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Factors affecting drug-induced liver injury: antithyroid drugs as instances.

Heidari R, Niknahad H, Jamshidzadeh A, Abdoli N - Clin Mol Hepatol (2014)

Bottom Line: The purpose of this article is to give an overview on possible susceptibility factors in liver injury induced by antithyroid agents.Age, gender, metabolism characteristics, alcohol consumption, underlying diseases, immunologic mechanisms, and drug interactions are involved in enhancing antithyroid drugs-induced hepatic damage.An outline on the clinically used treatments for antithyroid drugs-induced hepatotoxicity and the potential therapeutic strategies found to be effective against this complication are also discussed.

View Article: PubMed Central - PubMed

Affiliation: Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

ABSTRACT
Methimazole and propylthiouracil have been used in the management of hyperthyroidism for more than half a century. However, hepatotoxicity is one of the most deleterious side effects associated with these medications. The mechanism(s) of hepatic injury induced by antithyroid agents is not fully recognized yet. Furthermore, there are no specific tools for predicting the occurrence of hepatotoxicity induced by these drugs. The purpose of this article is to give an overview on possible susceptibility factors in liver injury induced by antithyroid agents. Age, gender, metabolism characteristics, alcohol consumption, underlying diseases, immunologic mechanisms, and drug interactions are involved in enhancing antithyroid drugs-induced hepatic damage. An outline on the clinically used treatments for antithyroid drugs-induced hepatotoxicity and the potential therapeutic strategies found to be effective against this complication are also discussed.

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The possible role of Grave's disease (GD) as a potential risk factor for antithyroid drugs induced hepatotoxicity. ROS, Reactive Oxygen Species; RNS, Reactive Nitrogen Species; SOD, Superoxide dismutase; GST, Glutathione-S-transferase; GSH, Glutathione.
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Figure 4: The possible role of Grave's disease (GD) as a potential risk factor for antithyroid drugs induced hepatotoxicity. ROS, Reactive Oxygen Species; RNS, Reactive Nitrogen Species; SOD, Superoxide dismutase; GST, Glutathione-S-transferase; GSH, Glutathione.

Mentions: Several different disorders can cause hyperthyroidism. Graves' disease (GD), is the most common cause of hyperthyroidism in humans.93 Many investigations have been carried out on the complications which occur in hyperthyroid patients with GD. It has been shown that, the activity of different enzymes which are involved in the antioxidant defense mechanism of liver, are changed in hyperthyroidism.94 Komosinska et al. showed that glutathione reductase (GR) activity, was lower in hyperthyroid patients.95 In another investigation it has been observed that oxidative stress occurred in liver tissue of hyperthyroid animals probably due to impaired antioxidant defense mechanisms.96,97 As antithyroid drugsinduced hepatotoxicity is deteriorated in experimental models with defected liver protective mechanisms,41,51 the question arises if GD (the disease which antithyroid drugs are prescribed against) can sensitize individuals to the antithyroid medications' adverse hepatic effects (Fig. 4). The hypothesis that GD itself has a role in antithyroid drugs-induced hepatic injury, needs more controlled and in depth investigations to be clarified.


Factors affecting drug-induced liver injury: antithyroid drugs as instances.

Heidari R, Niknahad H, Jamshidzadeh A, Abdoli N - Clin Mol Hepatol (2014)

The possible role of Grave's disease (GD) as a potential risk factor for antithyroid drugs induced hepatotoxicity. ROS, Reactive Oxygen Species; RNS, Reactive Nitrogen Species; SOD, Superoxide dismutase; GST, Glutathione-S-transferase; GSH, Glutathione.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4197171&req=5

Figure 4: The possible role of Grave's disease (GD) as a potential risk factor for antithyroid drugs induced hepatotoxicity. ROS, Reactive Oxygen Species; RNS, Reactive Nitrogen Species; SOD, Superoxide dismutase; GST, Glutathione-S-transferase; GSH, Glutathione.
Mentions: Several different disorders can cause hyperthyroidism. Graves' disease (GD), is the most common cause of hyperthyroidism in humans.93 Many investigations have been carried out on the complications which occur in hyperthyroid patients with GD. It has been shown that, the activity of different enzymes which are involved in the antioxidant defense mechanism of liver, are changed in hyperthyroidism.94 Komosinska et al. showed that glutathione reductase (GR) activity, was lower in hyperthyroid patients.95 In another investigation it has been observed that oxidative stress occurred in liver tissue of hyperthyroid animals probably due to impaired antioxidant defense mechanisms.96,97 As antithyroid drugsinduced hepatotoxicity is deteriorated in experimental models with defected liver protective mechanisms,41,51 the question arises if GD (the disease which antithyroid drugs are prescribed against) can sensitize individuals to the antithyroid medications' adverse hepatic effects (Fig. 4). The hypothesis that GD itself has a role in antithyroid drugs-induced hepatic injury, needs more controlled and in depth investigations to be clarified.

Bottom Line: The purpose of this article is to give an overview on possible susceptibility factors in liver injury induced by antithyroid agents.Age, gender, metabolism characteristics, alcohol consumption, underlying diseases, immunologic mechanisms, and drug interactions are involved in enhancing antithyroid drugs-induced hepatic damage.An outline on the clinically used treatments for antithyroid drugs-induced hepatotoxicity and the potential therapeutic strategies found to be effective against this complication are also discussed.

View Article: PubMed Central - PubMed

Affiliation: Pharmaceutical Sciences Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.

ABSTRACT
Methimazole and propylthiouracil have been used in the management of hyperthyroidism for more than half a century. However, hepatotoxicity is one of the most deleterious side effects associated with these medications. The mechanism(s) of hepatic injury induced by antithyroid agents is not fully recognized yet. Furthermore, there are no specific tools for predicting the occurrence of hepatotoxicity induced by these drugs. The purpose of this article is to give an overview on possible susceptibility factors in liver injury induced by antithyroid agents. Age, gender, metabolism characteristics, alcohol consumption, underlying diseases, immunologic mechanisms, and drug interactions are involved in enhancing antithyroid drugs-induced hepatic damage. An outline on the clinically used treatments for antithyroid drugs-induced hepatotoxicity and the potential therapeutic strategies found to be effective against this complication are also discussed.

Show MeSH
Related in: MedlinePlus