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PubMed2006

Evaluation of the antithyroid, antioxidative and antihyperglycemic activity of scopoletin from Aegle marmelos leaves in hyperthyroid rats.

Scopoletin (7-hydroxy-6-methoxy coumarin) was isolated from the leaves of Aegle marmelos and evaluated for its potential to regulate hyperthyroidism, lipid peroxidation and hyperglycemia in levo-thyroxine-induced hyperthyroid rats. Scopoletin (1.00 mg/kg, p.o.) administered daily for 7 days to levo-thyroxine-treated animals decreased the levels of serum thyroid hormones and glucose as well as hepatic glucose-6-phosphatase activity, demonstrating its potential to regulate hyperthyroidism and hyperglycemia. Scopoletin also inhibited hepatic lipid peroxidation and increased the activity of antioxidants, superoxide dismutase and catalase. Compared with the standard antithyroid drug, propylthiouracil, scopoletin exhibited a superior therapeutic activity, since unlike propylthiouracil, it also inhibited hepatic lipid peroxidation. These findings indicate that scopoletin has the potential to inhibit thyroid function and hyperglycemia without hepatotoxicity.

Aegle↗
PubMed1996

Effects of hyperthyroidism on expression of a phosphoenolpyruvate carboxykinase/bovine growth hormone gene in transgenic mice.

Thyroid hormone (T3) responsiveness of the PEPCK promoter in vivo was examined in both PEPCK/bGH(460) and PEPCK/bGH(335) mouse lines. Transgenic and non-transgenic littermates were treated with methimazole or PTU for 6 or 4 weeks, respectively, then treated +/- T3 for 10 days. In PEPCK/bGH(460) and PEPCK/bGH(355) transgenic mice, the bGH mRNA was decreased by 65% and 46%, respectively, in hyperthyroid mice when compared to euthyroid controls. Endogenous PEPCK mRNA was decreased by 33% in hyperthyroid non-transgenic mice. The conclusion of this study is that chronic hyperthyroidism in mice inhibits PEPCK-directed expression of the transgene when either the -460/+73 or the -355/+73 promoter/regulatory elements are used.

Animals↗
PubMed1993

Pathogenesis of thyroid-associated ophthalmopathy: an autoimmune disorder of the eye muscle associated with Graves' hyperthyroidism and Hashimoto's thyroiditis.

Thyroid-associated ophthalmopathy, the progressive eye disorder which occurs frequently in patients with Graves' hyperthyroidism and, occasionally, in those with Hashimoto's thyroiditis, may be a two-stage disorder of the eye muscle. In the first stage, which may occur in the great majority of patients with Graves' hyperthyroidism and in an unknown, but probably small, proportion of those with Hashimoto's thyroiditis, antibodies and CD4+ (helper) T lymphocytes reactive with eye muscle and thyroid shared antigens, of which 64-kDa membrane proteins are good candidates, may initiate a mild eye muscle inflammation, manifested as eye muscle swelling on orbital imaging. The second stage, which occurs in about 25% of patients with Graves' hyperthyroidism and in 2% of those with Hashimoto's thyroiditis, may be due to reactivity of cytotoxic antibodies against eye muscle-specific membrane antigens, one of which at approximately 35 kDa appears a likely candidate, and, possibly, cytotoxic T cells in the context of the appropriate class I MHC molecule. Orbital connective tissue inflammation, which plays an important role in the development of progressive orbital inflammation, is likely to be secondary to the eye muscle reaction. The recent cloning of a 64-kDa thyroid and eye muscle antigen which shares significant homology with the muscle protein tropomodulin and mapping of its antibody-reactive epitopes provide structural information about one candidate eye muscle autoantigen and promise for a more rational approach to the diagnosis and management of this common, progressive eye disorder.

Graves Disease↗
PubMed1997

Influence of hyperthyroidism on the activity of liver nitric oxide synthase in the rat.

Hyperthyroidism enhances the prooxidant activity of the liver by elevating superoxide radical and/or hydrogen peroxide generation in microsomal, mitochondrial, and peroxisomal fractions, with an increased respiratory burst of Kupffer cells. In this study, the influence of daily doses of 0.1 mg 3,3',5-triiodothyronine (T3)/kg for three consecutive days on liver nitric oxide (NO) synthase (NOS) was assessed, as a possible contributory mechanism to T3-induced liver prooxidant activity. Thyroid calorigenesis was paralleled by a progressive increment in the rate of NO generation, with significant increases after 2 (47%) and 3 days (70%) of T3 treatment, and a net 45% (P < 0.05) enhancement in the NG-methyl-L-arginine-sensitive NO production, compared to control values. These enhancement effects were reversed to control levels after 3 days of hormone withdrawal, concomitantly with the normalization of hepatic respiration. Enhancement of liver NOS activity in hyperthyroid animals was diminished by 27% (P < 0.05) by the selective in vivo inactivation of Kupffer cells by gadolinium chloride (GdCl3), without direct actions of GdCl3 on the enzyme. These data demonstrate that hyperthyroidism leads to a significant and reversible enhancement in rat liver NOS activity, an effect that is exerted at hepatocyte and Kupffer cell levels, thus representing an additional source of prooxidants to those of reactive oxygen species.

