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    Home > Active Ingredient News > Endocrine System > Seven categories of drugs can cause "thyroid disease", how to correctly identify and deal with it?

    Seven categories of drugs can cause "thyroid disease", how to correctly identify and deal with it?

    • Last Update: 2022-04-27
    • Source: Internet
    • Author: User
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    Drug-induced thyroid disease refers to thyroid disease caused by the application of certain drugs, including hyperthyroidism (hyperthyroidism), hypothyroidism (hypothyroidism), goiter, and subclinical thyroid disease
    .

    Because some drugs interfere with the test results of thyroid function and even lead to abnormal thyroid function, it is necessary to understand the relevant drugs in order to correctly identify the changes in thyroid function during the medication process and take corresponding measures
    .

     Drugs can affect thyroid function at all levels of the hypothalamic-pituitary-thyroid axis and the stages of thyroid hormone transport, metabolism, synthesis and secretion
    .

    A variety of drugs can cause changes in different types of thyroid hormones, resulting in mild thyroid dysfunction, but common drugs that cause clinically significant thyroid disease are as follows: ➤Interferon alpha; ➤Iodine preparations, such as amiodine Ketones, iodophors; ➤ lithium salts; ➤ hormones, such as corticosteroids, estrogens; ➤ non-steroidal anti-inflammatory drugs; ➤ beta-adrenoceptor blockers; Wait
    .

     Interferon alpha Interferon alpha is clinically used in the treatment of various diseases, such as chronic hepatitis C, hepatitis B, multiple sclerosis and neoplastic diseases
    .

    Interferon α-induced thyroid disease is divided into three types: ① autoimmune hypothyroidism (usually subclinical hypothyroidism); ② thyroiditis; ③ toxic diffuse goiter (Graves disease)
    .

    Studies have shown that in interferon alpha-induced thyroid disease, hypothyroidism occurs more frequently than hyperthyroidism
    .

    At the same time, hypothyroidism is prone to occur in autoantibody-positive cases, but can also occur in autoantibody-negative patients
    .

     For patients with hypothyroidism, it is not necessary to discontinue interferon alpha, and thyroxine (T4) replacement therapy can be given
    .

    For patients with Graves' disease, interferon alfa should be discontinued and anti-hyperthyroidism therapy should be performed
    .

    Most of the thyroid diseases induced by interferon alpha are subclinical, and about 60% of patients can get spontaneous remission regardless of whether the drug is discontinued or not
    .

    For patients with a history of thyroid disease or positive thyroid antibodies, thyroid function should be monitored during treatment with interferon alpha
    .

     Amiodarone Amiodarone is a commonly used drug for the treatment of arrhythmia.
    It is a phenylpropanoid derivative, and each molecule contains two iodine atoms (about 37% iodine content).
    Due to the presence of iodine and its molecules Similar in structure to thyroxine, it can be regarded as a thyroxine analog acting on the liver and pituitary gland
    .

    The effect of amiodarone on thyroid function is mainly due to the effect of iodine and the inherent effect of the drug itself, which is manifested in two aspects: blocking the synthesis and release of thyroid hormone and direct damage to thyroid cells
    .

    There are two main types of thyroid diseases induced by amiodarone: hyperthyroidism and hypothyroidism
    .

     Amiodarone-induced hyperthyroidism (AIT) can be divided into the following categories according to its pathogenesis: ① Type 1 AIT: that is, iodine-induced hyperthyroidism, which mainly occurs in patients with underlying thyroid dysfunction
    .

    ②Type 2 AIT: mainly destructive thyroiditis caused by amiodarone itself
    .

    The clinical symptoms of amiodarone-induced hypothyroidism are similar to those of primary hypothyroidism, mainly due to excessive iodine intake in patients, which can inhibit iodine oxidation when it reaches a higher concentration in the thyroid, showing an iodine blocking effect
    .

     Lithium Salts Lithium salts are used to treat manic depression
    .

    Thyroid abnormalities caused by lithium are mainly goiter and hypothyroidism
    .

    Lithium salts have also been reported in the literature to cause hyperthyroidism, but they are rare
    .

    Lithium-induced goiters are usually smooth in texture and not tender
    .

    It can occur within a few weeks after starting treatment with lithium, or months or years later
    .

    Thyroid function and thyroid antibodies should be tested before starting lithium treatment, and thyroid function should be monitored every 6 months after treatment
    .

    If hypothyroidism occurs, thyroxine supplementation can be given without discontinuation of lithium
    .

     Antithyroid drugs methimazole and propylthiouracil inhibit the activity of thyroid peroxidase and reduce the synthesis of thyroid hormones, resulting in a decrease in serum T4 and T3 levels and an increase in serum TSH levels
    .

