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PubMed1999

Liver volume, portal vein flow, and clearance of indocyanine green and antipyrine in hyperthyroidism before and after antithyroid treatment.

BACKGROUND: The aim of the study was to examine liver volume, portal vein flow, and indocyanine green (ICG) and antipyrine clearance in hyperthyroidism before and after antithyroid drug treatment. METHODS: Liver volume and blood flow in the portal vein were investigated in nine fasting patients with hyperthyroidism by means of computed tomography scan and Doppler ultrasound, respectively. ICG clearance was estimated by bolus injection of ICG (0.5 mg/kg body weight) and antipyrine clearance with a one-sample technique. All patients were investigated before and after 3 months of antithyroid treatment, when euthyroidism had been achieved. The Wilcoxon matched-pairs test was used for statistical analysis. RESULTS: The median liver volume increased by 238 (155-289) ml (median, 95% confidence interval), corresponding to 19%, and the weight by 5.0 (0.0-8.0) kg (8%), and the antipyrine clearance decreased by 8 (3.1-34.4) ml/min (16%). These changes were all significant (P < 0.05). The relation between liver volume and body weight increased from 19.9 (16.5-23.7) ml/kg to 21.4 (17.1-21.9) ml/kg (P = 0.11). The liver blood flow as estimated by ICG clearance and Doppler ultrasound was not altered significantly after the treatment period (P = 0.07 and 0.77, respectively). CONCLUSIONS: The liver volume increased by 19% in nine hyperthyroid patients during treatment with antithyroids. Antipyrine clearance was reduced by 16%, whereas liver blood flow, as estimated by ICG clearance and Doppler ultrasound examination of portal vein flow, was not significantly altered. A differential regulation of liver volume and oxidative metabolic capacity in hyperthyroidism was seen.

Adult↗
PubMed2000

Lung responses to hypothyroidism, hyperthyroidism, and lipopolysaccharide challenge in rats.

The objectives of this investigation were to study the effects of hypo- and hyperthyroidism on some factors involved in lung injury under basal conditions (air exposure) and during an inflammatory response induced by inhalation exposure to lipopolysaccharide (LPS; 100 microg/ml; 3 h) in adult rats. Thyroid status was altered by thyroidectomy or thyroxine injections for 15 d. Hyperthyroidism alone caused a greater degree of lung cell damage, an increase in the permeability of the alveolar-capillary barrier, a rise in the total number of phagocytic cells obtained by bronchoalveolar lavage (BAL), and enhanced nitric oxide (NO) release by phagocytic cells relative to that in euthyroid control animals. Hypothyroidism alone was associated with opposite effects. Exposure of animals to LPS produced inflammatory responses, which included significant increases in lung cell damage, permeability of the alveolar-capillary barrier, number of phagocytic cells obtained by BAL, and NO production by the phagocytic cells. In general, hyperthyroidism enhanced the effects of LPS, while hypothyroidism reduced LPS-induced responses. These results suggest that thyroid status alone can affect some of the factors involved in lung injury and also modulate some of the inflammatory effects of LPS. Hyperthyroidism tends to enhance lung injury, while hypothyroidism seems to reduce lung injury.

Albumins↗
PubMed1999

Thyroid function and energy intake during weight gain following treatment of hyperthyroidism.

