Hyperthyroidism (hyperthyroidism) is the most common form of hyperthyroidism, with a prevalence of about 1.2% in China. In recent years, the number of patients treated with Graves’ hyperthyroidism has been increasing. In order to further standardize the treatment, a number of nuclear medicine experts have jointly discussed and drafted this consensus on the clinical issues related to the treatment of Graves’ hyperthyroidism after several times and two years.
I. Definition and Etiology
Hyperthyroidism is a clinical syndrome caused by the dysfunction of the thyroid gland, which produces excessive thyroid hormones and releases them into the blood circulation, acting on the tissues and organs of the body, resulting in high metabolism and increased neuropsychological excitability of the body.
The main causes of hyperthyroidism include Graves’ hyperthyroidism, toxic multinodular goiter, hyperactive thyroid adenoma (Plummer disease), the hyperthyroid phase of various types of thyroiditis, and other special types of hyperthyroidism. Among them, Graves’ hyperthyroidism is the most common, accounting for about 85% of all hyperthyroidism. This consensus is only for Graves’ hyperthyroidism.
Graves’ hyperthyroidism is an organ-specific autoimmune disease characterized by an abnormal increase in thyroid hormone secretion, and its development is the result of a combination of genetic and environmental factors.
Clinical manifestations
The clinical manifestations of Graves’ hyperthyroidism vary with the progression of the disease, and may be characterized by abnormal excitation or metabolic changes in a single system or in multiple systems. Typical symptoms include agitation or irritability, insomnia, palpitations, fatigue, tremors, fear of heat, excessive sweating, weight loss, hyperphagia, increased stool frequency or diarrhea, and scanty menstruation in women. Other clinical manifestations may include photophobia, lacrimation, blurred and decreased vision, proptosis, redness or itching of the skin, swelling of the lower extremities, progressive weakness or even atrophy of the proximal muscles or periodic paralysis. A few patients, especially elderly patients, have atypical signs and symptoms, manifesting as weakness, anorexia, depression, lethargy, and significant weight loss (apathetic hyperthyroidism). Other rare first clinical manifestations may include fever, neck swelling and pain, or unexplained syncope.
The signs of Graves’ hyperthyroidism vary widely. Most patients have varying degrees of enlargement of the thyroid gland, characterized by diffuse, moderate texture (may become firm if the disease is prolonged or if the patient consumes more iodine-containing foods), no pressure pain, palpable tremor at the upper and lower poles of the gland, and vascular sounds on auscultation.
Vascular murmurs can be heard on auscultation. In cases with longer duration of hyperthyroidism, there may be enlarged blood vessels in the neck and significant vascular pulsations. If there are comorbidities, there are corresponding signs of comorbidity.
Laboratory tests and imaging examinations
1. Thyroid hormones and thyroid stimulating hormones. Serum thyroid hormone components include total thyroxine, free thyroxine, total triiodothyronine and free triiodothyronine, which can accurately reflect the functional status of the thyroid gland. These indicators are an accurate reflection of the functional status of the thyroid gland. High-sensitivity serum thyroid stimulating hormone (TSH) levels are now the internationally accepted indicator of choice for the diagnosis of hyperthyroidism and can be used as a single indicator to screen for hyperthyroidism. Some interfering factors should be excluded when analyzing TSH test results.
2. Thyroid autoantibodies. Thyroid autoantibodies are of guiding significance for the etiological diagnosis, differential diagnosis, efficacy evaluation and prognosis of hyperthyroidism. Currently, thyroid auto-antibodies are routinely tested: anti-thyroperoxidase (TPOAb), anti-thyroglobulin (TgAb) and thyroid stimulating hormone (TRA) receptor antibodies. All of these antibodies can be expressed positively in patients with Graves’ hyperthyroidism, with a positive TRAb being more clinically significant.
3. Thyroid uptake function test. An increased thyroid uptake rate is an important reference for the diagnosis and differential diagnosis of Graves’ hyperthyroidism, and is also one of the main bases for calculating the dose of treatment.