    Normal use can lead to primary hypothyroidism, and the hypothyroidism disappears after the drug is discontinued, and permanent hypothyroidism will not occur, and supplemental thyroxine treatment is not required
    .

    The use of methimazole and propylthiouracil in patients with hyperthyroidism can correct hyperthyroidism
    .

    It is currently used clinically for the treatment of hyperthyroidism
    .

     Anti-tumor drugs Tyrosine kinase inhibitors refer to small molecule kinase inhibitors, which inhibit the activity of kinases by blocking the binding of ATP, and are used for targeted therapy of various tumors
    .

    Commonly used drugs include sorafenib, sunitinib, axitinib, imatinib, nilotinib, and dasatinib
    .

    A variety of tyrosine kinase inhibitors can cause thyroid dysfunction and even drug-induced thyroid disease
    .

    It manifests as new-onset hypothyroidism or worsening of preexisting hypothyroidism, transient thyrotoxicosis, and persistent hyperthyroidism
    .

     There is no unified plan for the prevention and treatment of thyroid diseases caused by tyrosine kinases
    .

    Because thyroid dysfunction mostly occurs in the first few treatment cycles, it is recommended to monitor thyroid function on the 1st and 28th day of the first 4 treatment cycles.
    When hypothyroidism occurs, supplemental thyroxine replacement therapy is required.
    , When Graves' disease occurs, treatment of hyperthyroidism is given
    .

     In addition, some anticancer drugs can affect the concentration of thyroxine-binding globulin in the blood, such as pentafluorouracil, L-asparaginase, and hypothyroidism caused by them is more common, but its related clinical manifestations such as fatigue, fear Cold, depression, memory loss, etc.
    are often wrongly attributed to the primary disease, thus delaying the treatment of hypothyroidism
    .

     Hormones ➤ Glucocorticoids: Long-term treatment with glucocorticoids (eg, hydrocortisone) reduces TSH levels
    .

    Glucocorticoids also inhibit the conversion of T4 to T3, reduce thyroxine-binding globulin levels and enhance renal clearance of iodine
    .

    Moreover, glucocorticoids have a greater impact on the immune system, and are an important factor in causing autoimmune thyroiditis and thyroid nodules; ➤Estrogen: It can enhance the response of the pituitary gland to TRH and increase the secretion of TSH, which regulates thyroid function.
    and the main hormone that stimulates iodine accumulation, can promote the expression of sodium-iodine transporter through the cAMP pathway, thereby increasing the secretion of TH; ➤ Somatostatin: can directly affect the thyroid-stimulating cells of the pituitary and inhibit the secretion of TSH, but its role is usually It is temporary, so long-term treatment does not cause hypothyroidism
    .

     Other There are many drugs that can cause abnormal thyroid test indicators and even cause thyroid disease
    .

    ➤Sodium phenobarbital and rifampicin affect the metabolism of thyroid hormones, increase the metabolic rate and clearance rate of thyroid hormones until primary hypothyroidism is induced; ➤NSAIDs and high-dose furosemide can inhibit the The combination of T4, T3 and TBG increases the concentration of T4 and FT4 in serum in a short time, but long-term treatment leads to a decrease in the concentration of T4, and the concentration of T4 and FT4 is within the normal range; ➤ β-adrenoceptor blockers can inhibit the Inhibits the conversion of T4 to T3, resulting in a decrease in blood T3 concentration and an increase in T4 concentration; ➤ Phenytoin can induce liver drug enzymes, accelerate the metabolism of T3 and T4, and lead to a decrease in serum T3 and T4 concentrations, but the patient's thyroid function still remains normal, and TSH is normal or only slightly elevated
    .

     Many drugs can affect thyroid function through different mechanisms, leading to the occurrence of thyroid diseases.
    At present, domestic clinical medical personnel have not paid enough attention to this
    .

    Drug-induced thyroid disease is not uncommon, and with the continuous development and use of new drugs, the effects of drugs on the thyroid will become more common
    .

    Raising awareness is key to timely diagnosis and treatment of drug-induced thyroid disease
    .

     References: [1] Lian Xiaolan.
    Drug-induced thyroid disease [J].
    Drug Evaluation 2014, 11(11), 18-21.
    [2] Gu Xiulian, Dou Jingtao.
    Drug-induced thyroid dysfunction [J].
    Drugs Evaluation.
    2013(15).
    [3]Ma Minkang,Zhu Yong,Lv Xiaoqin.
    Analysis of 251 cases of adverse reactions of drug-induced thyroid dysfunction[J].
    Journal of Pharmacoepidemiology.
    2018,27(02),109-113 .
    [4] Qian Fengjuan, Ma Xianghua.
    Drug-induced thyroid dysfunction[J].
    Medical Review.
    2008, 15.
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