- Drug-induced thyroiditis - symptoms
- Which drugs can cause drug-induced thyroiditis?
- Monitoring of thyroid function during pharmacotherapy
- Drug-induced thyroiditis - diagnosis
- Drug-induced thyroiditis - treatment
- Drug-induced thyroiditis - prognosis
Drug-induced thyroiditis is a relatively rare disease; nevertheless, it is useful to know which drugs can cause them. Permanent control of the thyroid function during their use allows for quick detection of possible disorders. Learn about the symptoms of drug-induced thyroiditis, what drugs can cause them, and the diagnosis and treatment of drug-induced thyroiditis.
Drug-induced thyroiditisis an inflammation of the thyroid gland caused by the use of certain medications. It is most often caused by direct damage to the thyroid cells by a given pharmacological agent. We are talking then about drug-induced, toxic thyroiditis.
Some drugs, on the other hand, do not directly damage the thyroid gland, but cause the body to build antibodies responsible for the destruction of thyroid tissue. In this case, drug-induced thyroiditis is autoimmune.
Due to the course and duration of the disease, drug-induced thyroiditis is divided into
- acute drug-induced thyroiditis
- chronic drug-induced thyroiditis
In the case of acute inflammation, symptoms usually disappear after several days. Chronic inflammation can last for weeks or even months.
Drug-induced thyroiditis - symptoms
Drug-induced thyroid gland injury usually has a characteristic clinical course. In the acute phase of inflammation, there is a sudden destruction of thyroid cells, which causes a rapid release of thyroid hormones into the bloodstream. This condition is called thyrotoxicosis.
Excessive concentration of thyroid hormones causes the classic symptoms of hyperthyroidism:
- palpitations
- hot flashes
- shaking hands
- anxiety
- diarrhea
The overactive phase usually lasts no more than a few days. After this period, it often goes into hypothyroidism - damaged thyroid cells "threw out" all their hormones and do not produce new ones.
The clinical symptoms of hypothyroidism are:
- chronic fatigue
- slow heart rate
- constipation
- hair loss
- feeling cold
Clinical picture of drug-induced inflammationthe thyroid gland is heterogeneous - it can be accompanied by symptoms of both hyperthyroidism and hypothyroidism.
With long-term use of thyroid damaging drugs, these phases often alternate.
Drug-induced thyroiditis may or may not be accompanied by pain and swelling in the thyroid gland.
Which drugs can cause drug-induced thyroiditis?
There are many classes of drugs that affect the function of the thyroid gland. Not all of them cause direct damage or inflammation of the thyroid gland.
Many pharmacological agents modulate the activity of thyroid hormones by, for example, accelerating their breakdown in the liver. Some antiepileptic drugs (carbamazepine, phenytoin) and antibiotics (rifampicin) also work in this way.
There are also drugs that affect the entire hypothalamic-pituitary-thyroid axis. Their example is the frequently used glucocorticosteroids, which block the release of TSH in the pituitary gland, thus inhibiting the production of thyroid hormones.
It is worth remembering about the numerous drug interactions when prescribing thyroid hormones to patients as drugs for the treatment of hypothyroidism.
Concomitant use of other pharmacological agents (e.g. estrogens used in the form of contraceptives) can significantly change the effectiveness of the therapy.
Drug-induced thyroiditis affects a few selected drugs. Pharmacological agents that most often cause drug-induced thyroiditis are:
- amiodaron
- iodine-containing contrast agents
- lit and its derivatives
- alpha interferon
- interleukin 2
- some anti-cancer drugs (tyrosine kinase inhibitors)
Below is a brief description of the individual ignitions:
- drug induced thyroiditis caused by amiodarone
Amiodarone is a commonly used cardiac drug used to treat abnormal heart rhythms (arrhythmias).
Amiodarone is a preparation that has a significant impact on the function of the thyroid gland. Amiodarone molecules are built very similarly to thyroid hormones, which causes the drug to interfere with the thyroid gland.
In addition, one amiodarone molecule contains 2 iodine atoms. Iodine, in turn, is an important component of the chemical reactions that lead to the formation of thyroid hormones.
It's also important to know that amiodarone can have a direct toxic effect on thyroid cells.
As you can see, the relationship between amiodarone and thyroid function is quite complex. For this reason, the symptoms of drug-induced inflammationamiodarone-induced thyroid gland can be various.