OBJECTIVE: Individuals with hyperthyroidism lose weight despite increased appetite and food intake, and weight is regained after treatment of hyperthyroidism. We asked whether this weight regain is purely a function of lowered metabolic rate coincident with lowered thyroid hormone concentrations or if the weight gain is related to food-energy overconsumption. METHODS: Ten unselected patients with hyperthyroidism treated with 131I were studied. The following measurements were made at 0, 1, 2, 3, 6, and 12 months: total food energy, carbohydrate, fat and protein consumption; serum thyroxine (T4); serum triiodothyronine (T3); T3 resin uptake; serum thyroid stimulating hormone (TSH); weight; height; and 24-hour urinary urea excretion. RESULTS: Inverse changes in body weight and food energy consumption/kg throughout the period of observation was a striking finding (mean initial weight 67.1+/-5 kg, final weight 76.4 kg+/-3 kg, premorbid weight 77.1+/-5 kg). The initial and final food energy intake was 3005+/-199 and 2597+/-137 Kcal/24 hrs, respectively. The thyroid hormone concentrations declined inversely relative to weight gain during the first months of the study, but later the thyroid hormones increased while weight gain continued. Initial serum T4 15.0+/-1 value at three months was 4.0+/-1.0 mg/dl, final T4 11.0+/-1. CONCLUSION: We conclude that weight gain following treatment of hyperthyroidism is due to 1) reduction in metabolic rate consequent upon the decreased thyroid hormone concentrations and 2) food energy intake which was initially greater than required to maintain individuals' premorbid weight. As body weight increased, food intake declined and both reached an asymptotic limit.

Adult↗
PubMed2006

Subclinical hyperthyroidism due to a thyrotropin receptor (TSHR) gene mutation (S505R).

AIM: To identify the molecular defect by which non-autoimmune subclinical hyperthyroidism was caused in a 6-mo-old infant who presented with weight loss. METHODS: Congenital non-autoimmune hyperthyroidism is caused by activating germline mutations in the thyrotropin receptor (TSHR) gene. Therefore, the TSHR gene was sequenced directly from the patient's genomic DNA. RESULTS: Molecular analysis revealed a heterozygous point mutation (S505R) in the TSHR gene as the underlying defect. CONCLUSION: A constitutively activating mutation in the TSHR gene has to be considered not only in patients with severe congenital non-autoimmune hyperthyroidism, but also in children with subclinical non-autoimmune hyperthyroidism.

Adult↗
PubMed2004

Hyperthyroidism six years post-BMT for acute myeloblastic leukemia in a patient on long-term lithium therapy for bipolar affective disorder.

Lithium is commonly used to treat bipolar affective disorder. It is well known to adversely affect thyroid function, most commonly causing hypothyroidism. Hyperthyroidism is a rare complication. Similarly, total body irradiation (TBI) associated with BMT is well known to affect thyroid function frequently causing hypothyroidism. Hyperthyroidism secondary to TBI is unusual. To have both a history of chronic lithium therapy and TBI with a BMT in patient presenting with hyperthyroidism is an extremely atypical situation. We describe a 39-year-old male who presented with primary hyperthyroidism after 18 years of lithium use for bipolar affective disorder and 6 years post-BMT for AML-M4.

Adult↗
PubMed2001

Effects of oxidative stress on the erythrocyte Na+,K+ ATPase activity in female hyperthyroid patients.

This study was planned to determine the effects of free-radical-induced damage on the Na+,K+-ATPase activity of erythrocytes during hyperthyroidism and 4 wk after propylthiouracil (PTU) therapy (400 mg/d). The levels of plasma thiobarbituric acid-reactive substances (TBARS) as a marker of lipid peroxidation, erythrocyte glutathione (GSH) concentration as an antioxidant, blood ATP concentration, and erythrocyte membrane Na+,K+-ATPase activity were determined in female hyperthyroid patients (n = 22, mean age 40.5 +/- 6.5 yr). Before the PTU therapy, plasma TBARS concentration was significantly higher and the levels of blood ATP and erythrocyte GSH and the activity of membrane Na+,K-+-ATPase were significantly lower in the hyperthyroid patients (n = 15 women, mean age 40.8 +/- 7.3 yr). Four weeks after PTU therapy, plasma TBARS concentration was decreased, and levels of erythrocyte GSH and blood ATP and of Na+,K+-ATPase activity of erythrocytes were elevated in the treated patients. There was a significant positive correlation between blood ATP concentration and Na+,K+-ATPase activity, and a negative correlation between plasma TBARS concentration and Na+,K+-ATPase activity before PTU. Our results might help to clarify the effects of the oxidative mechanisms on the erythrocyte membrane Na+,K+-ATPase activity in hyperthyroid patients.

