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PubMed2006

Increased susceptibility of the lungs of hyperthyroid rats to oxidant injury: specificity of effects.

Results from previous studies indicate that hyperthyroidism increases the risk of ozone-induced lung toxicity. This observation raised the possibility that pulmonary damage from other oxidant substances might be greater in a hyperthyroid state. To address this hypothesis, pulmonary responses to crystalline silica, a particulate with oxidant properties, were evaluated in normal or hyperthyroid adult male rats. To induce a hyperthyroid condition, time-release pellets containing thyroxine were implanted subcutaneously; control rats received placebo pellets. After 7 days, the animals were exposed to saline or silica (0.1mg/100g BW or 1.0mg/100g BW) by intratracheal instillation. Following silica treatment, there was a dose-related increase in bronchoalveolar lavage (BAL) albumin levels and neutrophil numbers. However, the effects of silica were similar in both normal and hyperthyroid rats. These findings were confirmed and contrasted with those regarding ozone (1ppm, 4h inhalation) in a subsequent experiment. The results indicated that, although exposure to either ozone or silica resulted in increases in BAL albumin levels and neutrophil numbers, only responses to ozone were enhanced in hyperthyroid rats. These findings suggest that specificity exists in regards to the modulation of oxidant-induced lung damage and inflammation by thyroid hormones.

Albumins↗
PubMed1992

Transient hyperthyroidism and hyperemesis gravidarum: clinical aspects.

OBJECTIVES: Our objectives were to describe the presentation and course of hyperemesis gravidarum with respect to thyroid function and to test the hypothesis that patients with biochemical hyperthyroidism differ in clinical presentation from euthyroid hyperemesis patients. STUDY DESIGN: Sixty-seven patients seen at Los Angeles County Women's Hospital over a 10-month period with hyperemesis gravidarum were studied prospectively with respect to thyroid function. RESULTS: Forty-four patients (66%) had biochemical hyperthyroidism (increased free thyroxine index [n = 39] or suppressed thyroid-stimulating hormone [n = 40]) that was self-limited, resolving by 18 weeks' gestation. Hyperthyroid patients were more likely than euthyroid patients to have abnormal electrolyte levels (23/39 [59%] vs 6/28 [21%] and increased liver enzyme levels (23/59 [59%] vs 5/28 [18%], p less than 0.01). The severity of hyperemesis was found to vary directly with the degree of hyperthyroidism. CONCLUSIONS: Hyperthyroidism is a common, self-limited finding in hyperemesis. The cause of the hyperthyroidism may be linked to the cause of hyperemesis itself.

Adolescent↗
PubMed2006

[Evaluation of bone mineral density in hyperthyroid patients before and after medical therapy].

Osteoporosis is a common complication of hyperthyroidism, but it is not often evaluated. The aim of this study is to examine bone mineral density (BMD) (dual energy X-ray absorptiometry: DEXA) in lumbar spine (L1-L4), femoral neck (FN) and Ward's triangle (TW) in 45 hyperthyroid patients (group A: n 25 active hyperthyroidism, group B: n 20 controlled hyperthyroidism on medical therapy, after a mean of 7 months of euthyroidism), compared to control group (group C: n 22). These 3 groups are adjusted by age, sex, menopausal status and BMI. In hyperthyroid patients (group A), as compared to the control group, we noticed a significant reduction of BMD (z score) in different sites, more markedly in the lumbar spine (p L1-L4: 0,005; p FN: 0,011; p TW: 0,019). In group A, no differences were found between BMD values after adjustment for Z score whatever the menopausal status (p L: 0.12; p FN: 0.33; p TW: 0.09) and degree ofhyperthyroidism (p L: 0.48; p FN: 0.41; p TW: 0.21). The degree of BMD in group B patients was different from that of patients in group A (p L: 0.37; p FN: 0.28; p TW: 0.31). and was significantly lower than in those of group C except for the TW (p L: 0.009; p CF: 0.038; p TW: 0.068). We conclude that it is important to consider that after reaching euthyroidism hyperthyroidism patients present a bone risk.