4.Thyroxine imaging and ultrasonography. The use of thyroid nuclide imaging or thyroid ultrasonography can be used to estimate the quality of the thyroid gland and to calculate the therapeutic dose. Thyroxine imaging can assist in determining the nature of thyroid nodules and is of great importance in the diagnosis and differential diagnosis of Graves’ hyperthyroidism combined with nodular goiter. Ultrasonography of the thyroid gland can show the shape, size, and blood flow of the thyroid gland in patients with Graves’ hyperthyroidism, as well as detect the presence of thyroid nodules and the condition of lymph nodes in the neck.
IV. Diagnosis
Diagnostic criteria of Graves’ hyperthyroidism.
(1) Common clinical symptoms and signs of hyperthyroidism.
(2) Physical examination and imaging tests showing diffuse enlargement of the thyroid gland (in a few cases, there may be no obvious enlargement of the thyroid gland).
(3) Decreased serum TSH levels and increased serum thyroid hormone levels.
(4) Protruding eyes and other infiltrative eye signs.
(5) Anterior tibial mucinous edema.
(6) Positive TRAb or thyroid-stimulating antibody (TSAb).
(7) Increased thyroid uptake rate.
Among the above criteria, (1) (2) (3) are necessary for diagnosis, while (4) (5) (6) (7) are supplementary criteria for diagnosis, which can further clarify the diagnosis. The above criteria do not include subclinical hyperthyroidism.
A small number of hyperthyroidism patients have atypical clinical manifestations, such as arrhythmia, periodic paralysis, diarrhea or paroxysmal hypertension, which may be misdiagnosed clinically and can be diagnosed clearly only by combining serum thyroid hormone and TSH measurement and other tests.
V. Differential diagnosis
1. Differentiate Graves’ hyperthyroidism from thyrotoxicosis caused by thyroid hormone leakage due to thyroiditis. Both have clinical thyrotoxicosis, goiter and elevated serum thyroid hormone levels. The differential diagnosis is based on medical history, specific signs, thyroid uptake rate and serum TRAb test.
Graves’ hyperthyroidism is distinguished from autonomic hyperfunctioning thyroid adenoma or nodular toxic goiter. Graves’ hyperthyroidism is more likely to be associated with infiltrative proptosis and anterior tibial mucinous edema; the latter two are more likely to be considered if there are significant solitary or multiple thyroid nodules. In the latter two cases, the nodules appear as “hot” nodules on thyroid nuclear imaging, and the surrounding and contralateral thyroid tissues appear light or non-visible.
3. Differentiation between Graves’ hyperthyroidism and Hashimoto’s hyperthyroidism (Hashitoxicosis). Hashimoto’s hyperthyroidism refers to Hashimoto’s thyroiditis (also known as chronic lymphocytic thyroiditis) combined with Graves’ hyperthyroidism, and the presence of both lesions can be seen on thyroid biopsy. The disease has typical clinical manifestations of hyperthyroidism and laboratory findings, with abnormally elevated serum TgAb and TPOAb. The disease presents as Graves’ hyperthyroidism when the TSAb is predominant and as Hashimoto’s thyroiditis when the TPOAb is predominant. A small number of patients with Hashimoto’s thyroiditis have early destruction of follicles by inflammation and leakage of thyroid hormones leading to transient thyrotoxicosis, which may be called Hashimoto’s pseudohyperthyroidism or Hashimoto’s transient thyrotoxicosis. These patients have symptoms of thyrotoxicosis and elevated uptake rate, but the uptake rate is low and the thyrotoxicosis usually resolves on its own within a short period of time, with typical Hashimoto’s thyroiditis changes seen on thyroid puncture biopsy.
4. Differentiate from other causes of elevated and/or decreased TSH. For example, thyroid hormone resistance syndrome, severe systemic diseases, pituitary lesions and elevated thyroid hormone changes after estrogen or glucocorticoid use.
VI. Basic principles of treatment of Graves’ hyperthyroidism
Iodine (I) is one of the raw materials for the synthesis of thyroid hormones and is taken up by the follicular cells of the thyroid through the sodium/iodine transporter (NIS). The effective half-life in the thyroid gland is about 3.5-4.5 d. The duration of action of a single therapeutic dose on the thyroid gland can be 30-60 d, or even longer.