Adenosine Triphosphate↗
PubMed2001

Oxidative stress in heart tissue of hyperthyroid and iron supplemented rats.

This study was designed to investigate the effect of hyperthyroidism and/or iron supplementation or cardiac oxidative stress parameters--the lipid peroxidation end product glutathione (GSH), glutathione peroxidase (CSH-Px), and superoxide dismutase (CuZnSOD)--in rats. In plasma, ferritin as an indicator of iron status and glutamate oxaloacetate transaminase (GOT) as an indicator of damage to the heart tissue were analyzed. Our findings show that hyperthyroidism increased lipooxidative damage as reflected by higher lipid peroxidation end product levels and elevated antioxidant defense parameters-GSH and GSH-Px. Iron supplementation per se does not affect oxidative stress parameters studied in the euthyroid state. Although iron increased lipid peroxidation in the hyperthyroid state, this effect was less than that seen in euthyroidism. Iron supplementation to hyperthyroid rats significantly lowered plasma ferritin levels, suggesting increased iron elimination with consequently reduced oxidative stress.

Animals↗
PubMed2004

Oxidative damage to nuclear DNA in hyperthyroid rat liver: inability of vitamin C to prevent the damage.

The effects of hyperthyroidism on oxidative DNA damage in liver tissue and modification by vitamin C supplementation were investigated in rats. Animals were rendered hyperthyroid by administration of L-thyroxine (0.4 mg/100 g food) for 25 d. In the plasma samples, T(3), T(4), and thyroid-stimulating hormone (TSH) were measured by radioimmunoassay and ascorbate spectrophotometrically. Oxidative damage to hepatic nuclear DNA was determined by measuring deoxy-guanosine (dG) and 8-oxodG by high-performance liquid chromatography with diode array detector electrochemical detection (HPLC-DAD-ECD). In hyperthyroidism, 8-oxodG/(10(5) dG) levels were significantly higher and plasma vitamin C levels lower than in control rats. The results of this experimental study show that oxidative damage to hepatic nuclear DNA increases in the hyperthyroid state and that vitamin C was not effective in preventing this damage.

Animals↗
PubMed1994

Hyperthyroidism increases covalent binding and biliary excretion of 1,1-dichloroethylene in rats.

Distribution, covalent binding, and biliary excretion of 1,1-dichloroethylene (DCE) were examined in euthyroid (EuT) and hyperthyroid (HyperT) rats, which are more vulnerable to DCE hepatotoxicity. Male Sprague-Dawley rats were made hyperthyroid by 3 sc injections of thyroxine at 48-h intervals prior to experiments; euthyroid controls received vehicle injections. A time course study monitored the circulation and excretion of 14C-DCE label for 24 h after administration of 14C-labeled DCE (50 mg/kg in mineral oil) in serial blood and urine samples. At 24 h, total and covalently bound 14C-label were measured in liver, kidney, and lung. Hepatotoxicity of DCE was enhanced in the HyperT rats, as evidenced by elevated serum activities of aminotransferase and histopathology, and was associated with increases in circulating metabolite, and in metabolite bound to red blood cells and liver but not to kidney or lung. Hyperthyroidism had little effect on in vitro capacity of hepatic microsomes to convert DCE to reactive intermediates as reflected by covalent binding. A biliary excretion study in pentobarbital-anesthetized rats showed a striking, but transient, increase in toxicant metabolite excretion in bile of HyperT rats during the first 2 h after toxicant administration (14C-DCE, 100 mg/kg). During the next 2 h, biliary metabolite excretion by HyperT rats decreased while there was a rise in circulating amounts of total and bound 14C-label. Thus, although hyperthyroidism had little effect on the total extent of DCE metabolized, this hormonal disturbance may have transiently enhanced metabolite formation and definitely was associated with a lesser ability to detoxify reactive DCE metabolites capable of injuring hepatic cell constituents by covalent binding reactions.