Absorptiometry, Photon↗
PubMed1999

Effects of propylthiouracil, propranolol, and vitamin E on lipid peroxidation and antioxidant status in hyperthyroid patients.

OBJECTIVE: The purpose of this study was to examine lipid peroxidation and antioxidant states during hyperthyroidism states and after given different treatments. DESIGN AND METHODS: We examined 44 hyperthyroid patients and 19 euthyroid healthy controls. Patients were divided into three groups according to the treatment: Propylthiouracil (PTU) group, PTU + propranolol (PRP) group, PTU + PRP + vitamin E (vitE) group. RESULTS: In the hyperthyroid patients plasma malondialdehyde (MDA) levels were significantly high as compared to the control group (p < 0,001). There was a significant decrease in the MDA levels post-treatment (p < 0.001 in the PTU + PRP group and PTU + PRP + vitE group, p < 0.01 in the PTU group). In the hyperthyroidism, blood reduced glutathione (GSH) levels were lower, erythrocyte superoxide dismutase (SOD) and catalase (CAT) activities were higher than in the control group, but these changes were not significant. Post-treatment in each of the three groups the GSH levels were increased significantly as compared to the pretreatment levels (p < 0.001). There was significant decrease in the SOD activity post treatment (p < 0.01 in all three groups). Post-treatment CAT activity was decreased (p < 0.05 in the PTU group, p < 0.001 in the other two groups). The erythrocyte glutathione peroxidase (Gpx) activity was lower significantly in the hyperthyroidism as compared to the control group (p < 0.001). Post-treatment, in the three groups Gpx activity increased significantly as compared to the pretreatment levels (p < 0.05 in the PTU group, p < 0.001 in the PTU + PRP group and PTU + PRP + vitE group). CONCLUSION: We considered that giving all three treatments would be useful to the prevention of oxidative stress in the hyperthyroidism states.

Adult↗
PubMed2000

Effect of vitamin E on the response to ischemia-reperfusion of Langendorff heart preparations from hyperthyroid rats.

Hyperthyroidism has been reported to decrease heart antioxidant capacity and increase its susceptibility to in vitro oxidative stress. This may affect the heart response to ischemia-reperfusion, a condition that increases free radical production. We compared the functional recovery from in vitro ischemia-reperfusion (Langendorff) of hearts from euthyroid (E), hyperthyroid (H, ten daily intraperitoneal injections of T3, 10 microg/100g body weight), vitamin E-treated (VE, ten daily intramuscular injections, 20 mg/100g body weight) and hyperthyroid vitamin E-treated (HVE) rats. We also determined lipid peroxidation, tissue antioxidant capacity and the tissue capability to face an oxidative stress in vitro. A significant tachycardia was displayed during reperfusion following 20 min ischemia by the hyperthyroid hearts, together with a low recovery of left ventricular developed pressure (LVDP) and left ventricular dP/dt(max). When H hearts were paced at 300 beats/min, the functional recovery (LVDP and dP/dt(max)) was close to 100% and significantly higher than in E paced hearts. At the end of the ischemia-reperfusion protocol, myocardium antioxidant capacity was significantly lower, whereas lipid peroxidation and the susceptibility to in vitro oxidative stress were higher in the T3 treated (H) than in euthyroid rats. The in vitro tachycardic response, the reduction in the antioxidant capacity and the increase in lipid peroxidation were prevented by treatment of hyperthyroid rats with vitamin E (HVE). These results suggest that the tachycardic response to reperfusion following chronic T3 pretreatment was associated with the reduced capability of the heart to face oxidative stresses in hyperthyroidism.

Animals↗
PubMed1975

Hormonal pattern of relapse in hyperthyroidism.

