Detailed diagnosis of the etiology of hyperthyroidism

  Hyperthyroidism
  Hyperthyroidism is a condition in which the thyroid gland synthesizes and releases too much thyroid hormone, causing hyper-metabolism and sympathetic excitation, resulting in palpitations, sweating, increased eating and bowel movements, and weight loss. Most patients also often have proptosis, eyelid edema, and loss of vision.
  Causes
  The causes of hyperthyroidism include diffuse toxic goiter (also known as Graves’ disease), inflammatory hyperthyroidism (subacute thyroiditis, painless thyroiditis, postpartum thyroiditis, and Hashimoto’s hyperthyroidism), drug-induced hyperthyroidism (levothyroxine sodium and iodine-induced hyperthyroidism), hCG-associated hyperthyroidism (temporary hyperthyroidism due to pregnancy vomiting), and pituitary TSH tumor hyperthyroidism.
  More than 80% of clinical hyperthyroidism is caused by Graves’ disease, an autoimmune disease of the thyroid gland in which the patient’s lymphocytes produce an immunoglobulin that stimulates the thyroid gland – TSI, which we clinically measure as the thyrotropin receptor antibody: TRAb.
  Graves’ disease is often combined with other autoimmune diseases, such as vitiligo, alopecia areata, and type 1 diabetes.
  Clinical manifestations
  Thyroid hormones promote metabolism and redox reactions in the body, and hyper-metabolism requires the body to increase food intake; gastrointestinal activity is enhanced, and the number of stools increases; although food intake increases, oxidative reactions are enhanced, and the body consumes more energy, and patients show weight loss; increased heat production shows fear of heat and sweating, and individual patients show hypothermia; increased thyroid hormones stimulate sympathetic excitation, and clinical manifestations include palpitations, tachycardia, insomnia, and hypothermia. The increase in thyroid hormone stimulates sympathetic excitation, resulting in palpitations, tachycardia, insomnia, sensitivity to surrounding things, mood swings, and even anxiety.
  If hyperthyroidism is not treated properly for a long time, it can lead to wasting and hyperthyroid heart disease. Patients who lose weight are often susceptible to acute infections that can lead to disability or death. Hyperthyroid heart disease causes heart enlargement, arrhythmia, atrial fibrillation and heart failure, which can lead to loss of labor and even death.
  Examination
  Physical examination reveals an enlarged thyroid gland (mild to severe enlargement). In older patients, the enlarged thyroid gland is often inconspicuous and has a soft or medium texture. Most patients with hyperthyroidism have an increased heart rate, often exceeding 90 beats per minute at rest, and older patients may exhibit rapid atrial fibrillation.
  Many patients also show eyelid edema, widened lid fissures, less transient eyes, and bulbar conjunctival congestion and edema. Severe patients may have proptosis, limited eye movement, or even incomplete eyelid closure.
  Some patients with more severe hyperthyroidism show mucinous edema in front of the shins (tibia) of the lower limbs, thickened, rough, orange peel-like skin in front of the shins, and thickened sweat hair, similar to elephant skin legs, which is quite difficult to treat.
  Diagnosis
  Diagnosis of hyperthyroidism is not difficult, as long as hyperthyroidism is considered and thyroid function tests are performed to make the diagnosis.
  T3, T4, FT3 and FT4 secreted by the thyroid gland are significantly elevated, and TSH is often lowered due to the feedback effect of the thyroid and pituitary axis. If a patient has elevated T3, T4, FT3, and FT4 with decreased TSH, there is only one possibility, namely hyperthyroidism.
  Since most hyperthyroidism is Graves’ disease, an autoimmune disease of the thyroid gland, it is often accompanied by elevated thyroid autoantibodies, elevated thyroglobulin antibodies and elevated thyroid peroxidase antibodies. Patients with Graves’ disease are positive for thyrotropin (TSH) receptor antibodies-TRAb on clinical tests because the filter cells produce an immunoglobulin, TSI, that stimulates thyroid function.
  Some patients with hyperthyroidism may have elevated T3 and FT3, normal T4 and FT4, but decreased TSH, which we call “T3 hyperthyroidism”. “T3 hyperthyroidism” is most often seen in older patients with hyperthyroidism or in patients with toxic functional autonomic heat nodules.