Animals↗
PubMed1994

Glucose metabolism in a patient with hyperthyroidism and an insulinoma.

A 67-year-old woman was admitted in hypoglycemic coma, with fever and signs of hyperthyroidism. Diagnosis was made of both an insulinoma and subacute ("De Quervain") thyroiditis. This rare coincidence of two diseases with opposite effects on serum glucose levels, offered a rare opportunity to study glucose metabolism in this peculiar physiopathological situation. During the day abnormally high postprandial blood glucose levels were seen, pointing to the glucose intolerance usually seen in the hyperthyroid state. During the night and after prolonged fasting, however, hypoglycemia predominated, consistent with the clinical picture typical of an insulinoma. After resection of the insulinoma and spontaneous healing of hyperthyroidism, glucose metabolism reverted to normal. As shown in this case, concurrent hyperthyroidism and an insulinoma may lead to consecutive episodes of glucose intolerance and hypoglycemia within the same 24-hour period.

Aged↗
PubMed2003

Relationships existing between the serum cytokine levels and bone mineral density in women in the premenopausal period affected by Graves' disease with subclinical hyperthyroidism.

We examined the relationships existing between serum cytokine levels and bone mineral density (BMD) in women of premenopausal age affected by Graves' disease with subclinical hyperthyroidism. The study population consisted of 21 women with untreated hyperthyroid Graves' disease (group H) (age, 36 +/- 2 years), eight women with untreated subclinical hyperthyroid status (group SH) (age, 33 +/- 5 years) and 10 healthy women (group N) (age, 35 +/- 3 years). The following measurements were made in all patients: free T4 (fT4), free T3 (fT3), thyroid stimulating hormone (TSH), TSH receptor antibody (TRab), anti-thyroid peroxidase antibody (anti-TPO), anti-thyroglobulin antibody (anti-Tg), interleukin-2 receptor (IL-2r), interleukin-4 (IL-4), interleukin-8 (IL-8) and interleukin-13 (IL-13). IL-2r and IL-8 levels significantly increased in group H compared with group SH (p < 0.01 and p = 0.05, respectively) and group N (p < 0.001 and p = 0.02, respectively). IL-4 and IL-13 levels tended to be lower in groups H and SH compared with group N, although this difference did not reach statistical significance. Bone mineral density was significantly reduced in only two areas of the femur in group H compared with group N. There was no difference in BMD between groups SH and N. There was no correlation between thyroid hormones, serum cytokine levels and BMD in either group. In conclusion, these results suggest that there were no relationships existing between the serum level of these cytokines and BMD in women of premenopausal age affected by Graves' disease with subclinical hyperthyroidism.

Adult↗
PubMed2004

The prevalence and target antigens of antithyroid drugs induced antineutrophil cytoplasmic antibodies (ANCA) in Chinese patients with hyperthyroidism.