The average range of the rays in biological tissue is about 0.8 mm, and almost all of the energy is absorbed by the thyroid tissue after entering the thyroid gland. The strong ionizing radiation of the rays causes degeneration and necrosis of some thyroid follicular cells, reduces the synthesis and secretion of thyroid hormones, and reduces the size of the thyroid gland, thus achieving the treatment of hyperthyroidism. Because of its low distribution in the extra-thyroidal tissues and short retention time, the amount of radiation produced by the conventional treatment of hyperthyroidism is very low in the bone marrow, gonads, liver, spleen and gastrointestinal tract.
VII. Characteristics of Graves’ hyperthyroidism treatment
Treatment of Graves’ hyperthyroidism has the following characteristics.
(1) Simple method, easily accepted by patients.
(2) Definite efficacy, high cure rate, low recurrence rate, and significant reduction in thyroid volume.
(3) Safe and non-invasive, with no significant adverse effects.
(4) lower treatment cost and high benefit.
VIII. Indications and contraindications for treatment of Graves’ hyperthyroidism
Indications: All patients with Graves’ hyperthyroidism are suitable for treatment. It is especially suitable for the following cases: poor efficacy of antithyroid drugs or multiple relapses; long duration of disease or middle-aged or elderly patients; allergy or other adverse reactions to antithyroid drugs; hyperthyroidism combined with hepatic impairment; hyperthyroidism combined with leukocytopenia or thrombocytopenia; hyperthyroidism combined with heart disease; other special types of hyperthyroidism.
Contraindications: Pregnant and lactating patients.
Treatment of Graves’ hyperthyroidism
I. Diagnosis and related tests before treatment
The clinical diagnosis of Graves’ hyperthyroidism is based on the diagnostic criteria described in the Clinical Basis section above. The initial diagnosis is based on the typical symptoms and signs of hyperthyroidism.
Recommended basic tests: serum and TSH measurements, thyroid uptake rate, blood count, liver function, electrocardiogram, thyroid nuclear imaging and/or thyroid ultrasound.
Recommended tests: Thyroid autoimmune function indicators such as TRAb, TPOAb and TgAb, renal function, electrolytes, blood glucose and cardiac function. Fine needle aspiration cytology of the thyroid gland if necessary.
If there are comorbidities or concomitant disorders, other targeted tests are required to make differential diagnosis of the comorbidities or concomitant disorders and to assess the severity of the disease. In women of childbearing age, attention should be paid to exclude pregnancy.
Determination of treatment dose
There are three methods to determine the dose of treatment for Graves’ hyperthyroidism: calculated dose method or individualized dose plan, semi-fixed dose method and fixed dose method.
Calculated or individualized dose regimens: Calculations are based on thyroid mass and thyroid uptake rate. The usual dose range is 2.59 to 4.44 per gram of thyroid tissue.
Oral dose (MBq) = thyroid mass desired dose per gram of thyroid tissue (MBq) / maximum thyroid (or 24 h) uptake rate (%)
2. Semi-fixed dose method: Calculation based on the estimated thyroid mass. The dose is 185 MBq for small thyroids (up to 30 g), 370 MBq for medium-sized thyroids (30-50 g), and 555 MBq for larger thyroids (over 50 g).
This method is simple and has a high primary cure rate, but also has a high incidence of hypothyroidism (hypothyroidism).
Regardless of which dose method is used, the following factors can be referred to for dose adjustment before treatment. Factors that increase the dose are.
(1) Those with large and hard thyroid glands.
(2) Those with older age, longer duration of disease, and poor long-term antithyroid drug therapy.
(3) Short effective half-life;
(4) Poor or ineffective first treatment
(5) Those with serious comorbidities such as hyperthyroid heart disease and hyperthyroid myopathy.
Factors for dose reduction include
(1) Those who are young, have a short course of disease, and have a small thyroid gland
(2) Those who have not undergone any treatment or who have relapsed after surgery.
(3) Those who have been treated for one time but are not cured.
(4) The effective half-life is long.
