Thyroid hormones and the adrenergic nervous system

Nilsson, Ove; Karlberg, Bengt E.

doi:10.1111/j.0954-6820.1983.tb01610.x

Cited by 19 publications

(7 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It can be speculated that paracetamol liver toxicity is more pronounced in diseases accompanied by high catecholamine level such as congestive heart failure[ 12 13 ] or thyrotoxicosis. [ 14 ] Paracetamol in theses disease is expected to produce liver toxicity at therapeutic doses and that the use of adrenergic blockers may be beneficial in minimizing the toxicity of paracetamol. It can be concluded that adrenergic blockers are not the specific antidotes for paracetamol hepatotoxicity, however, concomitant use with paracetamol may minimize such toxicity.…”

Section: Discussionmentioning

confidence: 99%

Effect of adrenergic blockers, carvedilol, prazosin, metoprolol and combination of prazosin and metoprolol on paracetamol-induced hepatotoxicity in rabbits

2014

View full text Add to dashboard Cite

Objectives:To evaluate hepatoprotective potential of carvedilol, prazosin, metoprolol and prazosin plus metoprolol in paracetamol-induced hepatotoxicity.Materials and Methods:Thirty-six male rabbits were divided into six groups, six in each, group 1 received distilled water, group 2 were treated with paracetamol (1 g/kg/day, orally), group 3, 4,5 and 6 were treated at a dose in (mg/kg/day) of the following: Carvedilol (10 mg), prazosin (0.5 mg), metoprolol (10 mg), and a combination of metoprolol (10 mg) and prazosin (0.5 mg) respectively 1 h before paracetamol treatment. All treatments were given for 9 days; animals were sacrificed at day 10. Liver function tests, malondialdehyde (MDA) and glutathione (GSH) in serum and liver homogenates were estimated. Histopathological examinations of liver were performed.Results:Histopathological changes of hepatotoxicity were found in all paracetamol-treated rabbits. The histopathological findings of paracetamol toxicity disappeared in five rabbits on prazosin, very mild in one. In carvedilol group paracetamol toxicity completely disappeared in three, while mild in three rabbits. Paracetamol hepatotoxicity was not changed by metoprolol. In metoprolol plus prazosin treated rabbits, moderate histopathological changes were observed. Serum liver function tests and MDA in serum and in liver homogenate were elevated; GSH was depleted after paracetamol treatment and returned back to the control value on prior treatment with prazosin. MDA in serum and liver homogenate, alkaline phosphatase, total bilirubin were significantly decreased after carvedilol and prazosin plus metoprolol treatments.Conclusion:Carvedilol and prazosin are hepatoprotective in paracetamol hepatotoxicity, combination of prazosin and metoprolol have moderate, and metoprolol has a little hepatoprotection.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of adrenergic blockers, carvedilol, prazosin, metoprolol and combination of prazosin and metoprolol on paracetamol-induced hepatotoxicity in rabbits

2014

View full text Add to dashboard Cite

show abstract

“…However, the negative regulation of sterol regulatory element-binding protein-1c and angiopoietin-like protein 3 enhances fat catabolism and ketone body production (22,23). In addition, the activation of the sympathetic nervous system via the β-adrenergic system induces excessive glucagon secretion and enhances fat catabolism (24)(25)(26)(27)(28). Under fasting conditions, ketone body production may predominate over elevated blood glucose levels, and euDKA can develop.…”

Section: Discussionmentioning

confidence: 99%

Two Cases of Thyrotoxicosis and Euglycemic Diabetic Ketoacidosis Under Sodium-glucose Transport Protein 2 Inhibitor Treatment

et al. 2022

View full text Add to dashboard Cite

Thyrotoxicosis and sodium-glucose transport protein 2 inhibitors (SGLT2is) are associated with the induction of euglycemic diabetic ketoacidosis (euDKA). We herein report two cases of euDKA in patients with diabetes mellitus wherein both thyrotoxicosis and SGLT2i treatment were the underlying causes. One patient developed thyrotoxicosis during the course of type 2 diabetes mellitus, whereas the other patient was suspected of developing slowly progressive insulin-dependent diabetes mellitus during the course of Graves' disease. Although such cases are rare, there is some concern that similar cases may occur because of the increased frequency of SGLT2i use in recent years.

