Activity In Hyperthyroidism Research Articles

The Prevalence, Magnitude, and Reversibility of Elevated Liver Enzyme Activities in Hyperthyroid Cats Presenting for Iodine-131 Treatment.

ObjectivesThe primary objective of this study was to report the prevalence and magnitude of elevated liver enzyme activity in feline hyperthyroidism using a large cohort of cats presenting for iodine-131 treatment. The secondary objective was to determine if elevated liver enzyme activity was a reversible process following successful iodine-131 treatment.MethodsCases that presented for a single iodine-131 treatment were retrospectively reviewed. Short-term and long-term follow-up clinicopathologic data was then reviewed for the secondary objective.ResultsTwo hundred seventeen hyperthyroid cats met the inclusion criteria for the primary objective. In total, 123/217 (56.7%) of the cats had at least one liver enzyme elevation on their chemistry panel, with alanine transaminase activity being the most common. All cats who were successfully treated with iodine-131 had liver enzyme activity within the reference range at short-term follow-up and long-term follow-up points.Conclusion and RelevanceOur study demonstrates that elevated liver values are common in cats presenting for iodine-131 treatment. Additionally, our study demonstrates that even when liver values are markedly elevated prior to treatment, the liver enzyme activity will return to normal after successful resolution of hyperthyroidism using iodine-131 treatment. Investigation into hepatobiliary disease and liver function tests for cats with a diagnosis of hyperthyroidism may be unnecessary as the liver values will likely return to normal with successful iodine-131 treatment.

Evaluation of Arginine-Nitric Oxide Pathway in Patients with Hyperthyroidism

There is a reciprocal regulation of arginase and nitric oxide synthase in L-arginine metabolizing pathways. Nitric oxide has been claimed as an important role player in hyperthyroidism in recent years. The fact that arginase is an important part of regulation of arginine has not been investigated yet in terms of nitric oxide synthase activity in hyperthyroidism. This study aims to investigate arginase, manganese (a cofactor of arginase) and total nitrite levels (a metabolite of nitric oxide) and their relationship to the arginine- nitric oxide pathway in patients with hyperthyroidism. Arginase activities, manganese, and total nitrite levels were measured in plasma samples from 50 patients with hyperthyroidism and 50 healthy age- and gender-matched control subjects. Plasma arginase activities were found to be significantly lower and total nitrite level higher in patients with hyperthyroidism than those of controls. Manganese levels were not significantly different in hyperthyroidism group compared to those of controls. Our results demonstrate that the arginine-nitric oxide pathway is implicated in the cardiovascular manifestations of hyperthyroidism which may be of clinical relevance.

Abnormal spontaneous brain activity is associated with impaired emotion and cognition in hyperthyroidism: A rs-fMRI study

Hyperthyroid patients undergo emotional and cognitive dysfunction. However, the neurological basis for it remains ambiguous. Amplitude of low frequency fluctuation (ALFF) and regional homogeneity (ReHo) were used to investigate abnormal spontaneous activity in hyperthyroidism for the first time. 29 hyperthyroid patients and 29 healthy controls (HC) received 3.0T magnetic resonance imaging (MRI) scans and neuropsychological assessments. Compared with HC, hyperthyroid patients showed decreased ALFF in left medial frontal gyrus (MeFG) and left posterior cingulate cortex (PCC). Hyperthyroidism group exhibited decreased ReHo in left MeFG. Within hyperthyroidism group, ALFF values in left MeFG were positively correlated with Hamilton Anxiety Rating Scale (HARS) Z-scores, but negatively correlated with processing speed Z-scores. Besides, ALFF values in left precuneus had a positive correlation with HARS Z-scores. As a result, abnormal brain spontaneous activity mainly in default mode network (DMN) implicated the neuro-pathological substrate of relevant emotional and cognitive dysfunction in hyperthyroid patients.