22 patients with Grave's disease were followed up for up to a year after antithyroid drug therapy was discontinued. Clinical assessment and serum T3, T4, and thyroid-stimulating-hormone (T.S.H.) estimations were done serially and simultaneously. Serum T3 or T4 concentrations may be elevated briefly in the first few weeks after antithyroid drugs are stopped, as a rebound effect not necessarily indicative of subsequent relapsf. Clinical relapse of hyperthyroidism with subsequent improvement on antithyroid drugs occurred in 13 patients. Of these 13, serum T3 concentrations became elevated before serum T4 concentrations in 5, thus predicting the subsequent development of clinical hyperthyroidism. In the remaining 8 patients who relapsed, serum T4 was elevated a month before the serum T3. Hyperthyroidism was diagnosed clinically after elevated serum T3 concentrations in 11 patients and at the same time in 2 patients. The mean period of "biochemical hyperthyroidism" in these 11 patients was 12 weeks, with a range of 1 to 56 weeks. During this period 9 of the 11 had minor clinical changes attributable to hyperthyroidism. It is concluded that serial estimations of serum T3 provide the most reliable method of monitoring relapse in hyperthyroidism.

Carbimazole↗
PubMed1985

Fetal hyperthyroidism: experience of treatment in four siblings.

The outcomes of four pregnancies in a woman previously made hypothyroid by partial thyroidectomy for hyperthyroidism are reported. During the first two pregnancies she had no antithyroid therapy; the first resulted in late intrauterine death of a fetus with features compatible with fetal hyperthyroidism and the second in a child with skull deformities probably due to uncontrolled fetal hyperthyroidism. During the third and fourth pregnancies the mother received carbimazole to control fetal hyperthyroidism; both babies were euthyroid at birth and thrived. In mothers at risk of having hyperthyroid infants the fetal heart rate should be measured routinely to enable hyperthyroidism to be diagnosed and treated in utero.

Adult↗
PubMed1997

Hepatic amino nitrogen conversion and organ N-contents in hypothyroidism, with thyroxine replacement, and in hyperthyroid rats.

BACKGROUND/AIMS: The role of thyroid hormones in the regulation of hepatic conversions of amino nitrogen to urea is unresolved. The present study was designed to assess ureagenesis in rats with experimentally well-established hypo- and hyperthyroidism. The possible role of propylthiuracil (PTU), used for induction of hypothyroidism, was ascertained during thyroxine replacement of PTU treated hypothyroid rats. METHODS: Basal blood amino nitrogen concentrations (AAN), the urea nitrogen synthesis rate (UNSR) and the maximal hepatic capacity for urea nitrogen synthesis (CUNS) obtained during alanine infusion were determined together with N-contents in the soleus muscle and kidneys in experimentally hypothyroid rats (n = 19), upon thyroxine replacement (n = 14) and in experimentally hyperthyroid rats (n = 19). Hypothyroidism was induced by adding propylthiouracil (0.05%) to the drinking water for 5 weeks. Hyperthyroidism was induced by thyroxine 100 micrograms/100 g body weight. RESULTS: During hyperthyroidism, T3 fell to less than 10%, food intake was halved, and body weight fell by 13%. Basal blood AAN fell by 25% (p < 0.01), UNSR more than doubled (p < 0.01), and CUNS rose by 45% (p < 0.05). N-contents of the soleus muscle fell by 13% and by 20% in kidneys, respectively (p < 0.05). Thyroxine replacement normalized AAN, UNSR, CUNS and reduced N-loss to 7% in the soleus muscle (NS) and kidneys (p < 0.05), respectively. During hyperthyroidism, T3 rose five-fold, food intake rose by two thirds, and body weight fell by 10%. Basal AAN rose by 20% (p < 0.05), UNSR doubled (p < 0.01), and CUNS rose by 25% (p < 0.05). N-contents of the soleus muscle decreased by 19%, whereas kidney N-contents increased by 25% (p < 0.05). Overall liver function assessed by galactose elimination capacity did not differ among groups. Both conditions increased the rate of urea synthesis; in the hypothyroid state the hepatic waste of amino-N was limited by low blood concentration of amino-N, probably due to lower proteolysis. In the hyperthyroid state hepatic amino-N loss was aggravated by higher blood concentration of amino-N, probably due to higher proteolysis. This difference may explain the markedly different dietary nitrogen economy between the two groups. CONCLUSIONS: The findings suggest that distinct hepatic acceleration of urea synthesis may contribute to the protein loss seen in both myxedema and in thyrotoxicosis in humans.

