What Is Autoimmune Thyroiditis?

Chronic autoimmune thyroiditis is also called chronic lymphocytic thyroiditis, Hashimoto's thyroiditis, Hashimoto's disease, and so on. More common in middle-aged women, long course, slow onset, diffuse, mild to moderate swelling of the thyroid gland, tough texture, mostly asymptomatic, rare pain, occasionally mild pain or tenderness, seen in the formation of goiter growth Fast, significantly increased anti-thyroid antibody titers. May have pharyngeal discomfort, rare local symptoms caused by goiter, such as neck compression, difficulty swallowing and so on. No cervical lymphadenopathy.

Chronic autoimmune thyroiditis

Chronic autoimmune thyroiditis is also called chronic lymphocytic thyroiditis, Hashimoto's thyroiditis, Hashimoto's disease, and so on. More common in middle-aged women, long course, slow onset, diffuse, mild to moderate swelling of the thyroid gland, tough texture, mostly asymptomatic, rare pain, occasionally mild pain or tenderness, seen in the formation of goiter growth Fast, significantly increased anti-thyroid antibody titers. May have pharyngeal discomfort, rare local symptoms caused by goiter, such as neck compression, difficulty swallowing and so on. No cervical lymphadenopathy.

Overview of chronic autoimmune thyroiditis disease

Chronic autoimmune thyroiditis is also called chronic lymphocytic thyroiditis, Hashimoto's thyroiditis, Hashimoto's disease, and so on. In 1912, Hashimoto first reported four women with enlarged thyroid glands whose thyroid tissue metastasis into lymphoid tissue [strumalymphomatosa]. These patients developed hypothyroidism after surgery. Half a century later, thyroid autoantibodies were reported in this patient. In the past, autoimmune chronic thyroiditis refers to this disease, and it has now been redefined, that is, autoimmune chronic thyroiditis includes chronic thyroiditis (Hashimoto thyroiditis, lymphocytic thyroiditis or goiter thyroiditis) and atrophic Thyroiditis (primary atrophic hypothyroidism or non-thyroid goiter).
The two are actually different clinical manifestations or different clinical stages of the same disease. Either is characterized by the presence of thyroid autoantibodies in the serum. May or may not be accompanied by varying degrees of thyroid dysfunction. Some scholars believe that autoimmune thyroiditis can be classified as follows from histological diagnosis: lymphocytic thyroiditis (only lymphocyte infiltration) and Hashimoto thyroiditis (thyroid cells also have atrophy and eosinophilic changes, and fibrosis can also be seen To). This disease is closely related to Graves disease and together constitutes autoimmune thyroid disease (AITD).
This group of diseases share many similar genes and environmental factors, and often occur in the same family. It is not uncommon for certain individuals to progress from one form of disease to another. AITD involves complex interrelationships among genetic, environmental, and endogenous factors. In recent years, there has been a trend to simplify the definition of thyroiditis "lymphocyte infiltration and thyroid follicle destruction coexisting" in pathology to "intrathyroid lymphocyte infiltration", while thyroid follicular damage is not a necessary condition, so Graves' disease It can also be classified into the category of thyroiditis and become one of the types. It seems to be easier to explain the common relationship between the pathogenesis, pathophysiology and clinical evolution of this group of diseases.

Signs of chronic autoimmune thyroiditis

More common in middle-aged women, long course, slow onset, diffuse, mild to moderate swelling of the thyroid gland, tough texture, mostly asymptomatic, rare pain, occasionally mild pain or tenderness, seen in the formation of goiter growth Fast, significantly increased anti-thyroid antibody titers. May have pharyngeal discomfort, rare local symptoms caused by goiter, such as neck compression, difficulty swallowing and so on. No cervical lymphadenopathy.
Goiter is characteristic: diffuse goiter, or multinodular goiter, rare single nodule. If the thyroid gland appears as a single nodule, it is the only thyroid tissue left due to the destruction of most of the thyroid tissue, and it is not a true single nodule. Can be asymmetric, hard and tough texture, the surface is often not smooth, there are round protrusions, often can reach the cone leaves as one of its characteristics. May move up and down with swallowing.

Causes of chronic autoimmune thyroiditis disease

Hashimoto's thyroiditis is an organ-specific autoimmune disease. Its etiology is very complicated, and it may be caused by the interaction of genetic factors and environmental factors, as well as the coordination of age and sex hormones. The disease has a family aggregation phenomenon, and the production of thyroid autoantibodies is related to autosomal dominant inheritance.