Animals↗
PubMed1998

The effect of methimazole on the oxidant and antioxidant system in patients with hyperthyroidism.

The present study was designed to evaluate the changes in the plasma lipid peroxidation and antioxidant system in 15 adult volunteer patients in hyperthyroid and euthyroid states. In these patients, plasma concentrations of lipid peroxides were decreased and, ascorbic acid and vitamin E levels were significantly increased in euthyroid status in comparison to hyperthyroid status. A significant increase in the plasma GPx activity (P < 0.01) and a decrease in GST (P < 0.001) was observed after euthyroidism was sustained with methimazole therapy. In conclusion, hyperthyroidism tends to enhance lipid peroxide content and an increase in GST and decreases in GPx, vitamin E and ascorbic acid levels accompany to this change in the plasma. The achievement of euthyroidism led an improvement in these parameters.

Adult↗
PubMed1990

Concerning the decreased D-3-hydroxybutyrate dehydrogenase activity in the liver and heart of hyperthyroid rats.

Whereas in rat liver mitochondria the hyperthyroid state causes an increase both in fatty acid unsaturation and in the Ea of D-3-hydroxybutyrate dehydrogenase and a decrease in phase transition temperature, in hyperthyroid rat heart mitochondria these changes are negligible. D-3-hydroxybutyrate dehydrogenase in both the liver and the heart mitochondria of hyperthyroid rats is reduced by about 35% [12] but this reduction is not due to changes in membrane fluidity in either tissue. Hypothyroidism, on the other hand, affects BDH activity in neither heart nor liver.

Animals↗
PubMed1993

Evaluation of increased serum ferritin levels in patients with hyperthyroidism.

To further elucidate the mechanism of increased serum ferritin levels in hyperthyroidism, the changes in erythrocytes and serum iron and total iron-binding capacity levels were examined in addition to serum ferritin levels in 13 hyperthyroid patients. The mean values of hemoglobin, red blood cells, and packed cell volume were increased by antithyroid therapy. While the serum levels of iron did not change, those of total iron-binding capacity increased significantly after achieving a euthyroid state. Increased serum ferritin levels returned to normal through antithyroid therapy. Furthermore, the serum ferritin levels of four anemic patients were significantly higher than those of nine nonanemic patients. Thus it is concluded that the increase in serum ferritin levels in patients with hyperthyroidism may be due to the direct action of thyroid hormones on its synthesis, while in some cases complicated with anemia impaired iron utilization by erythropoietic cells may also be involved.

Adult↗
PubMed1982

Prolactin response to arginine in children with hyperthyroidism and primary hypothyroidism.

Plasma prolactin (PRL) response to arginine was examined in 16 prepubertal and 18 pubertal children with constitutional short stature, 5 patients with hyperthyroidism and 4 patients with primary hypothyroidism. The mean basal concentration of plasma PRL was significantly higher (P less than 0.01) in primary hypothyroidism than in other groups. Arginine infusion elicited significant (P less than 0.05) rises in plasma PRL in all groups. The maximal increment of plasma PRL above the baseline level after arginine stimulation was significantly larger (P less than 0.05) in pubertal than in prepubertal females and was significantly smaller (P less than 0.05) in patients with hyperthyroidism than in age- and sex-matched controls. There was no sex difference in arginine-stimulated PRL secretion. These data suggest that arginine produces a significant increase in plasma PRL and the PRL response to arginine was greater in pubertal than in prepubertal children. Plasma PRL response to arginine is suppressed in children with hyperthyroidism and the basal plasma PRL is markedly elevated in primary hypothyroidism.

Adolescent↗
PubMed1980

Effects and plasma levels of propranolol and metoprolol in hyperthyroid patients.