Animals↗
PubMed1998

Hyperthyroidism in pregnancy.

Hyperthyroidism is second to diabetes mellitus as the most common endocrinopathy in pregnancy. Inappropriate secretion of hCG is the most common cause of hyperthyroidism in the first part of gestation. In addition to hydatidiform mole and hyperemesis gravidarum, nonpathologic-conditions including multiple gestation, mild nausea and vomiting, and even normal pregnancies may present with transient undetectable or suppressed serum TSH values. The syndrome of transient hyperthyroidism of hyperemesis gravidarum is defined as severe nausea and vomiting, dehydration, ketonuria, and weight loss of more than 5% by 6 to 9 weeks of pregnancy. Thyroid tests are in the hyperthyroid range, and the abnormalities are related to the severity of symptoms. Tests normalize with resolution of the vomiting, and ATD therapy is not indicated. The natural history of Graves' disease in pregnancy is characterized by aggravation in the first trimester, amelioration in the second half, and recurrence in the year following delivery. ATD treatment is the therapy of choice in pregnancy. Either PTU or MMI may be used; the goal is to keep the FT4I in the upper limits of normal with the minimum dose of ATD. In approximately 30% of patients, ATDs may be discontinued in the last few weeks of gestation. Maternal, fetal, and neonatal complications are frequent when hyperthyroidism is not under control. Postpartum hyperthyroidism may be caused by an episode of silent thyroiditis or Graves' disease.

Antithyroid Agents↗
PubMed1988

Altered metabolism and decreased efficacy of prednisolone and prednisone in patients with hyperthyroidism.

To evaluate the effect of hyperthyroidism on the protein binding and metabolism of prednisolone, eight subjects with hyperthyroidism were investigated before and after thyroid status returned to normal. Hyperthyroidism was associated with a reduced volume of distribution of prednisolone, a decreased systemic availability of prednisolone after oral prednisone, a displacement of the prednisolone in equilibrium with prednisone equilibrium toward prednisone, and an increased nonrenal clearance of unbound prednisolone in the presence of an impaired 6 beta-hydroxyprednisolone formation. After oral prednisone or intravenous prednisolone, patients with hyperthyroidism had lower albumin-bound, transcortin-bound, and unbound concentrations of prednisolone but normal affinities of albumin and transcortin for prednisolone binding. These differences in prednisolone plasma concentrations were biologically relevant, because the capacity of these plasma samples to inhibit allogeneically stimulated lymphocytes was lower by 70% in the hyperthyroid than in the euthyroid state. Thus hyperthyroidism reduces the biologic effect of prednisolone and exhibits a differential effect on various enzymes involved in the catabolism of prednisolone.

Administration, Oral↗
PubMed1987

Hepatic carbon flux after re-feeding. Hyperthyroidism blocks glycogen synthesis and the suppression of glucose output observed in response to carbohydrate re-feeding.