Diagnosis of chronic autoimmune thyroiditis

Diagnosis of chronic autoimmune thyroiditis

Middle-aged women with diffuse, painless, hard goiter should first consider this disease. Thyroid autoantibodies (TG-Ab, TPO-Ab) and TSH measurements can often make a diagnosis. The antibody titer is high and long-lasting, with a positive rate of 59% for TG-Ab and 95% for TPO-Ab. The simultaneous determination of two items has a positive rate of 98% to 100% for complementary results. If the titer is very high, it is of great significance to the diagnosis. Of course, low or negative antibody titers cannot rule out the disease. If combined with needle aspiration cytology, the diagnosis rate is higher.

Laboratory tests for chronic autoimmune thyroiditis

1. ESR can be increased; 2-globulin and -globulin, immunoglobulins, and antinuclear antibodies also often increase.
2. When serum lipids are accompanied by hypothyroidism, serum total cholesterol and low-density lipoprotein cholesterol increase, which may also be accompanied by a decrease in high-density lipoprotein cholesterol and an increase in triacylglycerol levels.
3. The thyroid iodine uptake rate is normal, decreased or increased; it depends on the residual thyroid function and TSH level.
4. Potassium perchlorate release test was 50% to 75% positive, suggesting iodine organication disorder.
5. Increased plasma protein-bound iodine (PBI), often disproportionate to T4.
6. Thyroid function depends on the degree of lymphocyte infiltration and follicular cell proliferation. Early general function is normal. Some have elevated TSH to maintain a substantially normal serum thyroid hormone concentration, but TSH overreacts to TRH administration, indicating the presence of subclinical thyroid dysfunction. With the further destruction of the thyroid in the later period, T3 and T4 decreased.
7. Thyroid autoantibodies TGAb and TPOAb are present in the bloodstream at high titers. TPOAb is more common than TGAb and has a higher titer and longer duration. Young patients with chronic lymphocytic thyroiditis typically only have low titer antibodies. RIA double antibody method is often> 50%. Enzyme-linked immunosorbent assay (ELISA) and enzyme immunoassay (EIA) methods determined that 60% to 66% of patients with chronic lymphocytic thyroiditis were positive for TGAb and 80% to 95% for TPOAb. But chronic disease was not significantly increased. Most atrophic thyroiditis has a long course, and 80% of thyroid autoantibodies cannot be detected. Other thyroid autoantibodies can also be mildly elevated, with a TSAb positive rate of 14.2%, and Graves disease can be significantly increased. The TSBAb positive rate was 37.7%.
8. The cytokine IL-4 has good reproducibility and specificity, and is not affected by other ILs, hormones, and lactic acid. Chronic lymphocytic thyroiditis increases and decreases after treatment. Increased IL-8 levels in untreated patients with chronic lymphocytic thyroiditis.
9. As the release of iodine protein increases, Tg in the blood may increase.
10. Other hormones such as calcitonin (CT) levels are reduced in atrophic patients, and are more pronounced with hypothyroidism. In patients with chronic lymphocytic thyroiditis, 42.4% PRL levels increased when hypothyroidism was evident, and nearly 1/5 PRL levels were> 60 mg / L.

Other auxiliary tests for chronic autoimmune thyroiditis

1. Radionuclide inspection. Radionuclide testing is generally not required for patients with a high degree of suspicion of the disease. It is generally characterized by an enlarged thyroid gland, uneven distribution of iodine, or changes in "cold" and "cold" nodules. Due to the lack of specificity, it is difficult to distinguish it from other thyroid disorders. The loss of local iodine accumulation marks the severe part of the thyroid disease. MIBI scans show that "cold nodules" can basically exclude malignant nodules, and high MIBI uptake is highly likely to differentiate follicular thyroid cancer. The diagnosis rate of malignant nodules increased by 7.8 times with the second combined MIBI scan after the 99mTc scan. The 201Tl scan has the characteristics of high sensitivity and low specificity, and has no superiority in distinguishing benign and malignant thyroid nodules.
2. The specificity of ultrasound is not high. Diffuse or nodular thyroid enlargement, 18% to 95% accompanied by diffuse hypoechoic. 3mm nodules can be found using 10MHz high frequency.
3. The thyroid fine or thick needle pathological examination is helpful for patients with uncertain clinical diagnosis and isotope examination of "cold nodules". Especially for patients with autoantibodies, unnecessary surgery can be avoided. For chronic lymphocytic thyroiditis, the accuracy of the first fine needle aspiration cytology was 92%. The accuracy of fine-needle aspiration cytology in identifying benign and malignant thyroid nodules was 85.9%. It is possible to diagnose high-grade primary malignant thyroid lymphoma, but it is difficult to diagnose low-grade malignant lymphoma due to the lack of atypical nuclear characteristics. It is also difficult to distinguish proliferative follicular cell nodules and follicular adenomas by cytology. At this time, a thick needle or even an open biopsy is required.
4. The use of flow cytometry or immunotype -cell specific monoclonal antibodies can help determine the number of lymphocyte clones and prompt the diagnosis of lymphoma. Recently, the use of semi-quantitative needle aspiration biopsy-reverse transcription (RT) -PCR (ABRP) technology to detect monoclonal Ig heavy chain mRNA has been successful in diagnosing malignant thyroid lymphoma with a specificity of 100% and a sensitivity of 44.4%.