It is estimated that thyroid dysfunction will occur in 1/5 of patients using this drug. Thyroid damage caused by amiodarone can take two forms:
- amiodarone-induced thyrotoxicosis (AIT). The most common symptom of this condition is worsening of arrhythmias, despite the use of the antiarrhythmic amiodarone. Extreme forms of thyrotoxicosis can cause acute heart failure and be life-threatening. In such situations, the only therapeutic option is surgical removal of the thyroid gland (thyroidectomy).
- amiodarone-induced hypothyroidism (AIH). It is a variant more often associated with chronic amiodarone therapy. In situations where the drug cannot be discontinued, thyroid hormone substitution in the form of tablets is used.
- drug induced thyroiditis caused by iodine-containing agents
Iodine is an element that plays an important role in the production of thyroid hormones. The sudden introduction of large amounts of iodine into the body causes the so-called Wolff-Chaikoff effect. It is a phenomenon of a temporary inhibition of the production of thyroid hormones.
Iodine is used in many pharmacological preparations, and contrast agents are one of the most common. These are solutions administered intravenously in order to obtain more accurate results of imaging tests (e.g. computed tomography).
It is estimated that thyroid dysfunction occurs transiently in 20% of patients receiving iodine-based contrast agents.- drug induced thyroiditis caused by lithium derivatives
Lithium s alts are drugs used to treat bipolar disorder. The lithium builds up in the thyroid gland and blocks the release of thyroid hormones. Additionally, it may be toxic to thyroid follicular cells.
Due to the decrease in thyroid hormone levels, lithium causes an increase in TSH (which tries to "stimulate" the activity of the thyroid gland). These changes can cause an increase in the volume of the thyroid gland, or goitre. Lithium-induced thyroiditis usually presents clinically as hypothyroidism.
- interferon alpha drug induced thyroiditis
Interferon alfa is a preparation used in the treatment of viral hepatitis B and hepatitis C. Additionally, it is sometimes used in the treatment of certain types of cancer. Interferon alpha has a stimulating effect on the immune system.
One of the side effects of its action is increasethe frequency of autoimmune reactions directed against the body's own tissues.
The thyroid gland becomes a relatively frequent "target" of such reactions in the case of alpha interferon.
Drug-induced autoimmune thyroiditis caused by interferon alpha most often manifests as hypothyroidism. A rarer variant of this inflammation occurs in the form of hyperthyroidism.
- drug-induced thyroiditis caused by interleukin 2
Interleukin 2 belongs to cytokines, which are a group of proteins involved in the body's immune responses. The main role of interleukin 2 is to stimulate the growth of T cells (a type of white blood cell). Interleukin 2 is sometimes used to treat certain types of cancer, such as kidney cancer or melanoma.
The mechanism of thyroid damage in the course of interleukin 2 treatment is similar to that in the case of alpha interferon.
Inflammation of the thyroid gland is autoimmune, caused by the formation of anti-thyroid antibodies. This inflammation most often manifests as hypothyroidism.
- drug induced thyroiditis induced by anti-cancer drugs
Some anti-cancer drugs, introduced into therapy relatively recently, can cause thyroid inflammation. I am talking about the so-called tyrosine kinase inhibitors, specifically their two representatives: sunitinib and sorafenib. These preparations are used in the treatment of gastrointestinal cancer, kidney cancer and thyroid cancer.
Depending on the source, in 20-50% of patients using the above-mentioned drugs there is damage to the thyroid parenchyma with subsequent hypothyroidism (decrease in the concentration of thyroid hormones).
With repeated courses of therapy, there is a risk of permanent hypothyroidism.
Monitoring of thyroid function during pharmacotherapy
Knowing the risk of certain drugs causing thyroiditis, we need to ask ourselves: how to protect the patient from possible thyroid dysfunction? Unfortunately, it is not always possible to replace the drug with another one, which is associated with a lower risk of damage to the thyroid gland.
If there are indications for the use of a given preparation, constant monitoring of the thyroid function is usually carried out simultaneously with the therapy. Before treatment is started, a preliminary diagnosis is carried out: an ultrasound examination of the thyroid gland and the assessment of the levels of thyroid hormones, TSH and anti-thyroid antibodies (anti-TPO, anti-Tg, anti-TSHR).
Incorrect results of the above tests may constitute a contraindication to therapy (this is the case, for example, in the case of amiodarone).
Afterthe commencement of treatment, periodic monitoring of the above-mentioned parameters. Usually, basic tests (TSH, fT3, fT4) are performed after the first and third months of therapy, and then every six months.