The effects and plasma concentrations of different doses of propranolol and metoprolol were studied in 34 hyperthyroid patients. The initial daily doses were propranolol 160 mg or metoprolol 200 mg. If the resting heart rate remained above 75 beats per min after treatment for 4-7 days, the dose was increased and the patient re-examined after a further 4-7 days. Propranolol (n = 17) caused a reduced heart rate, a decrease in serum 3,3',5-triiodothyronine (T3) and an increase in serum 3,3',5'-triiodothyronine (reverse T3, rT3). In 10 patients, there was no change in T3 or rT3 until the daily dose of propranolol had been increased to 240 or 320 mg. The plasma level of propranolol was significantly correlated with the decrease in T3 and the increase in rT3. Metoprolol (n = 17) caused a reduction in heart rate similar to that following propranolol. However, serum T3 was only slightly reduced even after an increase in dose to 300 or 400 mg, and serum rT3 was not altered. Metoprolol concentrations were not significantly correlated with the fall in T3. It appears that the influence of beta-blockers on T4 conversion is of little importance for the clinical improvement in hyperthyroid patients, and rather it is a consequence of beta 1-adrenergic blockade interfering with the effect of T3. In addition, the findings support the assumption that therapeutic failure with beta-blockers in hyperthyroidism may be due to suboptimal treatment, and that individualized dosage is necessary.

Adult↗
PubMed1975

[Radio-iodine treatment of hyperthyroidism. Experience in more than 2000 patients (author's transl)].

Results of radioiodine therapy (131/125) of hyperthyroidism are reported. The individually calculated doses of 131-iodine were: 6000 rad in cases of small (not more than 60 g) diffuse goiters, 8000-10000 rad in large diffuse goiters, 10000-12000 rad in nodular goiter and 30000-40000 rad in autonomous adenoma. In about 75% of the patients a single application of 131-iodine was sufficient to control the hyperfunction. The cumulative risk of myxedema ten years after therapy was: 31% in small diffe goiters, 12% in large diffuse goiters and 6% in nodular goiter. All cases considered together, the cumulative myxedema risk was about 12%. This figure compares favourably with the results of surgical treatment and they document the necessity of individual calculation of the dose in order to get optimal results. 125-iodine was applied since October 1972 in cases of small diffuse goiters. The dose was standardized according to the gland weight, uptake and effective half value time (dose at the colloid-cell interface 12000-15000 rad). 5-12 months thereafter, there were about 60% of the patients euthyroid. The genetic and somatic risk of radiation is considered quantitatively and we conclude that there is no real argument aginst radioiodine therapy of hyperthyroidism except in children and in youth. Risks and efficiency of other treatments (surgical, antithyroid drugs) are compared with the radioiodine treatment and it is concluded that radioiodine is to be preferred in the major part of the hyperthyroid patients.

Humans↗
PubMed1978

[Hyperthyroidism (author's transl)].

Surgical cure of hyperthyroidism aims at removing enough functioning follicles to prevent hyperthyroidism while leaving sufficient tissue to maintain euthyroidism. In the case of Graves' disease the surgeon is faced with a goiter consisting of uniformly hyperstimulated follicles that are but one of the multiple targets of an immunologic attack. In contrast, autonomous follicles with an intrinsic functional abnormality are the hallmark of multinodular toxic goiter. These follicles may be clustered (toxic adenoma) or spread in different patterns throughout the gland. Partial thyroidectomy provides definite cure. While operating, the surgeon is unable to appreciate the functional quality of the tissue left behind. Thus, both postoperative hypo- and hyperthyroidism may occur independently of the surgical technique.

Goiter, Nodular↗
PubMed1978

[Hyperthyroidism: diagnosis (author's transl)].

In hyperthyroidism we differentiate two main forms: (1) hyperthyroidism due to Basedow's (Graves') disease, always characterized by endocrine eye signs, frequently with goiter; (2) hyperthyroidism due to nodular goiter or to Plummers' disease, without endocrine exophthalmos. The clinical diagnosis includes typical complaints (e.g., weight loss, heat intolerance, sweating) and findings (e.g., tachycardia, tremor, soft-warm skin). The technical diagnosis includes in vivo (scintigraphy, RI-uptake, X-ray examination) and in vitro (T3-RIA, T4-assay, TRH response to TRH) tests.

Goiter, Nodular↗
PubMed1991

Effects of subclinical hyperthyroidism on renal handling of water and electrolytes in patients with nodular goiter.

Evidence is beginning to accumulate that minor degrees of hyperthyroidism lead to adverse effects in various tissues, even though clinically the patients are euthyroid. To determine whether these anomalies in thyroid function have deleterious effects on renal function and electrolyte metabolism, the plasma concentrations of electrolytes, urea, and creatinine, the renal handling of water and sodium, and the urinary excretion of these substances were measured in patients with nodular goiter who were displaying stable subclinical hyperthyroidism. The studies were carried out before and after correcting the thyroid dysfunction. Restoration of euthyroidism did not modify any of the renal function parameters studied and did not cause changes in blood analyte levels. The data show that treatment of minor degrees of hyperthyroidism does not have any effects on renal function and electrolyte metabolism, and confirm the well-known capacity of the kidney to adjust its functions to changes induced by an abnormal secretion of thyroid hormones.