Differential diagnosis of chronic autoimmune thyroiditis

The diagnosis of chronic lymphocytic thyroiditis is generally not difficult, and the reasons for misdiagnosis may be: atypical symptoms, single or multiple nodules of the thyroid gland, coexistence with other thyroid disorders, lack of specific diagnostic methods, and the disease Lack of full awareness, etc.
1. Thyroid cancer and malignant lymphoma of the thyroid gland rapidly (2 to 3 months) progressively enlarged, fixed, hard, adherent to surrounding tissues, accompanied by compression symptoms such as hoarseness (recurrent laryngeal nerve compression), cervical lymphadenopathy Large, if necessary, the appropriate amount of thyroid hormone diagnosis and treatment for more than 4 weeks, the thyroid does not shrink or continue to increase asymmetry should be highly suspected of cancer. Imaging such as ultrasound or nuclide scanning: Cancer is mostly solitary nodules, while chronic lymphocytic thyroiditis shows heterogeneous diffuse lesions. Open thyroid biopsy can diagnose most patients. Needle aspiration cytology has diagnostic value in a small number of patients.
2. Non-toxic goiter Non-toxic nodular or diffuse goiter is difficult to distinguish from the disease, but the former is relatively soft and most of the thyroid functions are normal. The diagnosis depends on the measurement of thyroid antibodies and fine needle aspiration cytology if necessary. clear. Adolescent goiter may be more difficult to distinguish clinically from this disease. Therefore, chronic lymphocytic thyroiditis in the age group is less likely to have high titer circulating thyroid autoantibodies.
3. Others whose face is bloated and pale are easily misdiagnosed as chronic nephritis, anemia, etc., need to be more alert to this disease.