Drug-induced thyroiditis - diagnosis
A simple diagnostic tool - medical history - plays the most important role in the diagnosis of drug-induced thyroiditis.
Drug-induced thyroiditis usually follows a characteristic sequence: transient hyperthyroidism, then progressing to hypothyroidism. Of course, it is also possible to have only one group of symptoms (hyper or hypothyroidism).
Patient reporting the above-mentioned ailments in the doctor's office will usually hear a question about the medications you are taking. Recently applied measures are of particular importance. Very often, already at the stage of a medical interview, it is possible to establish the relationship between the appearance of symptoms and the initiation / change of a specific pharmacotherapy.
The diagnosis of any thyroid disorders, including drug-induced thyroiditis, requires a series of laboratory tests (the so-called thyroid panel). They include the determination of the level of thyroid hormones, TSH, as well as anti-thyroid antibodies (anti-TPO, anti-TG, anti-TSHR).
The above tests confirm the presence of hyperthyroidism or hypothyroidism in a given patient.
The presence of anti-thyroid antibodies suggests an autoimmune cause of thyroiditis. However, it should be remembered that this condition does not exclude drug-induced damage to the thyroid gland - some drugs may increase autoimmune reactions (see above) against the thyroid gland.
In the event of further diagnostic ambiguities, there is one more method to determine the cause of thyroiditis. You can - unless there are absolute contraindications - try to discontinue the drug suspected of having a thyrotoxic effect.
Observation of the patient's clinical and hormonal status usually allows us to answer the question of whether the drug was the cause of the ailments. However, such an attempt should be made only on the recommendation and under strict supervision of a doctor.
Drug-induced thyroiditis - treatment
Treatment of drug-induced thyroiditis depends on the stage of the disease development and the severity of clinical symptoms.
In the acute phase of inflammation associated with thyrotoxicosis (excess thyroid hormones), it is usually advisable to at least temporarily discontinue the drug suspected of damaging the thyroid gland.
The main symptoms of thyrotoxicosis are usually system relatedcirculatory system - these include palpitations, tachycardia and an increase in blood pressure. To relieve these discomforts, beta-blockers are usually given. These are drugs that slow down the heart rate and lower blood pressure.
Overproduction of thyroid hormones may be an indication for the administration of thyroid drugs (thiamazole, propylthiouracil). These are drugs that inhibit the formation of thyroid hormones. Their effects, however, are only visible after a few weeks of therapy.
Sometimes anti-inflammatory glucocorticosteroids are also used in the treatment of drug-induced thyroiditis.
Extremely severe cases of drug induced thyroiditis, in which the development of thyrotoxicosis is life-threatening, may require surgical treatment. I am talking about the thyroidectomy, i.e. the complete removal of the thyroid gland. Fortunately, such situations are relatively rare.
Drug-induced thyroiditis causing hypothyroidism is an indication for substitution therapy. There are many synthetic equivalents of levothyroxine (Euthyrox, Letrox) available on the market.
If there is no possibility of withdrawal from the thyrotoxic drug, treatment is usually continued by supplementing the thyroid hormone levels "externally" in the form of oral tablets.
Drug-induced thyroiditis - prognosis
The prognosis for drug-induced thyroiditis depends on many factors. If the source of the thyroid dysfunction is quickly identified and it is possible to withdraw the thyrotoxic drug, the chances of the thyroid gland return to normal are very high.
Sometimes, however, discontinuation / change of pharmacotherapy is not possible (e.g. in anticancer treatment). Then it is necessary to balance the balance of benefits and losses. If treatment causes symptoms of hypothyroidism, hormone replacement is used.
Obviously, the longer thyrotoxic treatment is administered, the greater the risk of irreversible damage to the thyroid gland and the development of permanent hypothyroidism. In such cases, the use of thyroid hormone preparations may be necessary for the rest of your life.
In drug-induced thyroiditis associated with acute thyrotoxicosis, we usually strive to temporarily discontinue / minimize the dose of the drug. After stabilizing the patient's hormonal status, chronic use of thyroid drugs is attempted in some cases.
Decisions on whether to continue therapy with thyroid damaging drugs are very difficult. You should always consider what carries a greater risk for the patient - discontinuation of the drug or damage to the thyroid gland.
Continuation of therapy with constant monitoring of functionsthe thyroid gland helps to keep the balance. Regular testing also allows you to capture the moment when discontinuation of the thyrotoxic drug is absolutely necessary.
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