1. The work investigated hepatic glycogen synthesis and glucose output after the intragastric administration of glucose or glycerol or the provision of chow ad libitum to 48 h-starved euthyroid or hyperthyroid rats. 2. After glucose administration, glycogen synthesis via the indirect pathway [Newgard, Hirsch, Foster & McGarry (1983) J. Biol. Chem. 258, 8046-8052] occurred concomitantly with reversal of glucose flux across the liver and re-activation of pyruvate kinase in the euthyroid controls. Glycogen synthesis was decreased and net glucose output continued in the hyperthyroid rats, but normal re-activation of pyruvate kinase was observed. 3. Use of 3-mercaptopicolinate indicated that the glucose released from liver of hyperthyroid rats was synthesized from substrates metabolized via the gluconeogenic pathway. 4. Hepatic glycogen synthesis was also impaired in hyperthyroid rats after administration of glycerol or chow. Measurement of portal-minus-hepatovenous concentration differences and arterial glucose concentrations after the administration of glycerol in combination with 3-mercaptopicolinate indicated that flux from triose phosphate to glucose 6-phosphate was not decreased. 5. Inhibited glycogen synthesis after chow re-feeding was associated with accelerated re-activation of hepatic pyruvate dehydrogenase complex in the hyperthyroid rats. 6. The results indicate three distinct and independent actions of hyperthyroidism after re-feeding: (i) it inhibits the reversal of glucose flux across the liver normally observed in response to carbohydrate; (ii) it affects glycogen deposition at a site distal to glucose 6-phosphate; (iii) it allows more rapid re-activation of liver pyruvate dehydrogenase complex in response to a mixed diet.

Animals↗
PubMed1990

Glucose utilization by skeletal muscles in vivo in experimental hyperthyroidism in the rat.

In the fed state, hyperthyroidism increased glucose utilization indices (GUIs) of skeletal muscles containing a lower proportion of oxidative fibres. Glycogen concentrations were unchanged, but active pyruvate dehydrogenase (PDHa) activities were decreased. Hyperthyroidism attenuated the effects of 48 h of starvation to decrease muscle GUI. Glycogen concentrations and PDHa activities after 48 h of starvation were low and similar in euthyroid and hyperthyroid rats. The increase in glucose uptake and phosphorylation relative to oxidation and storage in skeletal muscle induced by hyperthyroidism may contribute to increased glucose re-cycling in the fed hyperthyroid state and to glucose turnover in the starved hyperthyroid state.

Animals↗
PubMed1983

Changes in the number and activity of sodium pumps in erythrocytes from patients with hyperthyroidism.

1. The sodium content, the rate and rate constant of ouabain-sensitive sodium efflux and the number of sodium pumps (indicated by the ouabain-binding capacity) were measured in erythrocytes from patients with hyperthyroidism and compared with values obtained in euthyroid patients and healthy control subjects. Erythrocyte zinc content was measured as a simple estimate of the content of carbonic anhydrase. 2. In the hyperthyroid patients, erythrocyte sodium content was increased, whereas the rate and rate constant of ouabain-sensitive sodium efflux, the ouabain-binding capacity and erythrocyte zinc content were all decreased. 3. The sodium pumps in hyperthyroidism had the same affinity for ouabain and the same rate constant per pump as those in healthy controls. 4. The decrease in the efflux rate constant could be entirely accounted for by the decrease in the number of sodium pumps. 5. Although the sodium efflux was decreased in the hyperthyroid patients, the change was less than expected for the decrease in the efflux rate constant. This suggests that there is an increase in the ground permeability of the erythrocyte membrane in hyperthyroidism. 6. In the hyperthyroid patients the number of sodium pumps and erythrocyte zinc content were inversely related to the plasma levels of thyroxine and tri-iodothyronine, but more closely to the latter. 7. These results suggest that the thyroid hormones may influence the erythrocyte's content of a range of proteins which happens to include the sodium pump.

Adult↗
PubMed2001

Determinants of changes in plasma homocysteine in hyperthyroidism and hypothyroidism.

