with propylthiouracil and improved, but within 3 months she developed agranulocytosis. Propylthiouracil was discontinued, and the patient was treated with antibiotics and recovered. She was then given 131I to control her hyperthyroidism. The case is an example of the rare association of hyperthyroidism with lithium, which usually suppresses thyroid function, and demonstrates that lithium carbonate cannot prevent agranulocytosis caused by propylthiouracil.

Agranulocytosis↗
PubMed1985

Urinary free cortisol levels and dexamethasone suppression testing in organic affective disorder associated with hyperthyroidism.

Eleven of 32 newly diagnosed untreated patients with hyperthyroidism met DSM-III criteria for organic affective syndrome. Thirty of these patients submitted 24-hour urine specimens for measurement of urinary free cortisol levels, and 31 were given a 1-mg dexamethasone suppression test (DST) before antihyperthyroidism therapy was started. There was no difference in the mean +/- SD urinary free cortisol excretion levels between depressed and nondepressed hyperthyroid patients. One nondepressed patient demonstrated nonsuppression (greater than 5 micrograms/dl) at 8:00 a.m. These results suggest that cortisol abnormalities as reflected by urinary free cortisol levels and DST findings are uncommon in patients with hyperthyroidism whether they are depressed or nondepressed.

Depressive Disorder↗
PubMedDate not supplied

Hyperthyroidism as a cause of pulmonary arterial hypertension: a prospective study.

The authors assessed the prevalence of pulmonary arterial hypertension (PAH) in patients with hyperthyroidism and evaluated the response to treatment of the thyrotoxicosis. They assessed the pulmonary artery systolic pressure (PASP) at rest (estimated by echocardiography) in 23 consecutive patients diagnosed with hyperthyroidism due to Graves' disease or toxic multinodular goiter. Twelve of 23 patients (52%) did not show antithyroglobulin and antithyroperoxidase antibodies. Seventeen patients were followed up for at least 9 months after achieving a stable euthyroid status. Fifteen (65%) patients demonstrated PAH at admission. Four patients were lost to follow-up; therefore they were able to evaluate 17 patients serially with echocardiography. Sixteen patients normalized their PASP value: 13 after methimazole, 2 after total thyroidectomy, and 1 after (131)I treatment. In 1 patient no significant change in PASP was observed. This patient experienced an acute myocardial reinfarction during follow-up. They found a higher prevalence than that previously reported in observational studies. In addition, they demonstrated that the PAH reverses after correction of hyperthyroidism. Elevated PASP at rest on echocardiography may be considered a frequent finding of thyrotoxicosis. Moreover, the data seem not to support an autoimmune pathogenesis for PAH.

Adult↗
PubMed1990

Atrial natriuretic factor in untreated hyperthyroidism.

Increased plasma concentration of atrial natriuretic factor (ANF) in untreated hyperthyroid patients is reported. A significant positive correlation between the concentration of ANF and serum thyroid hormones (T4 and T3) has been found when hyperthyroid patients and healthy controls were pooled together. The mechanism by which thyroid hormones raise plasma ANF concentration and its relevance to the symptomatology of hyperthyroidism is discussed.

Adult↗
PubMed1993

Hyperthyroidism after treatment with lithium.

The association between treatment with lithium and hypothyroidism is well documented. Reports of hyperthyroidism are rare and it is less well known among patients treated with lithium. It may be overlooked simply because the clinician will be watching for hypothyroidism, the reverse phenomenon. This paper describes the cases of four patients who have been on long term lithium treatment, all of whom developed Graves' disease, or an atypical form of hyperthyroidism. Some suggestions are offered to account for the mechanism underlying this unusual association. Although hyperthyroidism may be rare among patients receiving lithium, astute clinical observation and appropriate laboratory tests are called for to detect the early stages of such thyroid dysfunction and to provide appropriate intervention.

Adult↗
PubMed1999

Derangement of Kupffer cell functioning and hepatotoxicity in hyperthyroid rats subjected to acute iron overload.