Increased BAT Activity in Hyperthyroidism Is Still a Fascinating Hypothesis that Awaits Confirmation

Increased BAT Activity in Hyperthyroidism Is Still a Fascinating Hypothesis that Awaits Confirmation

Serum paraoxonase-1 activity as a novel marker in the diagnosis and prognosis of hyperthyroidism

Thyrotoxicosis or hyperthyroidism is the clinical syndrome caused by an excess of circulating free thyroxine and free triiodothyronine, or both. It was first diagnosed in 1979 in the US. Since this time, the frequency of this diagnosis has increased. It is common, affecting about 2% of women and 0.2% of men. The most common causes of Thyrotoxicosis are Graves' disease and formation of multinodular goiter and autonomously functioning solitary thyroid nodule. In excessive production of thyroid hormones, the basal metabolic rate can be increased by 100%. Hyperthyroidism also induces a hyperdynamic cardiovascular state that is associated with tachycardia, systolic hypertension, atrial fibrillation and increased cardiovascular mortality. The present study was designed to investigate the relationship among the serum PON-1 activity, lipid profile, and thyroid hormone level in patients with hyperthyroidism. In our research, we have estimated PON 1 activity in hyperthyroidism. We found the PON 1 activity decreased in the hyperthyroid patients (144.89 ± 3.27 U/ml) as compared to controls (214.71 ± 5.46 U/ml) significantly (p < 0.05). The thyroid hormones T3 and T4 also significantly increases (p < 0.001) in hyperthyroidism. In case of lipid profile triacylglycerol, HDL cholesterol, LDL cholesterol as well as VLDL cholesterol was also found significantly decreased (p < 0.05) in hyperthyroidism. In our study, we found a decrease in triacylglycerol, HDL cholesterol, LDL cholesterol as well as VLDL cholesterol. However, the decrease in HDL, LDL and VLDL cholesterol may also be associated with other disorders. Further, the blood quantity required for lipid profile is large (5 ml) and patients have to be fast for at least 14 hours. Similarly, estimation of lipid profile is time consuming method and hence it is not preferable as a marker. The increase in thyroid hormones T3 and T4 significantly correlates with hyperthyroidism. However, estimation of thyroid hormone also required large (5 ml) quantity of blood sample. Similarly, the sample required should be always fresh. The estimation is carried generally by enzyme linked immune sorbent assay (ELISA) which is time consuming and costly method. But, on the other hand quantity of blood sample required for estimation of PON 1 activity is very less (1 ml). The estimation of PON 1 activity is easy and the method is chief. The most important thing is that PON 1 activity is decreased only in few disorders. Further, it correlates well with severity of hyperthyroidism. Thus, PON 1 activity is a novel marker in the diagnosis and prognosis of hyperthyroidism.

Lithium and thyroid

One in 200 people receive lithium for treatment of bipolar disorder. The common clinical side effects of the drug are goitre in up to 40% and hypothyroidism in about 20%. Lithium increases thyroid autoimmunity if present before therapy. Treatment with levothyroxine is effective and lithium therapy should not be stopped. Lithium may cause hyperthyroidism due to thyroiditis or rarely Graves' disease. As lithium inhibits thyroid hormone release from the thyroid gland it can be used as an adjunct therapy in the management of severe hyperthyroidism. It also increases thyroidal radioiodine retention and may be effective in reducing administered activity in hyperthyroidism. There is no clinical benefit of lithium therapy in thyroid cancer. More research is required on the cellular proliferative effects of lithium as well as its impact on the immune system.

Serum Chromogranin A Concentration in Hyperthyroidism before and after Medical Treatment

The aim was to evaluate changes in chromogranin A (CgA) concentration in hyperthyroidism and to assess its metabolic correlations. We studied CgA levels in hyperthyroidism. First, 38 hyperthyroid patients matched with 86 normal controls were studied after an overnight fast. Second, 30 if the 38 patients were followed up for 6 months with medical antithyroid drug therapy (carbimazole). In the first study, after 10-12 h overnight fasting, blood was collected for measurement of CgA, glucose, insulin, intact proinsulin, and thyroid function. These variables were remeasured in the second study for the patients after attainment of euthyroidism with the antithyroid drug carbimazole for 6 months. Pretreatment CgA level was significantly higher in patients compared with controls. CgA levels dropped significantly to levels similar to those of controls after antithyroid therapy. Although baseline and follow-up fasting glucose, insulin, and intact proinsulin demonstrated similar pattern of CgA changes before and after medical treatment, CgA did not correlate with any of them. However, CgA levels demonstrated a significant positive correlation with free T(3) and free T(4) only. These studies demonstrate that untreated hyperthyroidism is associated with elevated CgA level that changes in parallel to thyroid status. It is therefore possible to use CgA concentration as a potential marker of disease activity in hyperthyroidism.

