The thyroid gland is an endocrine organ in the neck, in the anterior lower region of the trachea, close to the breastbone. It is the largest endocrine gland in our body. It weighs 20-30 grams. It has two lobes. It has two symmetrical lobes on the right and left. It produces thyroid hormones and calcitonin hormone.
Hyperthyroidism is a syndrome that expresses excessive secretion of thyroid hormone from the thyroid gland. Hyperthyroidism and thyrotoxicosis are not the same. Thyrotoxicosis is a condition in which the body is affected by these excess thyroid hormones. This effect may not be present in every case of hyperthyroidism. That is, hyperthyroidism can lead to thyrotoxicosis.
Thyroid hormones are produced in the follicles of the thyroid gland as a result of the conversion of iodides in the colloid structure called thyroglobulin into thyroid hormones by the thyroid peroxidase enzyme and secreted into the blood. In order for thyroid hormones to be secreted into the blood, stimulation is expected from the pituitary gland with the hormone TSH. Depending on the diurnal rhythm of the body, this warning usually peaks between midnight and 04:00 in the morning, and thyroid hormone secretion is increased.
The majority of thyroid hormones are secreted as T4, which is inactive thyroid hormone, and a small amount as T3, which is active thyroid hormone. The T4 hormone is then activated by converting to T3 in the circulation.
Thyrotoxicosis is a clinical condition that occurs when symptoms occur in the body due to overactivity of thyroid hormones. These clinical pictures can range from the slightest symptom to life-threatening conditions such as thyroid storm. These symptoms are usually caused by an extreme metabolic state caused by an excess of thyroid hormones. Thyrotoxicosis can lead to serious complications if not properly diagnosed and treated. These complications can range from delirium, altered mental status, osteoporosis, muscle weakness, atrial fibrillation, congestive heart failure, thromboembolic diseases, cardiovascular collapse, and death.
Thyrotoxicosis is most common between the ages of 20-50.
Table of contents
Causes of thyroitoxicosis:
- Causes that increase thyroid hormone
- Graves’ disease
- Toxic multinodular goiter
- Toxic thyroid adenoma
- Struma ovarii
- Gestational trophoblastic neoplasia
- Thyrotoxicosis factitia (infections)
- Activation mutations of the TSH receptor
- Tonic thyroid cancer
- TSH producing pituitary adenoma
- HCG-mediated hyperthyroidism
- Thyroiditis
- Subacute thyroiditis
- Painless thyroiditis
- Gestational thyroiditis
- Radiation
- Drug-related causes
- Amiadaron
- Radioactive iodine
- Lithium
- Interferon-alpha
- Immunosuppressive drugs
- External thyroid hormone intake
- Artificial hyperthyroidism
- Excessive replacement therapy with levothyroxine
Thyrotoxicosis causes complications arising from the accelerating effect of increased thyroid hormone activity on body metabolism. It affects almost all tissues. It accelerates energy production and cell proliferation in tissues. Even the acceleration of the heart muscle increases. Blood pressure rises. The body’s oxygen consumption rate increases. The work of the kidneys increases. More sodium begins to be reabsorbed by the kidneys. The liquid content of the circulatory system increases and begins to burden the heart. In the later period, heart failure develops.
Graves’ disease is the most common cause of thyrotoxicosis. It is an autoimmune disease. It secretes antibodies that stimulate TSH hormone receptors in the thyroid gland. These thyroid-stimulating immunoglobulins stimulate the production of thyroid hormones. The thyroid gland reacts as if TSH is secreted and thyroid hormone production increases.
In diseases such as toxic multinody goiter and toxic adenoma, the thyroid gland begins to produce excess hormones by itself. In thyroiditis, inflammation develops in the hormone-producing follicles of the thyroid gland, and this inflammation leads to the breakdown of the walls of the follicles. Thyroid hormones in the contents of the follicles pass into the bloodstream.
In gestational hyperthyroidism, human chorionic gonadotropin, which is secreted due to pregnancy in the first trimester of pregnancy, increases the stimulus for thyroid hormone production by binding to TSH receptors due to its TSH-like structure. This is why hyperthyroidism develops in the first trimester of pregnancy.
Symptoms of thyrotoxicosis:
Patients who develop thyrotoxicosis naturally develop complaints due to overproduction of thyroid hormones. These:
- Excessive appetite increase
- Weight loss
- Heat intolerance
- Sweating
- Anxiety
- Shake
- Palpitation
- Alopecia
- Weakening in the muscles
- Tiredness
- Tachycardia
- Arrhythmia
- Atrial fibrillation
- Amenorrhea or oligomenorrhea
- Depression
- Shortness of breath
- Tenderness in the abdomen
- Increase in reflexes
- Gynecomastia
In more advanced stages of thyrotoxicosis, a life-threatening condition called thyroid storm may develop.