  Differential Diagnosis
  Inflammatory hyperthyroidism (or destructive hyperthyroidism) is a clinical condition in which the inflammatory response of the thyroid gland leads to changes in the membrane permeability of the thyroid follicular cells, resulting in the release of large amounts of thyroid hormones from the follicular cells into the blood, causing a significant increase in thyroid hormones and a decrease in TSH in the blood, with clinical manifestations and biochemical tests resembling hyperthyroidism.
  Inflammatory hyperthyroidism includes the hyperthyroid phase of subacute thyroiditis, the hyperthyroid phase of painless thyroiditis, the hyperthyroid phase of postpartum thyroiditis, and iodine-induced hyperthyroidism type 2. It is important to differentiate between Graves’ disease and inflammatory hyperthyroidism because the former requires aggressive treatment and the latter does not. The major difference between the two is the thyroid uptake rate of 131I, which is elevated or normal in the former and suppressed in the latter; in addition, TRAb is positive in the former and negative in the latter; and thyroid-associated ophthalmopathy is combined in the former and not in the latter.
  Complications
  1. Hyperthyroidism combined with pregnancy
  Because of the teratogenic effect of antithyroid drugs on the fetus, it is necessary to discuss with the doctor to decide whether to keep or give up the fetus according to the condition.
  Pregnant patients with hyperthyroidism are contraindicated to radioactive iodine therapy. Most of the patients with hyperthyroidism who need to continue pregnancy are treated with medication, using the minimum effective dose as much as possible, and try not to add thyroid hormones at the same time during treatment.
  2. Thyroid-related ophthalmopathy
  Most hyperthyroidism is Gravs disease, an organ autoimmune disease. Organ autoimmune diseases often combine with other organ autoimmune diseases. Patients with hyperthyroidism often combine with proptosis, which is an organ autoimmune disease of the eye orbit (including extraocular muscles and posterior fat of the eye).
  In addition to Graves’ disease, other thyroid autoimmune diseases, such as chronic lymphocytic thyroiditis, can also manifest proptosis, which is why we call it “thyroid-associated ophthalmopathy”. There is no direct relationship between thyroid-related ophthalmopathy and Graves’ disease, they are not “father and son” but “brother”.
  Treatment
  There are three types of treatment for hyperthyroidism: anti-thyroid medication, radioactive iodine therapy and surgery.
  Anti-thyroid medication can be used for a wide range of conditions, including adults and children, men and women, mild or severe hyperthyroidism, first time onset or relapse of hyperthyroidism, and pregnant or breastfeeding women. There are two types of anti-thyroid medications – imidazole and thiopyrimidine, represented by methimazole (also known as “tabazol”) and propylthiouracil (also known as “propyrim”).
  Medication is suitable for pregnant women, children, and patients with mildly enlarged thyroid gland, and treatment usually takes 1 to 2 years. There are some side effects of drug therapy, including granulocytopenia, drug allergy, impaired liver function, joint pain, and vasculitis. The side effects of drug therapy need to be monitored closely at the beginning of drug therapy, especially granulocyte deficiency. Discontinue the drug immediately for emergency treatment.
  Another disadvantage of drug therapy is the high recurrence rate after discontinuation of the drug, which is around 50%.
  Radioactive iodine therapy and surgery are both destructive treatments, and hyperthyroidism is not prone to relapse, with only one treatment required. Radioactive iodine is suitable for patients with moderate enlargement of the thyroid gland or recurrence of hyperthyroidism. The doctor calculates the radiation dose needed for each patient based on the uptake rate of radioactive iodine by the patient’s thyroid gland. Radioactive iodine is absolutely contraindicated in pregnant and nursing women. Since radioactive iodine has a delayed effect, the incidence of hypothyroidism with time follow-up is 3-5% per year. Radioiodine treatment is not suitable for hyperthyroid patients with thyroid eye disease, as the eye disease may worsen after treatment.
  Surgery is appropriate for those with significant goiter, or those with high suspicion of thyroid malignancy, or those with goiter that is compressing the trachea and causing breathing difficulties. Medication is required to control the thyroid function to normal range before surgery, and oral compound iodine solution is also required for preoperative preparation before surgery.