Third, the method of drug administration
Generally use 1 time oral method (i.e. one-time treatment). Pay attention to verify the patient’s name, gender and age before administration, and approve the treatment dose. Special attention should be paid to the routine preparation and treatment instructions before treatment, as well as the follow-up instructions after treatment, and patients with comorbidities should be treated accordingly.
IV. Pre-treatment routine preparation and treatment instructions
First of all, determine whether there are any factors affecting the uptake of thyroid medication and whether the patient has received or is receiving anti-thyroid medication and Chinese herbal medicine (whether there are iodine-containing ingredients in Chinese herbal medicine, such as seaweed, etc.). In general, patients should be advised to stop taking methimazole for 2-7 d and propylthiouracil (PTU) for 2-4 weeks, but special cases (e.g. severe hypermetabolic symptoms) should be treated specifically. Patients are advised to abstain from seaweed, nori, deep-sea fish oil, iodine-containing multivitamins, etc. for about 2 weeks.
Before treatment, the patient should be introduced to the characteristics of treatment for Graves’ hyperthyroidism and treatment-related precautions, and the patient and/or family should be informed of its efficacy and possible near-term and long-term complications. Have the patient sign an informed consent form. The main points of communication with the patient prior to treatment are.
(1) Post-treatment self-management. If the patient has recently experienced nausea and vomiting or is expected to vomit immediately after oral administration, antiemetic medication should be administered first. Fasting for 2 hours after treatment (with moderate water intake). Within 2 d after treatment, it is advisable to increase the amount of water, urinate in a timely manner, avoid splashing urine during defecation, and flush immediately after defecation.
(2) Advise the patient to take rest, avoid straining and mental stimulation, do not press the neck frequently, and pay attention to keeping warm and preventing infection.
(3) Advise of possible adverse reactions and countermeasures after treatment. For example, the condition may worsen in the short term after treatment, and although the incidence of hyperthyroidism crisis and cardiac emergencies after treatment is low, attention should be paid to prevention and timely management accordingly. In case of heavy sweating or fever (temperature >38 ℃); severe vomiting and/or diarrhea; irritability and ineffectiveness of common sedatives, severe palpitations (heart rate >140 beats/min), ineffectiveness of receptor blockers; and other special circumstances, patients should go to the hospital promptly.
(4) Inform The time to see the effect of treatment is 2 to 3 weeks later. The appearance of fatigue, drowsiness, weight gain, coldness, convulsions, increased menstrual flow and constipation in women within a short period of time after treatment suggests the possibility of early onset hypothyroidism and should be reviewed promptly.
(5) Inform about the occurrence of distant hypothyroidism after treatment and its management. Avoid close and prolonged contact with others (within 1 m, for more than 3 h) for 1 week after treatment. Avoid close contact with infants and pregnant women for 2 weeks after treatment, and avoid sharing utensils with others.
(6) Men and women of childbearing age should use contraception for 6 months after treatment. Patients with severe disease or comorbidities or complications before treatment should be treated according to the characteristics of the disease and the comorbidities (see the treatment of Graves’ hyperthyroidism comorbidities below).
V. Early reactions after treatment and principles of management
Some patients with Graves’ hyperthyroidism may experience weakness, poor appetite, nausea, skin pruritus and swelling of the thyroid gland within a few days after treatment. Most of these reactions will gradually subside after 1 to 2 weeks, and no special medication is needed.
VI. Treatment of special cases after treatment
1. Severe Graves’ hyperthyroidism. These patients may be at higher risk after treatment. Consider a short course of antithyroid medication first, and then proceed to treatment after the condition has resolved. Short courses of antithyroid drugs may also be added 48 h after administration. It is recommended that patients with severe hyperthyroidism should be hospitalized or closely followed up, and that any exacerbation or complication of infection after treatment should be treated promptly.