Symptoms in patients who develop thyroid storm:
- Fever
- Mental status changes
- Heart failure
- Liver dysfunction
- acute muscle paralysis
- Symptoms of hypokalemia
Patients who develop thyrotoxicosis also have symptoms of the disease causing thyrotoxicosis. For example, eye problems may occur in patients with graves.
Diagnosis of thyrotoxicosis:
Excessive increase in thyroid hormones causes a decrease in the level of TSH hormone, which essentially stimulates the production of thyroid hormones. However, T3 and T4 hormone levels were increased in thyroid hormone profile tests. Concomitantly, thyroid receptor antibodies and thyroid peroxidase antibodies may be increased.
Imaging can be performed with radioactive iodine uptake to investigate the causes of thyrotoxicosis. Regions of increased uptake of radioactive iodine in thyroid tissues are considered hyperactive regions. Radioactive iodine uptake may be absent in some cases.
In diseases with inflammation such as thyroiditis, laboratory signs of inflammation can be seen in patients. Sedimentation increase and CRP elevation are one of them.
When evaluating T3 and T4 levels in pregnant women, a thyroid hormone reference range of approximately 1.5 times higher than in normal individuals is used due to the physiological effects of pregnancy. In patients who receive thyroid hormone externally, artificial hyperthyroidism can be mentioned. Thyroglobulin levels are also suppressed in these patients.
Treatment of thyrotoxicosis:
The treatment of thyrotoxicosis is twofold. While treating the complications and symptoms of thyrotoxicosis, on the one hand, the root cause of thyrotoxicosis should be treated, on the other. First of all, beta-blockers are frequently used to protect the heart in patients with thyrotoxicosis.
Basic approach in the treatment of thyrotoxicosis:
- Antithyroid drugs
- Propylthiouracil
- Metamizole
- Radioactive iodine therapy
- Surgical treatment
The use of antithyroid drugs in which patients and in which situations, in what dose and for how long may vary depending on the patient’s clinic and diagnosis. For example, in Graves’ disease, the hormone balance of the patient can be achieved by using metamizole for 4-8 weeks. The decision for metamizole or propylthiouracil also depends on the patient’s circumstances. Metamizole is considered more reliable because of the negative effects of propylthiouracil on liver functions. However, metamizole is not used in pregnant women due to the risk of teratogenic effects.
Radioactive iodine therapy is also a frequently preferred treatment because it is administered as a single dose. Radioactive iodine causes inflammation in thyroid cells, causing destruction of thyroid tissue and suppression of hormone production. However, hypothyroidism develops 6 or 12 months after this treatment, and these patients may have to take oral thyroid hormone for life.
Thyroid surgery is one of the effective treatment methods of thyroid. Surgical treatment has risks from surgery. They are usually controllable risks. After surgical treatment, patients may have to take lifelong thyroid replacement therapy. Before the surgical treatment, the hormones of the patients are reduced to normal levels. Otherwise, thyrotoxicosis or thyroid storm may develop as a complication after surgery.
In the case of thyrotoxicosis in children, successful results are obtained in the treatment with metamizole. Radioactive iodine therapy is not recommended for children under 5 years of age. The use of propylthiouracil in children is also not recommended. Surgical treatment is one of the treatments that can be used in children.
Thyrotoxicosis treatment during pregnancy can be done with drug therapy by strictly following dose settings. Tight control is important so that the fetus does not experience hypothyroidism. Matemizole is not used in the first three months of pregnancy. Propylthiouracil is preferred.
The prognosis is generally good in cases of medically treated thyrotoxicosis. In the absence of medical treatment, thyroid storm may develop. In case of acute thyroid storm in the absence of hyperthyroidism, the possibility of many diseases should be investigated.
Differential Diagnosis for Thyrotoxicosis presenting acutely as Thyroid Storm
Neuro/Psychic
- Anxiety, Acute panic
- Psychosis
- Meningitis
Cardiovascular
- Heart valve disease
- Tachyarrhythmias such as atrial flutter, atrial fibrillation, and supraventricular tachycardia
- Decompensated heart failure
Gastrointestinal
- Acute liver failure
- Dehydration from gastroenteritis
Endocrine
- Adrenal crisis
- Pheochromocytoma
Infectious diseases
- Septic shock
Other
- Overdose from adrenergic or anticholinergic drugs
- Electrolyte imbalance