OBJECTIVE: Hyperhomocysteinaemia is a risk factor for premature atherosclerotic vascular disease and venous thrombosis. The aim of the present study was to assess plasma total homocysteine (tHCys) concentrations in hypo- as well as hyperthyroid patients before and after treatment, and to evaluate the role of potential determinants of plasma tHCys levels in these patients. DESIGN: Prospective follow up study. PATIENTS: Fifty hypothyroid and 46 hyperthyroid patients were studied in the untreated state and again after restoration of euthyroidism. MEASUREMENTS: Fasting plasma levels of tHCys and its putative determinants (plasma levels of free thyroxine (fT4), folate, vitamin B(12), renal function, sex, age, smoking status and the C677T polymorphism in the methylenetetrahydrofolate reductase (MTHFR) gene were measured before and after treatment. RESULTS: Restoration of the euthyroid state decreased both tHCys (17.6 +/- 10.2-13.0 +/- 4.7 micromol/l; P < 0.005) and creatinine (83.9 +/- 22.0-69.8 +/- 14.2 micromol/l; P < 0.005) in hypothyroid patients and increased both tHCys (10.7 +/- 2.5-13.4 +/- 3.3 micromol/l; P < 0.005) and creatinine (49.0 +/- 15.4-66.5 +/- 15.0 micromol/l; P < 0.005) in hyperthyroid patients (values as mean +/- SD). Folate levels were lower in the hypothyroid group compared to the hyperthyroid group (11.7 +/- 6.4 and 15.1 +/- 7.6 nmol/l; P < 0.05). Pretreatment tHCys levels correlated with log fT(4) (r = - 0.47), folate (r = - 0.21), plasma creatinine (r = 0.45) and age (r = 0.35) but not with C677T genotype. Multivariate analysis indicated that pretreatment log(fT(4)) levels and age accounted for 28% the variability of pre-treatment tHCys (tHCys = 14.2-5.50 log(fT(4)) + 0.14 age). After treatment the logarithm of the change (Delta) in fT(4) (expressed as the post-treatment fT(4)/pre-treatment fT(4) ratio) accounted for 45% of the variability in change of tHCys ( tHCys = - 0.07-4.94 log ( fT(4))); there was no independent contribution of changes in creatinine which was, however, strongly related to changes in tHCys (r = 0.61). CONCLUSIONS: Plasma tHCys concentrations increased in hypothyroidism and decreased in hyperthyroidism. Plasma fT(4) is an independent determinant of tHCys concentrations. Lower folate levels and a lower creatinine clearance in hypo-thyroidism, and a higher creatinine clearance in hyperthyroidism only partially explain the changes in tHCys.

Adult↗
PubMed2002

Serum concentrations of tumour necrosis factor-alpha (TNF-alpha) and soluble TNF-alpha receptor p55 in patients with hypothyroidism and hyperthyroidism before and after normalization of thyroid function.