2. Hyperthyroid crisis (refer to the Chinese Medical Association Endocrinology Branch “Chinese Guidelines for the Diagnosis and Treatment of Thyroid Diseases”. Hyperthyroidism crisis is an acute aggravation or worsening of symptoms related to hyperthyroidism, which can occur when severe hyperthyroidism is untreated or inadequately treated. Although the onset or complication of hyperthyroidism after treatment is rare, clinical vigilance is required. To prevent the occurrence of hyperthyroid crisis, anti-thyroid medication and symptomatic treatment can be considered for severe hyperthyroidism, and treatment can be given after the condition has resolved. If a condition similar to hyperthyroidism crisis occurs after treatment, prompt management is required.
Consider hyperthyroidism crisis in patients with the following conditions: high or excessive fever, profuse sweating, tachycardia (>140 beats/min), irritability and anxiety or even delirium, severe vomiting or diarrhea, or heart failure, shock and coma. Principles of management of hyperthyroidism crisis.
(1) Remove all kinds of causative factors, and attention should be paid to anti-infection.
(2) Replenish body fluids and ensure electrolyte balance in a timely manner. (2) promptly replenish body fluids and ensure electrolyte balance. Actively lower the temperature in cases of hyperthermia (artificial hibernation if necessary).
(3) Combined with heart failure, take cardiac treatment, such as digitalis and diuretics, etc.
(4) Use anti-thyroid drugs and give iodine. The initial dose can be increased and gradually reduced after the critical signs are controlled. (4) Use of antithyroid drugs with oral iodine (compounded iodine solution) followed by intravenous drips.
(5) Use glucocorticoids, dexamethasone or hydrocortisone intravenously. If the treatment is effective, the disease begins to remit within 1 to 2 d, and remits significantly in about 1 week. At this time, the amount of iodine and glucocorticoids should be gradually reduced until the drug is discontinued. If the above conventional treatment is ineffective, peritoneal dialysis, hemodialysis or plasma exchange are proposed as measures to rapidly reduce plasma thyroid hormone concentration.
The mechanism by which hypothyroidism occurs after treatment of Graves’ hyperthyroidism is not clear. Hypothyroidism after treatment can be divided into early-onset hypothyroidism and late-onset hypothyroidism. Early onset hypothyroidism is defined as hypothyroidism that occurs within one year after treatment, which may be related to the patient’s thyroid gland being more sensitive to radiation and the high dose of treatment. Some patients with early onset hypothyroidism (especially younger patients) may recover on their own. The occurrence of early onset hypothyroidism cannot be accurately predicted clinically. Lowering the treatment dose may reduce the incidence of early-onset hypothyroidism, but this may reduce the one-time clinical cure rate. Late onset hypothyroidism is defined as hypothyroidism that occurs after 1 year of treatment. Late onset hypothyroidism is increasing annually (2% to 3% per year) and may be primarily related to abnormalities in the patient’s autoimmune function, not to the dose.
Post-treatment hypothyroidism is easy to diagnose and treat clinically, but only those who have been untreated for a long time and whose hypothyroidism has gradually worsened will develop serious hypothyroid complications. The key to managing hypothyroidism is early detection and timely thyroid hormone replacement therapy.
Efficacy evaluation, follow-up and safety of treatment of Graves’ hyperthyroidism
According to evidence-based medical evidence and several treatment centers at home and abroad, the efficacy of one-time treatment for Graves’ hyperthyroidism is about 50% to 80%, and the total effective rate is over 95%. The relapse rate after treatment is 1% to 4%, and the failure rate is about 2% to 4%. The overall efficiency of treatment for Graves’ hyperthyroidism is higher compared to other treatments, and the price effectiveness of treatment is higher.
I. Evaluation of the efficacy of treatment of hyperthyroidism
After oral administration, the effect of Graves’ thyroid treatment usually appears gradually after 2 to 3 weeks, with relief of symptoms, reduction of thyroid size and weight gain. Graves’ hyperthyroidism treatment is more effective and has a higher cure rate. In cases of nodular goiter or oversized and hard thyroid gland, several treatments are needed to heal. The higher the dose, the higher the one-time cure rate, but also the higher the incidence of early onset hypothyroidism. The criteria for evaluating the efficacy are as follows.
(1) Clinical cure: the patient’s hyperthyroidism symptoms and signs completely disappear and the serum returns to normal after more than six months of follow-up.