Liver oxidative stress, Kupffer cell functioning, and cell injury were studied in control rats and in animals subjected to L-3,3',5-tri-iodothyronine (T3) and/or acute iron overload. Thyroid calorigenesis with increased rates of hepatic O2 uptake was not altered by iron treatment, whereas iron enhanced serum and liver iron levels independently of T3. Liver thiobarbituric acid reactants formation increased by 5.8-, 5.7-, or 11.0-fold by T3, iron, or their combined treatment, respectively. Iron enhanced the content of protein carbonyls independently of T3 administration, whereas glutathione levels decreased in T3- and iron-treated rats (54%) and in T3Fe-treated animals (71%). Colloidal carbon infusion into perfused livers elicited a 109% and 68% increase in O2 uptake in T3 and iron-treated rats over controls. This parameter was decreased (78%) by the joint T3Fe administration and abolished by gadolinium chloride (GdCl3) pretreatment in all experimental groups. Hyperthyroidism and iron overload did not modify the sinusoidal efflux of lactate dehydrogenase, whereas T3Fe-treated rats exhibited a 35-fold increase over control values, with a 54% reduction by GdCl3 pretreatment. Histological studies showed a slight increase in the number or size of Kupffer cells in hyperthyroid rats or in iron overloaded animals, respectively. Kupffer cell hypertrophy and hyperplasia with presence of inflammatory cells and increased hepatic myeloperoxidase activity were found in T3Fe-treated rats. It is concluded that hyperthyroidism increases the susceptibility of the liver to the toxic effects of iron, which seems to be related to the development of a severe oxidative stress status in the tissue, thus contributing to the concomitant liver injury and impairment of Kupffer cell phagocytosis and particle-induced respiratory burst activity.

Animals↗
PubMed1981

Prolonged effect of nadolol on heart rate in hyperthyroidism.

There is extensive experience in the treatment of hyperthyroidism with beta-blockade. Because of the short half-life of propranolol the drug must be taken in divided doses. The effect of a single daily dose of a long-acting beta-blocking drug, nadolol, was investigated in 7 hyperthyroid patients. A satisfactory and prolonged reduction in heart rate was observed during continuous monitoring over a 24-hour period. Nadolol, therefore, is a possible alternative to propranolol in the treatment of hyperthyroidism with an advantage in the poorly-compliant patient.

Adolescent↗
PubMed2004

Dissociation between iodide-induced thyroiditis and antibody-mediated hyperthyroidism in NOD.H-2h4 mice.

NOD.H-2h4 mice are genetically predisposed to thyroid autoimmunity and spontaneously develop thyroglobulin autoantibodies (TgAb) and thyroiditis. Iodide administration enhances TgAb levels and the incidence and severity of thyroiditis. Using these mice, we investigated the interactions between TSH receptor (TSHR) antibodies induced by vaccination and spontaneous or iodide-enhanced thyroid autoimmunity (thyroiditis and TgAb). Mice were immunized with adenovirus expressing the TSHR A-subunit (or control adenovirus). Thyroid antibodies, histology, and serum thyroxine levels were compared in animals on a regular diet or on a high-iodide diet (0.05% NaI-supplemented water). Thyroiditis severity and TgAb levels were enhanced by iodide administration and were independent of the type of adenovirus used for immunization. In contrast, TSHR antibodies, measured by TSH-binding inhibition, thyroid-stimulating activity, and TSH-blocking activity, were induced in the majority of animals immunized with TSHR (but not control) adenovirus and were unaffected by dietary iodide. The NOD.2h4 strain of mice was less susceptible than BALB/c or BALB/k mice to TSHR adenovirus-induced hyperthyroidism. Nevertheless, hyperthyroidism developed in approximately one third of TSHR adenovirus-injected NOD.2h4 mice. This hyperthyroidism was suppressed by a high-iodide diet, probably by a nonimmune mechanism. The fact that inducing an immune response to the TSHR had no effect on thyroiditis raises the possibility that the TSHR may not be the target involved in the variable thyroiditis component in some humans with Graves' disease.

Adenoviridae↗
PubMed1978

Insulin secretion and the morphological and metabolic characteristics of pancreatic islets of hyperthyroid ob/ob mice.

Thyroxine treatment induced experimental hyperthyroidism in ob/ob mice, inhibited glucose-induced insulin secretion from the isolated perfused ob/ob mouse pancreas, and reduced total pancreas insulin content. In contrast, glucose-induced insulin release from incubated pancreatic islets and insulin content of pancreatic islets from ob/ob mice isolated by freehand microdissection were not reduced after thyroxine treatment when expressed per microgram dry islet. Histological examination of the ob/ob mouse pancreas revealed islets without degenerative lesions of islet cells. Granularity of beta cells was well preserved. The average number of pancreatic islets was unchanged. However, the beta cell area was significantly decreased in relation to the total pancreatic parenchyma after thyroxine treatment. This implies that insulin release and content per pancreatic islet was half of that of the controls. ATP content of islets was slightly reduced. Glucose oxidation and glucose utilization by islets from treated mice were slightly increased. Thyroxine treatment of the animals did not abolish the stimulation of 45Ca2+ uptake by glucose, but it did suppress the potentiating effect of fasting on the stimulatory effect of glucose on 45Ca2+ uptake. The metabolic characteristics of islets from experimentally hyperthyroid mice are those of all hyperthyroid tissues. The results provide no evidence for the view that the effects of thyroxine treatment may be due to disturbed metabolic function or energy deprivation of pancreatic islets. Inhibition of insulin secretion from the pancreas after thyroxine administration is apparently due to a reduction in pancreas insulin content and a diminished pancreatic islet volume. Reduced pancreatic islet volume represents most probably a reduction of individual islet cell volume.