BACKGROUND: Tumour necrosis factor-alpha (TNF-alpha) is a cytokine with numerous immunological and metabolic activities. Receptors for TNF-alpha have been demonstrated in thyroid follicular cells and TNF-alpha and its receptors have been implicated in the cytotoxic mechanisms that characterize the thyroid destruction in autoimmune thyroid disease. In patients with Graves' disease, serum levels of TNF-alpha have been reported to be elevated and administration of TNF-alpha to humans has been shown to induce hormonal alterations resembling those seen in the nonthyroidal illness syndrome. OBJECTIVE: To evaluate serum concentrations of TNF-alpha and the soluble receptor for TNF-alpha (sTNFR-I) in a group of patients with thyroid dysfunction before and after normalization of thyroid function with appropriate therapy. DESIGN: We studied 20 patients with hypothyroidism (18 women and 2 men, mean age +/- SD, 48.8 +/- 16.1 years) and 20 patients with hyperthyroidism (14 women and 6 men, age 44.6 +/- 15.9 years). Patients were assessed at the time of diagnosis and again after normalization of thyroid function tests with appropriate therapy. A group of 20 healthy subjects (15 women and 5 men, age 44.9 +/- 15.1 years) were also studied as a control group. SETTING: All subjects were ambulatory and were studied as outpatients during visits to the endocrinology clinic. MEASUREMENTS: Serum concentrations of free T4 (FT4), total T3, TSH, TNF-alpha and sTNFR-I were measured in all subjects. TNF-alpha and sTNFR-I were measured using a quantitative enzyme immunoassay. RESULTS: In patients with hypothyroidism serum concentrations of TNF-alpha (3.17 +/- 1.18 pg/ml) and sTNFR-I (1273 +/- 364 pg/ml) were significantly higher than those found in controls (2.42 +/- 0.76 pg/ml, P < 0.05, and 971 +/- 235 pg/ml, P < 0.01, respectively). Normalization of thyroid function with l-thyroxine therapy did not significantly modify TNF-alpha or sTNFR-I levels. There were no differences in pre- and post-therapy values of TNF-alpha and sTNFR-I in patients with autoimmune (n = 14) or nonautoimmune (n = 6) hypothyroidism. Before therapy, patients with hyperthyroidism showed elevated serum concentrations of TNF-alpha (3.36 +/- 1.21 pg/ml; P < 0.01) and sTNFR-I (2274 +/- 579 pg/ml; P < 0.001) in relation to the control group. Treatment of hyperthyroidism was accompanied by a normalization of TNF-alpha levels (2.46 +/- 0.89 pg/ml; P < 0.001) and by a significant decrease in sTNFR-I concentrations (1369 +/- 475 pg/ml; P < 0.001). Post-therapy levels of TNF-alpha and sTNFR-I showed a significant correlation with loss of weight (r = 0.674, P < 0.01, and r = 0.629, P < 0.01, respectively) in hypothyroid patients. No correlation between these parameters was found in the group of patients with hyperthyroidism. CONCLUSIONS: In summary, these results confirm the relevance of activation of the TNF-alpha system in patients with thyroid dysfunction, as high plasma concentrations of TNF-alpha and sTNFR-I have been demonstrated in patients with hypothyroidism or hyperthyroidism. Treatment of hyperthyroidism is accompanied by a significant reduction in the previously elevated concentrations of both TNF-alpha and sTNFR-I. However, these changes are not seen when normalizing thyroid function in patients with hypothyroidism.

Adult↗
PubMed2003

Serum concentrations of adipocytokines in patients with hyperthyroidism and hypothyroidism before and after control of thyroid function.

OBJECTIVE: Adipose tissue is a hormonally active system that produces and releases different bioactive substances. Leptin, adiponectin and resistin are some of the recently discovered adipocytokines that participate in the regulation of intermediate metabolism. The aim of this study was to evaluate the circulating levels of leptin, adiponectin and resistin in patients with thyroid dysfunction before and after normalization of thyroid function with appropriate therapy. PATIENTS AND MEASUREMENTS: We studied 20 patients with hyperthyroidism (16 women and 4 men; mean age 47.2 +/- 3.9 years) and 20 patients with hypothyroidism (17 women and 3 men; 51.5 +/- 4.1 years). A group of 20 euthyroid subjects served as control group. Patients were evaluated at the time of diagnosis and again after normalization of thyroid function with appropriate therapy. Serum concentrations of free T4 (FT4), total T3, TSH, insulin, leptin, adiponectin and resistin were measured in all subjects. RESULTS: Hyperthyroid patients showed significantly decreased leptin levels in comparison with controls (11.0 +/- 1.1 vs. 30.4 +/- 5.0 microg/l, P < 0.001). No significant differences in adiponectin levels between hyperthyroid and control groups were found (27.8 +/- 4.0 vs. 46.0 +/- 12.0 mg/l, NS). Patients with hyperthyroidism exhibited reduced resistin levels in comparison with euthyroid subjects (6.4 +/- 0.8 vs. 8.4 +/- 0.7 microg/l, P < 0.05). Normalization of circulating thyroid hormone was accompanied by a nonsignificant increase in leptin levels (12.9 +/- 1.7 microg/l, P < 0.01 vs. control) and no significant modification both in adiponectin (32.0 +/- 7.1 mg/l, NS) and resistin (5.4 +/- 0.7 microg/l, NS) levels. Adjustment of adipocytokine concentrations for body mass index (BMI) showed that treatment of hyperthyroidism induced a significant reduction in adjusted resistin concentrations (0.21 +/- 0.03 vs. 0.28 +/- 0.03 microg/l/BMI units, P < 0.05), with no changes in adjusted leptin and adiponectin. Hypothyroid patients showed significantly lower leptin levels compared with the controls (16.0 +/- 3.5 vs. 30.4 +/- 5.0 microg/l, P < 0.05). Adiponectin levels in patients with hypothyroidism (71.8 +/- 16.0 mg/l) were similar to those in the control group and were not modified with therapy. Resistin levels were significantly reduced among hypothyroid patients (5.8 +/- 1.0 microg/l, P < 0.05), and were not increased after levothyroxine therapy. A significant rise in BMI-corrected leptin levels was observed after replacement therapy, with no changes in adiponectin- and resistin-corrected values. CONCLUSIONS: The results suggest that (1) low serum leptin levels are present in both hyperthyroid and hypothyroid patients but are only increased after therapy in the latter; (2) resistin might be implicated in the insulin resistance state that accompanies thyrotoxicosis; and (3) inadequate secretion of adiponectin seems to have no role in metabolic changes associated with thyroid dysfunction.