(2) Improvement: the symptoms of hyperthyroidism are reduced, the signs and symptoms partially disappear, and the serum is significantly reduced, but not to normal level.
(3) Ineffective: the patient’s symptoms and signs do not improve or worsen, and the serum does not decrease significantly.
(4) Relapse: After the treatment reaches the standard of recovery, the symptoms and signs of hyperthyroidism appear again, and the serum thyroid hormone level rises again.
(5) Hypothyroidism: After treatment, symptoms and signs of hypothyroidism appear, serum thyroid hormone level is lower than normal and TSH is higher than normal.
Follow-up
Follow-up is a very important part of the treatment of Graves’ hyperthyroidism, and the requirements for follow-up vary from patient to patient. For mild to moderate Graves’ hyperthyroidism with no serious comorbidities, a follow-up visit can be made within 1 to 3 months after treatment to initially evaluate the efficacy. The follow-up interval can be extended if the patient is determined to be clinically cured after 6 months of treatment, and the follow-up review can be conducted once a year. Follow-up content.
(1) Patient symptoms and signs.
(2) Laboratory tests: TSH and, if necessary, TPOAb, TgAb and TRAb.
A significant reduction in the size of the thyroid gland about 6 weeks after treatment is a reliable indication of the effectiveness of the treatment. Before the treatment, the original symptoms should start to be significantly relieved, but the serum thyroid hormone may still be at a high level and the TSH is still low. If fatigue, drowsiness, weight gain, chills, convulsions, increased menstrual flow and constipation in young and middle-aged women appear after treatment, it indicates the possibility of early onset hypothyroidism and should be followed up in a timely manner. If only the thyroid hormone level is below the normal range, even if TSH is still suppressed, early onset hypothyroidism should be considered.
If hypothyroidism occurs, replacement therapy with levothyroxine sodium or thyroid tablets may be used, and the dosage should be adjusted under the guidance of a physician to bring the thyroid hormone levels to normal. The dosage of levothyroxine sodium or thyroid tablets should be adjusted under the guidance of the physician to bring the thyroid hormone level to normal. Regular follow-up examinations should be conducted during the replacement therapy.
For patients who are not cured or have poor outcome after 3-6 months of treatment, re-treatment may be considered according to the needs of the patient, with an interval of 3-6 months between the initial treatment. The dose should be increased for patients who are not effective or who have worsened; the dose should be reduced for patients who have improved but have not recovered. A small number of patients with large and hard thyroid glands require multiple treatments to achieve clinical recovery.
Safety of treatment of Graves’ hyperthyroidism
A large number of studies have shown that treatment of Graves’ hyperthyroidism is safe, does not affect fertility, and does not lead to genetic damage; after treatment of Graves’ hyperthyroidism combined with infertility or sexual dysfunction, fertility can be restored and sexual function can be significantly improved. Treatment does not increase the incidence of thyroid cancer, leukemia, or other cancers in patients with Graves’ hyperthyroidism. Long-term follow-up studies have confirmed that the incidence of leukemia and thyroid cancer in treated patients with hyperthyroidism does not differ from the natural incidence of this type of cancer.
Safety of treatment in adolescent and pediatric patients with hyperthyroidism: The literature reports no significant differences in fertility and offspring growth after several years of follow-up in patients with hyperthyroidism under 20 years of age compared to the general population.
Management of Graves’ hyperthyroidism comorbidities
I. Hyperthyroid heart disease
The incidence of hyperthyroidism in Graves increases with the duration of the disease or with age, and its pathogenesis is unknown. Studies have shown that myocardial metabolism can be altered by the combined effects of excessive thyroid hormone and other factors, causing a range of cardiovascular symptoms and signs. Reference criteria for the diagnosis of hyperthyroid heart disease.
(1) A clear diagnosis of hyperthyroidism.
(2) The presence of one or more of the following cardiac signs: severe arrhythmias such as atrial fibrillation, atrial flutter, frequent atrial premature, frequent ventricular premature, degree II or III AV block; heart failure; enlarged heart; angina pectoris or myocardial infarction.