Adenosine Triphosphate↗
PubMed1982

The effect of experimental hyperthyroidism and hypothyroidism on 5'-monodeiodination of 3,3',5'-triiodothyronine and 3',5'-diiodothyronine by rat liver and kidney.

To study the effect of alterations in thyroid status on 5'-monodeiodinase activity, conversions of rT3 to 3,3'-diiodothyronine and 3',5'-diiodothyronine (3',5'-T2) to 3'-monoiodothyronine were examined in vitro. Rats were injected either with T4 (10 micrograms/100 g BW, ip, daily for 12 days) to make them thyrotoxic or thyroidectomized to render them hypothyroid, and liver and kidney homogenates were prepared. Liver homogenates from hyperthyroid animals demonstrated a 2-fold increase in 5'-monodeiodination of both rT3 and 3',5'-T2; both reactions were also significantly increased in the kidneys of hyperthyroid rats. Hypothyroidism produced a significant decrease in 5'-deiodination of both rT3 and 3',5'-T2 in liver and kidney homogenates. These data indicate that the in vitro 5'-deiodination of both rT3 and 3',5'-T2 is increased in hyperthyroidism and decreased in hypothyroidism and suggest that these two iodothyronines are metabolized in a similar fashion in rat liver and kidney homogenates in states of altered thyroid function.

Animals↗
PubMed1984

Effect of hypothyroidism and hyperthyroidism on triiodothyronine production in perfused rat liver.

This study was undertaken to evaluate the effect of altered thyroid states on hepatic T3 production in a functioning intact organ system, the isolated perfused liver. Thyroidectomized rats were treated for 3-4 weeks with vehicle, T4, 1.5 micrograms/100 g-1 day-1, or T4, 20 micrograms/100 g-1 day-1, to produce hypothyroidism, euthyroidism, or hyperthyroidism. Livers were perfused for 1 h with medium containing T4, 10 micrograms/dl, and T3 production was estimated by RIA. T3 production in the hypothyroid, euthyroid, and hyperthyroid groups, respectively, was 1.61 +/- (SE) 0.50, 5.18 +/- 0.55, and 15.62 +/- 1.61 ng/g-1 liver h-1. These differences in T3 production resulted entirely from changes in percent conversion of T4 to T3 which were 0.87 +/- 0.25%, 3.21 +/- 0.38%, and 12.02 +/- 1.82% in the hypothyroid, euthyroid, and hyperthyroid groups, respectively. The measured hepatic uptake of T4 decreased slightly with T4 administration from 188 +/- 13 to 162 +/- 7 and 144 +/- 10 ng/g liver in these same groups. The changes in T3 production were not accounted for by differences in biliary excretion or deiodination of T3. These studies demonstrate a stimulatory effect of T4 on the conversion of T4 to T3 which is important to altering net hepatic T3 production.

Animals↗
PubMed1991

Effects of hyperthyroidism on rat liver glutathione metabolism: related enzymes' activities, efflux, and turnover.

The effect of hyperthyroidism on liver glutathione (GSH) metabolism was studied in fed rats after the administration of 0.1 mg T3/kg body wt, for 1-3 consecutive days. T3-calorigenesis resulted in elevated rates of O2 consumption by the liver, together with higher lipid peroxidative processes and GSH depletion, compared to the euthyroid state. The study of the enzymes related to GSH metabolism revealed no significant changes in the activity of glutathione peroxidase and glutathione reductase, with decreases (27-41%) in the activity of glutathione-S-transferases and marked elevation (133%) in that of gamma-glutamyl transferase, 3 days after T3 treatment. At this experimental time, the activity of the NADPH generating enzyme glucose-6-phosphate dehydrogenase was enhanced by 84% in the liver of T3-treated rats, compared to that in the controls. In these conditions, the canalicular efflux of GSH was not altered by T3, whereas net and fractional rates of sinusoidal GSH efflux were enhanced by 86% and 288%, respectively. The latter effect of hyperthyroidism was found in parallel with an enhancement in sinusoidal lactate dehydrogenase and protein release, suggesting that loss of GSH might be related to a permeabilization of the hepatocyte plasma membrane. Liver GSH turnover assessed after a pulse of [35S]cysteine resulted in a 209% increase in the fractional turnover rate in hyperthyroid rats over controls, under steady state conditions for both hepatic GSH pools, leading to a 62% enhancement in the respective turnover flux. Data suggest that the elevation in the sinusoidal GSH efflux from the liver and in the hepatic capacity to degrade the tripeptide are major mechanisms leading to GSH depletion in the liver of T3-treated rats. As the increased GSH use is not balanced by the elevation in GSH synthesis, a lower steady state level of GSH is attained in the liver.