Elevated numbers of reticulated platelets in hyperthyroidism: direct evidence for an increase of thrombopoiesis.

We studied thrombopoietic activity in hyperthyroidism by determination of reticulated platelet counts. At the time of hyperthyroidism 14/15 patients had higher reticulated platelets than after achievement of euthyroidism (P<0.001). There was no difference in peripheral platelet counts and mean platelet volumes at the time of hyperthyroidism when compared to euthyroidism. Three patients had pan- and auto-reactive platelet antibodies during hyperthyroidism. These antibodies were directed against GPIIb/IIIa in two patients and against GPIb/IX in one patient. Our findings provide direct evidence that hyperthyroidism is associated with increased platelet production, as reflected by an increase in reticulated platelets.

Ceruloplasmin and vitamin E levels in toxic multinodular goiter

The effect of the enhanced metabolic rate over antioxidant status was investigated in hyperthyroid individuals. Serum total T 3 and T 4 levels were measured by radioimmunoassay in 45 patients and 25 controls. The serum vitamin E was assayed fluorometrically in the hexane extract of serum. Serum ceruloplasmin activity was measured spectrophotometrically. Statistical significance was asessed by correlation regression analysis and paired t-test. The serum vitamin E levels decreased significantly as the levels of the thyroid hormones increased. For ceruloplasmin the opposite changes were observed: mean serum ceruloplasmin of hyperthyroid patients was greater than that of control group. Although the changes in vitamin E and ceruloplasmin concentrations did correlate with the levels of thyroid hormones in hyperthyroid patients, we observed no associations between these parameters in the euthyroid state. As these two parameters are the measure of oxidation potential, it may be suggested that raised free radical activity in hyperthyroidism cause the increased oxidative stress and increased general radical scavenging. The present data may indicate a direct effect of thyroid hormones on vitamin E and ceruloplasmin metabolism.

Altered muscle sympathetic nerve activity in hyperthyroidism and hypothyroidism

To determine whether sympathetic nerve activity is altered in hyperthyroidism and hypothyroidism we microneurographically measured muscle sympathetic nerve activity in patients with these thyroid dysfunctions and compared the results with those of normal controls. Patients with hyperthyroidism tended to have less muscle sympathetic nerve activity than normal controls, and patients with hypothyroidism had significantly greater muscle sympathetic nerve activity than normal controls ( P < 0.05). In all subjects, there was a significantly negative correlation between the serum concentration of free triiodothyronine or free thyroxine and muscle sympathetic nerve activity, and there was a significantly positive correlation between the serum concentration of thyroid-stimulating hormone and the muscle sympathetic nerve activity. These results suggest an inverse relationship between thyroid function and sympathetic nerve activity.

Effect of pyridostigmine and pirenzepine on GH responses to GHRH in hyperthyroid patients

We wished to investigate whether thyrotoxicosis can influence the cholinergic modulation of GH secretion. Pyridostigmine was given orally, then GHRH injected i.v., and levels were measured. In a separate study, pirenzepine was injected i.v., then GHRH, and growth hormone levels were measured. Thyrotoxic patients were compared with normal subjects. GH was measured from -30 to +120 minutes at intervals of 15 minutes. Pyridostigmine markedly increased GH responses to GHRH in normal subjects, but not in thyrotoxic patients. Pirenzepine abolished the GH response to GHRH in thyrotoxic patients. GH responses to GHRH in hyperthyroid patients were suppressed by cholinergic muscarinic receptor blockade with pirenzepine. Activation of cholinergic pathways with pyridostigmine did not increase GH responses to GHRH in these patients. This may be a consequence of increased hypothalamic cholinergic function or reduced hypothalamic GHRH activity in hyperthyroidism. Our findings demonstrate a further mechanism by means of which thyroid status may affect the secretory activity of the somatotroph.