OBJECTIVE: Antithyroid drugs such as propylthiouracil (PTU) and methimazole (MMI) are common medications in Chinese patients with hyperthyroidism and PTU-induced antineutrophil cytoplasmic antibody (ANCA) positive vasculitis has been reported. The current cross-sectional study aimed to investigate the prevalence and the target antigens of ANCA in Chinese patients with hyperthyroidism pre- and post-antithyroid medication therapy. METHODS: Sera from 216 patients with hyperthyroidism in our hospital were collected from January to July in 2002. Patients were divided into four groups: untreated (n = 34); treated with PTU (n = 62); treated with MMI (n = 77); and treated with both PTU and MMI (n = 43). Indirect immunofluorescence (IIF) assay was used to detect ANCA and ANA. Antigen-specific ELISAs were used to detect antigen specificities. The known antigens included myeloperoxidase (MPO), proteinase 3 (PR3), human leukocyte elastase (HLE), lactoferrin, bactericidal/permeability-increasing protein (BPI), cathepsin G and azurocidin. RESULTS: 33/216 sera were IIF positive, 20 of the 33 samples were ANCA positive, 11 samples were ANA positive, and two samples were both P-ANCA and ANA positive. The prevalence of positive ANCA in patients receiving PTU (14/62, 22.6%) was significantly higher than that of untreated patients (1/34, 2.9%) and patients treated with MMI (0/77, 0), P < 0.017. Of the 22 IIF-ANCA positive samples, 12 (54.5%) sera recognized lactoferrin, seven (31.8%) sera recognized HLE, four sera recognized MPO and azurocidin respectively, three sera recognized PR3 and cathepsin G respectively, and one serum recognized BPI. Six of the 22 (27.3%) patients with ANCA positive had clinical evidence of vasculitis. All patients with MPO-ANCA and two of the three patients with PR3-ANCA had clinical vasculitis. CONCLUSION: PTU is associated with the production of ANCA in patients with hyperthyroidism. PTU-induced ANCA are due to polyclonal activation of B cells. Anti-MPO and anti-PR3 antibodies may associate the occurrence of clinical vasculitis.

Adult↗
PubMed2001

Surgical treatment of hyperthyroidism: a ten-year experience.

Hyperthyroidism is treated either by antithyroid drugs, radioiodine (I131) or surgery. In Sweden, surgery is often performed in patients with large goiter or severe hyperthyroidism with infiltrative endocrine ophthalmopathy. To evaluate indications and results of surgical treatment, data from 380 patients operated on for hyperthyroidism at our department during 1986-1995 were analyzed. Twenty-six percent were referred for surgery because of failure of treatment with antithyroid drugs or I131. Ninety-one percent were subjected to subtotal thyroidectomy with a median remnant weight of less than 2 g. In the remaining patients, total thyroidectomy was performed. Transient vocal cord affection occurred in 2.6%, none of which was permanent. Prolonged postoperative hypocalcemia occurred in 3.1%, and permanent hypoparathyroidism in 1%. There was no difference in complication rate between subtotal or total thyroidectomy. In patients with Graves' disease, 5% worsened with regard to ophthalmopathy initially after surgery but later improved. Recurrent disease occurred in 2% of the patients, all of whom had undergone subtotal thyroidectomy. Surgery is not first-line therapy in all patients with hyperthyroidism. However, in experienced hands, surgery is a good therapeutic alternative that can be carried out with no mortality, few complications, and, provided that a minimal remnant is left, very few recurrences.

Adenoma↗
PubMed2001

Hyperplacentosis: a novel cause of hyperthyroidism.

Human chorionic gonadotropin (hCG), which is capable of thyrotropic activity, is believed responsible for the hyperthyroidism of gestational trophoblastic disease and hyperemesis gravidarum. Hyperplacentosis is a condition of heightened trophoblastic activity characterized by increased placental weight and circulating hCG levels higher than those associated with normal pregnancy. We report the first case of hyperthyroidism associated with hyperplacentosis. Correction of the hyperthyroidism occurred after hysterotomy and correlated with declining hCG levels. Hyperplacentosis should be included among the causes of hCG-mediated hyperthyroidism.

Adult↗
PubMed2001

Cilazapril prevents cardiac hypertrophy and postischemic myocardial dysfunction in hyperthyroid rats.