Treatment options for chronic autoimmune thyroiditis

Those with no obvious symptoms and insignificant thyroid enlargement were followed up. Some patients can remain stable for several years without treatment.
1. When the thyroid hormone is markedly enlarged with compression symptoms, thyroid preparations should be given to shrink the glands and compensate for the damaged thyroid function, and reduce the antibody titer. Pain relief can also be achieved in patients with pain or tenderness. After a few months of proper treatment, 25% of the glands fully retracted, 50% shrank to half of their original size, and 10% to 20% remained unchanged. Generally, patients with newly developed goiter or younger respond better to treatment, and older patients shrink more slowly. Patients with pre-existing fibrosis tend to respond poorly. Start with small doses:
(1) Thyroid powder (tablets): The hormone content is not accurate enough, and the T3 ratio is high, which has been used less. 10 40mg / d, gradually increased (2 4 weeks) to 120 240mg / d as appropriate. The initial dose of patients with long-term disease, elderly patients or coexisting ischemic heart disease should be smaller, and the increase should be slower (4 8). week). If there are no contraindications in children and developmental patients, they can be given in sufficient amount or close to sufficient amount to facilitate their growth and development.
(2) Levothyroxine sodium (L-T4): 12.5 to 50 g / d, and gradually increased to 150 to 200 g / d as appropriate. Choose an effective maintenance amount for long-term use. In the past, levothyroxine sodium (L-T4) was considered to be the most physiologically suitable for the treatment of hypothyroidism, and it was also the most suitable for long-term thyroid replacement therapy. Recent studies have reported that partial replacement of thyroxine with liothyronine (T3) can significantly improve patients' emotional and neuropsychological functions. Regarding the timing of thyroid hormone application: opinions are not completely consistent. Some people have suggested that once the disease is diagnosed, a certain amount of thyroid preparations should be administered, which is considered to be possible to prevent and prevent malignant changes. Most clinicians use hypothyroidism (subclinical and clinical reduction) and compression symptoms as indications. Some authors recommend treatment indicators: serum TSH> 10mU / L, accompanied by high risk factors for progression to hypothyroidism: high titer thyroid autoantibodies, patients aged 45 years or older, and no heart disease. Otherwise, follow-up is possible. If it is an epidemiological investigation instead of diagnosis and treatment, the above TSH serum level will be reviewed after half a year, and it will be repeated every 1 to 2 years, and treated as appropriate. Studies have found that when serum TSH> 10mU / L, thyroid hormone therapy can significantly reduce total cholesterol and low-density lipoprotein cholesterol levels, while TSHL, the above indicators are not affected by thyroid hormone therapy. In chronic autoimmune thyroiditis with hypothyroidism, about 10% to 24% of patients remain functional for more than one year after thyroid hormones return to normal thyroid function and are discontinued. Some authors have studied the indicators that can predict the return to normal thyroid function: family history of thyroid disease, youth, obvious goiter (usually> 35g before treatment), increased 131 uptake, normal response of thyroxine to TSH, and blockade of TSH receptors Antibody turned negative. Some authors suggest that patients with the above characteristics should undergo a thyroid hormone withdrawal test after 1 year of replacement therapy. This clinical remission may be due to the disappearance of TSHR [Block] Ab or termination due to some influencing factors: such as the discontinuation of cytokines, lithium, amiodarone, or other iodine-containing agents. However, these patients need to be closely monitored for changes in thyroid function after discontinuation of the drug, especially when eating a high or low iodine diet or reactivating the above drugs. Among these patients, the existence of self-limiting hypothyroidism, such as subacute, postpartum, or painless thyroiditis, for which no etiology diagnosis has been previously made is not excluded. Pregnant women taking thyroid hormone should be appropriately increased, but it should be noted that excessive thyroid hormone is not conducive to fetal brain development. During the increase of thyroid preparations, there have been reports of pseudogout (the presence of pyrophosphate crystals in the synovial fluid).
2. Glycocorticoids only temporarily shrink the glands, and those with acute onset or with pain can be used for a short time. It has certain effects on controlling the progress of the disease, improving symptoms, and reducing antibody titers, but relapses after discontinuation of the drug, and taking into account the side effects, generally do not advocate long-term application. Steroids have a positive effect on chronic lymphocytic thyroiditis-associated polymyositis. Some authors compared the effects of thyroid local injection of dexamethasone with oral thyroid powder (tablets) on thyroid morphology, antibodies, and therapeutic effects of chronic lymphocytic thyroiditis. The results showed that local hormone treatment can significantly reduce the levels of TPOAb, TGAb, and the maximum thyroid diameter. And area, and significantly increase thyroid hormone levels and reduce TSH levels. Its curative effect is large and the course of treatment is short. No adverse reactions.
3. Surgery should be considered when the surgery has severe compression symptoms and drug treatment cannot alleviate or exclude malignant lesions. Some people claim that patients with diffuse thyroid tissue damage can also be treated surgically if they have progressive thyrotoxicosis or neck compression. Wortsman pointed out the indications for surgical exploration in chronic lymphocytic thyroiditis: combined with cold nodules; obvious goiter with pain; enlarged cervical lymph nodes with adhesions; hoarseness; continued thyroid during treatment Increase or nodules do not shrink. After the routine application of thyroid hormone replacement therapy. Some authors also believe that proper thyroid resection (5 to 6 g on each side) is a safe and effective method for the treatment of chronic lymphocytic thyroiditis. After 3 months to 7 years of follow-up, the incidence of hypothyroidism was 9.7%. The incidence of hypothyroidism in the follow-up group for 3 to 10 years was 4.7%. It may be related to the place where the surgical removal of antibodies occurs.
4. Biotherapy antigen specific technology (such as intravenous injection of soluble Tg, Tg-specific T lymphocytes), non-specific therapy (such as injection of anti-MHC-II antibody, anti-CD4 antibody, IFN- monoclonal antibody, etc. But All are in the research stage. Plasma depletion therapy alone has a good effect, but it is expensive. 5. Single local radiation therapy or combined chemotherapy is required for concurrent thyroid lymphoma. The 5-year survival rate is 13% ~ 92%. Above 65 years old, tumor Larger, faster growth, and poorer prognosis for high-level histology. Avoid using iodine-containing drugs in women with a history of this disease to avoid hypothyroidism. When women with this disease are pregnant, avoid excessive iodine intake to avoid Iodine is transmitted through the placenta, which results in an increase in fetal TSH and neonatal hypothyroidism.

Prognosis prevention of chronic autoimmune thyroiditis

Prognosis : The prognosis of this disease depends on the state of thyroid function. Generally, it can maintain normal function for several years or slowly progress to hypothyroidism or combined with hyperfunction, but no matter hyperfunction or hypofunction, as long as it is detected in time and actively treated, the prognosis is good. .
Prevention : The use of iodine-containing drugs in women with a history of this disease should be avoided to avoid inducing hypothyroidism. When women with this disease are pregnant, excessive intake of iodine should be avoided to prevent the transmission of iodine through the placenta and increase fetal TSH and neonatal hypothyroidism. [1]

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