Adult↗
PubMed1989

[Early changes in thyroid hormones following radioiodine therapy of hyperthyroidism with reference to etiology and accompanying medication].

Radioiodine therapy (RITh) is an effective mode of treatment of different types of hyperthyroidism (immunogenic, IH; nonimmunogenic, NIH). The aim of this study was to evaluate the risk of thyroid storm after RITh. For this purpose a systematic determination of thyroid hormones (TT3, TT4) 5 and if possible 12 days after RITh was performed in 416 patients with borderline or overt hyperthyroidism. Additional antithyroid medication after RITh was necessary in 20 patients. Among the remaining 396 patients 48% had been pretreated with antithyroid drugs because of more severe clinical symptoms. This medication was canceled 10 to 5 days before RITh in all cases. After RITh the mean TT3 and TT4 levels of the subgroups, with and without antithyroid premedication, decreased nearly in parallel course. The whole group of 396 patients presented a significant decrease in TT3 levels with a mean from 1.9 to 1.4 ng/ml. In 18 cases (5%) an increase in TT3 level (greater than or equal to 0.5 ng/ml) was detected without requiring antithyroid therapy. No case of thyroid storm was observed in the entire patient group. TT3 decrease appeared to be more pronounced in patients with higher pretreatment levels. TT4 showed a significant decrease only in case of elevated levels. Post-therapeutic hormone levels were not dependent on the etiology of hyperthyroidism (IH, NIH). The decrease of TT3 levels in the IH group was more pronounced after application of 150 Gy compared with 60 Gy. The additional medication with propranolol (greater than or equal to 60 mg/day) enforced the TT3 decrease. Accompanying glucocorticoid medication had no influence on the hormone levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Indications for conservative and operative therapy of thyroid autonomy and Basedow hyperthyroidism from the internal medicine viewpoint].

The risk of recurrent hyperthyroidism can be eliminated indefinitely in patients with autonomously functioning thyroid tissue (AFTT) by selective surgery or radioiodine, whereas medical treatment inhibits only the actual thyroid hormone over-production. Therefore, AFTT should be removed. In immunogenic hyperthyroidism the natural history of the disease can be influenced only symptomatically. The relapse rate after medical treatment is more than 50%. After surgical or radioactive therapy long-term remission of hyperthyroidism, not of the underlying thyroid disease can be achieved more effectively. Therefore surgical treatment should be preferred.

Goiter, Nodular↗
PubMed1985

[Operative strategy in thyroid autonomy and Basedow hyperthyroidism].

The different extra- and intrathyroid origin of hyperthyroidism, the advantages of the surgical procedure and the criteria for the extent of thyroid resection determine the operative tactics. For both forms of hyperthyroidism we recommend a rather extended resection of the diseased thyroid gland in order to prevent recurrent hyperthyroidism and recurrent thyroid growth as well. These recurrences require subtotal thyroidectomy for Graves' disease, monolateral partial lobectomy for a so-called toxic adenoma and bilateral partial lobectomy for toxic multi-nodular goiters. With these procedures lesions of the recurrent nerves and parathyroid glands can be prevented.

Adenoma↗
PubMed1981

Breast cancer concurrent with hyperthyroidism: a case report.

A case of breast cancer concurrent with hyperthyroidism was reported and the relation between breast cancer and thyroid dysfunction was reviewed. It has been frequently suggested that the incidence of breast cancer is decreased in patients with hyperthyroidism and breast cancer coincidental with hyperthyroidism is rare.

Adult↗
PubMed1988

Adenomatous goiter with hyperthyroidism.

Adenomatous goiter with hyperthyroidism is a rare disease entity in Japan. Over a five-year period, we operated on 20 patients with this disease. Pre-operatively, basal thyrotropin was not necessarily suppressed and the thyrotropin-binding inhibiting immunoglobulin activity, which had been recently measured in five patients, showed normal values. Uneven patches of cold areas were noted on 131I thyroidal scintigrams. Thyroid function tests carried out three years after surgery in one lobectomy case and in eleven subtotal thyroidectomy cases revealed hypothyroidism in seven, hyperthyroidism in two and euthyroidism in only three cases. These results suggest that the pathogenesis and clinical features of adenomatous goiter with hyperthyroidism are quite different from those of Graves' disease, and that routinely performing near-total thyroidectomy may be considered as the treatment of choice.

Adenoma↗