We evaluated the effects of hyperthyroidism on cardiac structural changes and postischemic myocardial function, and also studied how an angiotensin-converting enzyme (ACE) inhibitor, cilazapril, can alter these changes. Hyperthyroidism was induced by daily intraperitoneal injection of thyroxine (T4) (600 microg/kg) with or without cilazapril (10 mg/kg per day, orally), and control rats were given by vehicle. After 2 weeks of treatment, T4-treated rats showed increases in blood pressure and heart weight to body weight ratio (HW:BW). Cilazapril decreased blood pressure to control values and reduced HW:BW. In the isolated working heart preparation, T4-treated rats showed a poor postischemic recovery of left ventricular pressure-rate product (14% of baseline at 30 minutes of reperfusion vs. vehicle 85%) and cardiac work (6% vs. 71%). Cilazapril recovered both values to 49% and 43%. Propranolol (500 mg/L in drinking water) decreased blood pressure to the same extent as cilazapril in hyperthyroid rats, but changed neither HW:BW nor the postischemic myocardial dysfunction. Percent recovery of cardiac work was inversely well correlated with HW:BW (R2 = 0.998, p < 0.001). Results indicate that T4-induced cardiac hypertrophy enhances postischemic cardiac dysfunction. Results also indicate renin-angiotensin system (RAS), but not sympathetic nerve activation, is involved in cardiac hypertrophy and postischemic myocardial dysfunction in hyperthyroid rats.

Adrenergic beta-Antagonists↗
PubMed2004

Medullary thyroid carcinoma associated with hyperthyroidism: a case report and review of the literature.

Thyroid cancer is occasionally associated with hyperthyroidism. Papillary thyroid carcinoma is the most frequently reported histologic type followed by follicular thyroid carcinoma. Medullary thyroid carcinoma (MTC) has been rarely described in association with Graves' disease or other forms of hyperthyroidism. To our knowledge, only 14 cases have been described in which MTC was associated with hyperthyroidism. We report a 70-year-old male who had a clinically significant MTC discovered in the course of diagnostic work-up for hyperthyroidism. We also summarize the clinical features of the other 14 reported cases.

Aged↗
PubMed1991

Hyperthyroid myopathy and the response to treatment.

Hyperthyroidism is accompanied by significant dysfunction of both proximal and distal skeletal muscles. The purpose of this study was to quantitate the degree of muscle weakness in newly diagnosed patients with Graves' disease and to assess the response to treatment. Ten patients were prospectively studied with objective measures of strength and endurance of proximal and distal muscles while hyperthyroid (stage I), after 2 weeks of propranolol (stage II), and about 6 months later when euthyroid (stage III). Propranolol treatment for 2 weeks resulted in a subjective decrease in weakness, which was accompanied by a statistically significant improvement in grip strength (P less than 0.01), shoulder strength (P less than 0.02), and grip endurance (P less than 0.01) but not shoulder endurance. Muscle function further improved and attained control levels when the patients were chemically and clinically euthyroid. In contrast, a control group subjected to the same muscle testing protocol before and after 1 week of propranolol treatment showed no improvement in grip, shoulder strength, or shoulder endurance but had decreased grip endurance (P less than 0.01) and increased subjective weakness. These results confirm that muscle weakness commonly is associated with hyperthyroidism and can be quantitatively profound. In contrast to the effects of beta-blockade in normal controls, propranolol partially improves muscle weakness in thyrotoxic patients. We conclude that thyroid hormone and catecholamines in concert mediate the muscle dysfunction of hyperthyroidism.

Adrenergic beta-Antagonists↗
PubMed1994

Serum amino-terminal propeptide of type III procollagen in patients with hyperthyroidism or hypothyroidism during therapy.

Changes in serum amino-terminal type III procollagen propeptide (PIIIPN) and hydroxyproline were compared with indices of thyroid function in 33 patients with hyperthyroidism and 16 patients with hypothyroidism before and after treatment. Control values were obtained from 26 healthy individuals. Hyperthyroidism was shown to be associated with an increased level of PIIIPN and hypothyroidism with a decreased PIIIPN level. An increase in PIIIPN was found in 100% of hyperthyroid patients and a decrease in 31% of those with hypothyroidism, while hydroxyproline increased in only 54% of patients with hyperthyroidism and its level was decreased in only 6% of patients with hypothyroidism. Correlation between PIIIPN and thyroxine and triiodothyronine levels was shown. The results obtained suggest that PIIIPN is a valuable index of tissue response to thyroid hormones.

Adolescent↗