Pleiotropic Effects of Thyroid Hormones: Learning from Hypothyroidism

Franco, Martha; Chávez, Edmundo; Pérez-Méndez, Óscar

doi:10.4061/2011/321030

Cited by 29 publications

(14 citation statements)

References 110 publications

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“…Treatment of hyperthyroidism is important to prevent arrhythmic complications and even a subclinical hyperthyroid state should be treated, especially in high-risk patients. Another important point is prevention of iatrogenic hypothyroidism during treatment, because hypothyroidism also brings some other cardiovascular and general risks [ 98 – 100 ].…”

Section: Discussionmentioning

confidence: 99%

State of the art paper Hyperthyroidism and cardiovascular complications: a narrative review on the basis of pathophysiology

Ertek¹,

Cicero²

2013

aoms

124

107

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Cardiovascular complications are important in hyperthyroidism because of their high frequency in clinical presentation and increased mortality and morbidity risk. The cause of hyperthyroidism, factors related to the patient, and the genetic basis for complications are associated with risk and the basic underlying mechanisms are important for treatment and management of the disease. Besides cellular effects, hyperthyroidism also causes hemodynamic changes, such as increased preload and contractility and decreased systemic vascular resistance causes increased cardiac output. Besides tachyarrythmias, impaired systolic ventricular dysfunction and diastolic dysfunction may cause thyrotoxic cardiomyopathy in a small percentage of the patients, as another high mortality complication. Although the medical literature has some conflicting data about benefits of treatment of subclinical hyperthyroidism, even high-normal thyroid function may cause cardiovascular problems and it should be treated. This review summarizes the cardiovascular consequences of hyperthyroidism with underlying mechanisms.

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Section: Discussionmentioning

confidence: 99%

State of the art paper Hyperthyroidism and cardiovascular complications: a narrative review on the basis of pathophysiology

Ertek¹,

Cicero²

2013

aoms

124

107

View full text Add to dashboard Cite

show abstract

“…Moreover, Franco et al, 2011 [31] reported that hypothyroidism also could increase the formation of polyunsaturated fatty acids which in turn changed plasma membrane composition. Isman et al [28] and Hataya et al, [32] were in agreement with that explanation and reported that this change of lipid composition caused lipid peroxidation sensitivity in rats membranes with hypothyroidism and could decrease the vulnerability to oxygen radical which caused cell injury.…”

Section: Discussionmentioning

confidence: 99%

samar.zag1234@gmail.com

Khatab¹,

Hulail²,

Hegazy³

et al. 2018

Zagazig University Medical Journal

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Kidney and thyroid functions interact with each other. Drugs used in treatment of any of them could have side reactions on any other organ. The effects of antithyroid medications on extrathyroidal organs could be due to oxidative stress and to damage in the renal cells. Aim: This work is designed to demonstrate the role of T4 in protection against the increase in oxidative stress caused by methimazole, and to detect if antithyroid drug-induced hypothyroidism (methimazole) or removal of thyroid by surgery causes damage of kidney cells or not. Methods: Twenty-five healthy adult male albino rats were used in the study. The animals were randomly separated into groups. Each group contained five rats: Group I (control group): This group received no drugs or treatment. Group II included rats with false thyroidectomy. Group III included thyroidectomized albino rats. Group IV included methimazole-induced hypothyroidism albino rats through receiving 60 mg/kg/day of methimazole in drinking water. Group V were administered methimazole (60 mg/kg/day) and l-thyroxine (T4) subcutaneous injection (20 μg/kg/day).The animals were anasethized and their abdomens were opened and both kidneys were removed, and immediately processed for histological & immunohistochemical study. Also oxidative enzymes were estimated. Rresults: Light microscopic examination of H&E stained sections showed marked damage of the structure of renal cortex in methimazole induced hypothyroidism group. This damage was concomitant with a decrease in kidney antioxidant enzymes. This damage was less pronounced in group of rats administrated T4 in association with methimazole. The cortex of kidney in rats of thyroidectomized group did not show any alterations in its micro structure. Conclusion: Methimazole causes both of hypothyroidism and alteration of the kidney cortex. This alteration is not noticed in case of surgical thyroidectomy inducing hypothyroidism. L-Thyroxine (T4) could decrease the effect of methimazole on kidney cortex.

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“…The role of various hormones such as thyroid-stimulating hormone, cortisol, prolactin, and thyroid hormones in the pathogenesis of psoriasis has been studied previously. [ 7 ] The severity of the disease has been correlated with levels of thyroid hormones, since like prolactin, the thyroid hormone receptors are expressed in the skin[ 8 ] and their levels change during the active phase of disease and alleviation of the disease by antithyroid therapy.…”

Section: Introductionmentioning

confidence: 99%