Erythrocyte sodium fluxes, ouabain binding sites, and Na +, K +-ATPase activity in hyperthyroidism

Erythrocyte sodium pump activity, in contrast to other tissues, is decreased in hyperthyroidism. In order to examine whether the effect of thyroid hormones on erythrocytes is part of a generalized effect on other transport pathways, we measured sodium pump activity, Na +,K +-adenosine triphosphatase (ATPase) activity, ouabain binding sites, bumetanide-sensitive sodium potassium cotransport (SPC), sodium lithium countertransport (SLC), and ouabain- and bumetanide-insensitive passive efflux of sodium (sodium “leak”) in erythrocytes from 20 healthy subjects and 18 untreated hyperthyroid subjects. Sodium pump activity (ouabain-sensitive sodium efflux rate constant), Na +,K +-ATPase activity, and the number of ouabain binding sites were lower and the erythrocyte sodium content was higher in hyperthyroid subjects. The rate constants of erythrocyte SPC ( P < .05), SLC ( P < .001), and sodium “leak” ( P < .05) were also significantly lower in hyperthyroidism. In 11 of the hyperthyroid subjects, sodium flux measurements were repeated after 20 weeks of treatment. Sodium pump activity, the number of ouabain binding sites, and the rate constant for SLC increased. These results suggest that the effect of thyroid hormones on the erythrocyte sodium pump is part of a generalized effect on membrane proteins, rather than a specific effect.

Fibrinogen and fibrinolytic activity in hyperthyroidism before and after antithyroid treatment

Plasma concentration of fibrinogen and B beta 15-42, a specific product of fibrinogen metabolism induced by plasmin, were measured in a group of patients with untreated hyperthyroidism and in controls. Significantly increased plasma levels of both parameters were observed in hyperthyroid patients. The restoration of euthyroidism either by antithyroid drug or by radioiodine caused a significant decrease of fibrinogen and B beta 15-42. These data indicate that hyperthyroidism is another clinical condition associated with increased concentration of fibrinogen and B beta 15-42.

Effects of variations in thyroid hormone serum concentrations on serum ACE-activity.

Serum angiotensin converting enzyme activities were significantly increased in 26 untreated hyperthyroid patients (20.3 +/- 5.4 U/ml; P less than 0.001) compared with healthy control subjects (13.1 +/- 2.3 U/ml). In 12 patients a significant fall in enzyme activities was observed after treatment compared with pretreatment serum ACE levels (P less than 0.001). Eight patients with hypothyroidism (15.7 +/- 5.1 U/ml) and 11 athyreotic patients, totally thyroidectomized for well-differentiated thyroid cancer, showed no significant differences in serum ACE activities (14.3 +/- 2.2 U/ml) compared with control subjects. After thyroid hormone supplementation a significant increase in serum ACE activity (P less than 0.05) was found in the athyreotic patients. Addition of increasing amounts of L-thyroxine to a serum sample of an athyreotic patient showed no significant effect on ACE activity in vitro. We suggest that the elevated serum ACE activity in hyperthyroidism is not from the thyroid gland, but represents a direct effect of thyroid hormone on ACE synthesis and/or release from endothelial cells.

Increased levels of serum angiotensin-converting enzyme activity in hyperthyroidism.

Serum angiotensin-converting enzyme activity was significantly elevated in 21 patients with hyperthyroidism (65 +/- 18 U/mL) as compared with levels in healthy control subjects (30 +/- 9 U/mL). In eight patients treated with thionamide drugs, the enzyme activities decreased to a normal range as thyroid hormone concentrations returned to euthyroid levels. When two patients became hyperthyroid due to an insufficient maintenance dose of antithyroid drugs, the increase in the serum thyroid hormone concentration was followed by the re-elevation of serum angiotensin-converting enzyme levels with a time lag of about 2 weeks. Levels of this enzyme are increased reflecting the elevated serum thyroid hormone levels in hyperthyroidism. The hyperthyroid state should be considered when serum angiotensin-converting enzyme levels are high.

Parathyroid activity in hyperthyroidism

Even in the absence of PTH, serum P levels rose in response to thyroxine. Thus, PTH secretion is not suppressed in hyperthyroidism as assumed hitherto. In contrast, the findings suggest an activation of endogenous PTH secretion in thyrotoxic animals. These results agree with the finding of increased serum PTH levels in thyrotoxic patients (radioimmunoassay*), reported elsewhere (3). After parathyroidectomy TRP of hyperthyroid animals was not different from that of euthyroid animals, although the serum P levels were elevated. At high serum P levels, TRP was higher in hyperthyroid PTX animals, pointing to a raised renal “threshold”. In view of the contracted extracellular space in hyperthyroid animals, this effect of thyroxine might be mediated by changes of extracellular volume, although alternative mechanisms are not excluded.

Some observations on the mechanism of increase of plasma renin activity in hyperthyroidism

Some observations on the mechanism of increase of plasma renin activity in hyperthyroidism