Hashimoto’s thyroiditis, also known as chronic lymphocytic thyroiditis, is an autoimmune disease.
1. They all have a common name, “Hashimoto”
In the family of thyroid diseases, chronic lymphocytic thyroiditis is the oldest in order of prevalence. The disease is more prevalent in women than in men, with a male to female ratio of about 1:10 and a high incidence in the 30s and 50s. In recent years, the incidence of this disease is increasing year by year, and the trend is toward younger age. Since the disease was first discovered and reported by a Japanese doctor named “Hashimoto” in the early 1900s, it is also called “Hashimoto’s thyroiditis” or “Hashimoto’s disease”.
Hashimoto’s thyroiditis is an autoimmune thyroid disease with hypothyroidism as its ultimate outcome. If treatment is delayed, the patient’s metabolism will slow down, making him or her cold and lethargic, affecting the quality of life, and causing increased blood lipids, aggravating arteriosclerosis and leading to cardiovascular disease.
2, “Hashimoto’s disease” of the various stages of performance
The disease starts insidiously and progresses slowly, often with no obvious discomfort at first or only symmetrical and progressive enlargement of the thyroid gland. At different stages of the disease, thyroid function may be transient hyperthyroidism, normal thyroid function, and eventually progress to permanent hypothyroidism. This change is due to the destruction of thyroid follicular cells by autoantibodies.
Transient hyperthyroidism: The thyroid follicular cells are destroyed and the thyroid hormones (T3, T4, FT3, FT4) stored in the follicles are released into the blood, resulting in mild “transient hyperthyroidism”, which may cause palpitations, shaking hands, fear of heat and sweating, excessive food and weight loss, insomnia and excitement, etc. This stage usually lasts for several months.
Normal thyroid function: After the transient hyperthyroidism, there will be a period of normal thyroid function.
Permanent hypothyroidism: As more and more thyroid follicular cells are destroyed, the amount of T3 and T4 eventually tends to be depleted, eventually leading to hypothyroidism. At this stage, the patient may experience chills, slow heartbeat, swelling, hair loss, constipation and other symptoms, and the enlargement of the thyroid gland becomes more and more obvious, usually diffuse symmetrical enlargement, clear borders, firm texture like rubber, no tenderness, no swollen lymph nodes in the neck.
3. How is Hashimoto’s thyroiditis diagnosed?
Clinically, the presence of diffuse enlargement of the thyroid gland in young and middle-aged women should be suspected, regardless of changes in thyroid function. If the patient also has a significant increase (>400) in thyroid autoantibodies (e.g. TPOAb, TgAb), the diagnosis is basically clinically confirmed. For patients with atypical clinical manifestations and insignificantly elevated antibody titers, fine needle aspiration cytology or tissue biopsy may be used to confirm the diagnosis.
4.What is the treatment for Hashimoto’s disease?
The goal of treatment is to improve symptoms, reduce goiter, and prevent or delay the onset of hypothyroidism. Each patient should be treated according to the stage of the disease.
(1) For patients with only elevated antibodies and normal thyroid function, regular follow-up and observation is sufficient without intervention. It is generally recommended to follow up every six months to one year, mainly to check thyroid function and, if necessary, to perform ultrasound examination of the thyroid gland.
(2) In principle, anti-thyroid drugs (ATD) should not be used for patients in the hyperthyroid phase because the hyperthyroidism in patients with Hashimoto’s thyroiditis is mostly transient and mild, and the medication can easily lead to hypothyroidism. In order to control the symptoms of hyperthyroidism in such patients, oral beta-blockers such as Tretinoin 10mg, tid can be administered. iodine 131 and surgical treatment (unless there are severe pressure symptoms) are in principle not considered.
(3) For patients with advanced clinical hypothyroidism and subclinical hypothyroidism with TSH ≥ 10 mIU/L, thyroid hormone replacement therapy can be taken, which generally needs to be maintained for life.
At present, there are no particularly effective drugs for patients with elevated autoantibody titers, so in principle, they can be ignored.
5. How is goiter treated?
Oral thyroxine tablets (L-T4) and adrenocorticotropic hormone are mostly used clinically, which can reduce goiter in some patients (especially young patients). For patients with significant, painful and tracheal compression goiter, surgical removal can be considered if medical treatment is ineffective, but post-operative patients will inevitably become hypothyroid and require long-term thyroid hormone replacement therapy.
6.How to prevent “Hashimoto’s disease”?
A: So far there are no preventive and therapeutic measures for the cause of this disease. Since the incidence of the disease increases significantly with the increase of iodine intake, excessive iodine intake can trigger the development of clinical hypothyroidism in occult patients, so the basis of prevention is to control iodine intake and prevent the destruction of thyroid follicular cells by autoimmunity. It is important to eat less iodine-containing foods, mainly seaweed and shellfish: seaweed, kelp, hairy vegetables, jellyfish, sea cucumber, moss, various shellfish, shrimp skin, etc.