Animals↗
PubMed2002

Plasma concentration of asymmetric dimethylarginine, an endogenous inhibitor of nitric oxide synthase, is elevated in hyperthyroid patients.

Cardiovascular manifestations are frequent findings in patients with thyroid hormone disorders. Nitric oxide (NO) plays a key role in vascular, endothelial-mediated relaxation. NO is synthesized from L-arginine by NO synthase, an enzyme inhibited by endogenous compounds, mainly asymmetric dimethylarginine [asymmetric N(G),N(G)-dimethyl-L-arginine (ADMA)]. The aim of our work was to investigate whether plasma L-arginine and dimethylarginine concentrations and NO production are altered in hypo- and hyperthyroid patients, compared with control subjects. L-arginine, ADMA and symmetric dimethylarginine were analyzed by HPLC. NO was measured as plasma nitrite plus nitrate (NO(x)) concentration by a colorimetric method based on Griess reagent. L-arginine, ADMA, and symmetric dimethylarginine plasma levels in the hypothyroid group were similar to those of the control group; whereas in hyperthyroidism, these values were significantly increased. However, the L-arginine/ADMA ratio was decreased in hyperthyroid patients, resulting in diminished NO(x) production. When all subjects were analyzed together, free T(4) levels were directly correlated with ADMA and inversely correlated with NO(x).

Adult↗
PubMed2003

The effects of early antithyroid therapy for endogenous subclinical hyperthyroidism in clinical and heart abnormalities.

Subclinical hyperthyroidism has been associated with harmful cardiac effects, but its treatment remains controversial. This study was designed to assess the cardiac effects of the normalization of serum TSH concentration in patients with endogenous subclinical hyperthyroidism. Ten patients (median age, 59 yr; range, 16-72 yr) with normal serum free T(4) and free T(3) concentration and a stable suppression of serum TSH levels were evaluated by Doppler-echocardiography, by standard and 24-h electrocardiography monitoring (Holter), and by the clinical Wayne index. Ten subjects, matched for age and sex, were used as controls. Patients were reevaluated 6 months after achieving stabilized euthyroidism by using methimazole with a median initial dose of 20 mg daily (10-30 mg daily). After reaching euthyroidism, we found a significant decrease in the heart rate (P = 0.008), the total number of beats during 24 h (P = 0.004), and the number of atrial (P = 0.002) and ventricular (P = 0.003) premature beats. Echocardiographical data resulted in a reduction of the left ventricular mass index (P = 0.009), interventricular septum thickness (P = 0.008), and left ventricular posterior wall thickness (P = 0.004) at diastole. Furthermore, the early diastolic peak flow velocity deceleration rate was significantly higher (P = 0.02) in the untreated patients compared with controls. The Wayne clinical index was higher in patients than in controls (P = 0.001) and decreased after treatment (P = 0.004). Serum TSH concentration returned to normal values after 2.5 months (range, 1.0-7.0 months) on methimazole therapy (0.05 vs. 1.42 mU/liter; P = 0.002). Serum free T(4) values were normal in patients before treatment but significantly decreased after reaching the euthyroidism (16.9 vs. 11.5 pmol/liter; P = 0.002). In contrast, serum free T(3) concentration did not differ among the groups. In conclusion, our findings support that early antithyroid therapy should be considered in patients with endogenous subclinical hyperthyroidism, where it is needed to prevent potential progression to a more advanced heart disease.

Adolescent↗
PubMed2004

Treatment of hyperthyroidism associated with thyrotropin-secreting pituitary adenomas with iopanoic acid.

TSH-secreting tumors comprise less than 2% of all pituitary adenomas. All patients present with hyperthyroidism with a detectable TSH level, and a majority have macroadenomas. Oral cholecystographic agents (e.g. iopanoic acid) potently inhibit the activation of T(4) to the more potent T(3). They have been used successfully to treat primary thyroidal hyperthyroidism and thyroxine overdose. However, they have not been employed in the treatment of central hyperthyroidism. We report, herein, the first two patients with thyrotropinomas, in whom iopanoic acid (Telepaque) has been used perioperatively to safely and rapidly achieve euthyroidism. In case 1, free T(3) index improved from a value of 634 to 175 (normal range 78-162) after 3 d of therapy with iopanoic acid. In case 2, free T(3) by dialysis improved from 697 pg/dl (10.7 pmol/liter) to 195 pg/dl (3.0 pmol/liter) (normal range 210-440 pg/dl; 3.2-6.7 pmol/liter) after 7 d of therapy with iopanoic acid.

Adenoma↗