show abstract

“…PSV STA represents the level of autonomic nervous system (ANS) stimulation [38,39] and indicates the role of peripheral ANS in the activation of the thyroid gland function, with which the blood flow is directly associated [40]. Meanwhile, the direct involvement of conductive autonomic innervation in hormonogenesis within the thyroid gland is natural and evidenced by studies [41][42][43][44][45][46]. For example, according to Park et al [47], ANS directly affects thyrocytes and increases the production of thyroid hormones independently from TSH and TSHR antibodies.…”

Section: Discussionmentioning

confidence: 99%

“…In hypothyroidism, serum FT4 and FT3 are often at normal levels [50,51], which is indicative of the functional capability of the thyroid gland to provide the level of thyroid hormones necessary for the body in response to stimulation by the nervous system and TSH. At the same time, the facts indicate the leading role of the nervous system in regulating thyroid hormone production [42][43][44][45][46]. Therefore, the excessive ANS-mediated stimulation of the thyroid gland in hypothyroidism can cause hyperthyroidism without the involvement of the immune system.…”

Section: Discussionmentioning

confidence: 99%

Conversion From Hypothyroidism to Hyperthyroidism and Back After Anti-SARS-CoV-2 Vaccination

Ушаков

2022

J Endocrinol Metab

View full text Add to dashboard Cite

Cases presenting with changes in various organs caused by anti-severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccination are rare. In particular, after such instances of vaccination, onset of subacute thyroiditis, Hashimoto thyroiditis, and Graves' disease was observed. We present the case of a 55-year-old woman whose hypothyroidism converted to hyperthyroidism after vaccination with Gam-COVID-Vac (Sputnik V). After the first dose of vaccine, a hormonal metabolism alteration was noted, i.e., conversion from hypothyroidism to euthyroidism. After the second dose of vaccine, onset of hyperthyroidism with thyrotoxicosis was noted without signs of subacute thyroiditis. Hyperthyroidism persisted for several weeks before reverting to hypothyroidism. Assessments did not reveal an increase in the patient's thyroid-stimulating hormone receptor antibody levels throughout the indicated period. However, after hyperthyroidism reverted to hypothyroidism, a significant increase in the peak systolic velocity of the superior thyroid arteries was observed, which is characteristic of hyperthyroidism. Owing to the known involvement of the autonomic nervous system (ANS) in blood vessel tone regulation, thyroid hormonogenesis, and stress, the ANS-mediated conversion from hypothyroidism to hyperthyroidism in certain individuals after receiving a vaccine, which may serve as a sufficient stimulus for ANS nerve centers, is highly probable. Therefore, diagnostic assessment of ANS condition should be performed before vaccination in patients with chronic thyroid disorders or diseases of other organs or organ systems. If changes in ANS are found, providing preemptive treatment before vaccination is recommended.

show abstract

Thyroid hormones and the adrenergic nervous system

Cited by 19 publications

References 38 publications

Effect of adrenergic blockers, carvedilol, prazosin, metoprolol and combination of prazosin and metoprolol on paracetamol-induced hepatotoxicity in rabbits

Effect of adrenergic blockers, carvedilol, prazosin, metoprolol and combination of prazosin and metoprolol on paracetamol-induced hepatotoxicity in rabbits

Two Cases of Thyrotoxicosis and Euglycemic Diabetic Ketoacidosis Under Sodium-glucose Transport Protein 2 Inhibitor Treatment

Conversion From Hypothyroidism to Hyperthyroidism and Back After Anti-SARS-CoV-2 Vaccination

Contact Info

Product

Resources

About