Adiponectin↗
PubMed1997

Hyperthyroidism and pulmonary hypertension.

OBJECTIVES: To identify patients with hyperthyroidism and coincidental pulmonary hypertension and to document reversibility of pulmonary hypertension after treatment of hyperthyroidism. DESIGN: Patients with hyperthyroidism referred for transthoracal echocardiography for any reason that showed elevated pulmonary arterial pressures were collected. After therapy for the thyreotoxic state with documented normalization of thyroid hormone (IT4), pulmonary arterial pressure was measured again noninvasively. SETTING: An out-patient tertiary referral centre. SUBJECTS: The medical records were used to identify, retrospectively, patients with hyperthyroidism and pulmonary hypertension over a three-year period (April 1993 to April 1996). INTERVENTIONS AND MAIN OUTCOME MEASURES: Systolic pulmonary artery pressure (PAPs) was determined by adding up right ventricular systolic pressure (RVSP) and mean right atrial pressure (RAP) measured by continuous-wave Doppler echocardiography according to standard techniques. All patients were treated for hyperthyroidism to normal IT4 levels. After successful therapy. Doppler echocardiography was repeated. RESULTS: Four patients with pulmonary hypertension showing elevated PAPs of 40 +/- 11 mmHg were identified. After therapy. PAPs decreased in all patients to a mean of 25 +/- 6 mmHg. CONCLUSION: The observation of four patients with pulmonary hypertension and hyperthyroidism is striking and suggests a possible pathogenetic link of these disorders.

Adult↗
PubMed2001

Platelet Na,K-adenosine triphosphatase as a tissue marker of hyperthyroidism.

Platelet Na(+),K(+)-adenosine triphosphatase (ATPase) activity was measured in 34 (15 males, 19 females) healthy subjects, 89 (35 males, 54 females) hyperthyroid patients, and 34 (7 males, 27 females) treated hyperthyroid patients to assess the potential of this measurement as a tissue marker and diagnostic test for hyperthyroidism. Platelet Na(+),K(+)-ATPase activity was measured in platelet lysates by the rate of release of phosphate from adenosine triphosphate (ATP) in the presence and absence of ouabain. Platelet Na(+),K(+)-ATPase activity (median and range) in the hyperthyroid group (271, 169 to 821 pmol/h/g protein) was significantly higher compared with the healthy group (125, 74 to 185 micromol/h/g protein, P <.001 by Mann-Whitney U test). The treated hyperthyroid group had slightly, but significantly higher, free triiodothyronine (FT3) and free thyroxine (FT4), as well as platelet Na(+),K(+)-ATPase activity (147, 98 to 246 micromol/h/g protein, P <.05). If a platelet Na(+),K(+)-ATPase activity of 190 micromol/h/g protein was used as a cut off value, the specificity and sensitivity were 90% and 93%, respectively. We conclude that platelet Na(+),K(+)-ATPase may be a useful tissue marker of hyperthyroidism.

Adolescent↗