(3) Excluding other known causes of heart disease, such as hypertensive heart disease, coronary heart disease, rheumatic heart disease, etc.
(4) Improved or significantly improved heart disease after control of hyperthyroidism symptoms .
Most of the patients with Graves’ hyperthyroidism have palpitations. Before and after treatment, appropriate amount of receptor blocker can be given to slow down the heart rate, and the palpitations can be improved gradually with the relief of hyperthyroidism. For those who are nervous, a small amount of sedative can be given on the day of treatment. For those who have atrial fibrillation alone but no obvious heart failure, no special treatment is needed. If heart failure is combined, treatment should be considered after improving cardiac function and controlling heart failure. If there is a combination of coronary artery disease, it is appropriate to improve myocardial blood supply first. If combined with hypertension, it is proposed to continue anti-hypertensive treatment or adjust the treatment plan appropriately according to the condition. For patients with severe hyperthyroid heart disease who are determined to have no significant adverse reaction to antithyroid drug therapy, short courses of antithyroid drugs can be given first to relieve hyperthyroidism or combined with antithyroid drug therapy can be started on the third day after oral administration.
The long-term goal of treatment for hyperthyroid heart disease may be directly related to hypothyroidism. Hypothyroidism can also cause heart problems, including congestive heart failure. Therefore, thyroid hormone levels should be monitored regularly to correct the symptoms of hypothyroidism in a timely manner. It is recommended that patients with hyperthyroid heart disease be treated with intensive cardiac ambulatory monitoring and hospitalization for close observation. In most patients with hyperthyroid heart disease, after treatment and normalization of thyroid function, their cardiac function can return to normal or partially normal. Paroxysmal atrial fibrillation usually does not occur again after hyperthyroidism is controlled or cured; and in those with persistent atrial fibrillation, 1/3 of them can automatically return to sinus rhythm. Studies [26,27] have shown that treatment is less effective in relieving hyperthyroid heart disease if it has a long duration and a significant goiter.
In conclusion, it is advisable to take decisive one-time treatment as soon as possible after the diagnosis of hyperthyroid heart disease.
Hyperthyroidism combined with liver function impairment
Graves’ hyperthyroidism is more likely to cause or complicate liver function abnormalities than other types of hyperthyroidism. The mechanisms by which hyperthyroidism impairs liver function are multifaceted and are related to genetic, psychiatric and autoimmune reactions. The main ones are.
(1) Direct toxic effects of thyroid hormones on the liver.
(2) Long-term overproduction of thyroid hormone, which causes metabolic disorders and contributes to accelerated decomposition of liver glycogen and protein, liver malnutrition and hepatocyte degeneration.
(3) In a high metabolic state, energy consumption of organs is greater than synthesis, and the burden on the liver increases relatively, but the blood supply does not increase accordingly, leading to hepatocyte hypoxia.
(4) Damage involving autoimmune mechanisms.
(5) Liver stasis and hepatocyte necrosis can occur when hyperthyroidism is combined with heart failure. There are no uniform diagnostic criteria for hyperthyroidism liver damage, but it is generally considered that hyperthyroidism can be diagnosed in patients with any of the following conditions: elevated transaminases, hepatomegaly and jaundice, provided that other causes of liver function abnormalities are excluded.
Most patients with Graves’ hyperthyroidism have varying degrees of abnormal liver serum enzymes, but these abnormalities are temporary and reversible, and with the remission of hyperthyroidism, the abnormal liver serum enzymes will return to normal. A small number of patients with Graves’ hyperthyroidism may develop severe liver damage and may develop severe jaundice or even cirrhosis due to long-term untreated or ineffective treatment.
The principle of treatment for hyperthyroidism combined with liver damage is to control hyperthyroidism in a timely and effective manner, and to supplement it with liver-protective therapy. When hyperthyroidism with liver damage is clinically diagnosed, it should be the first choice for definitive treatment. Even for those with severe liver damage, treatment can be considered along with liver protection, stress management and immune suppression. After treatment, most of the Graves’ hyperthyroidism liver damage can be gradually restored after the thyroid hormone level is normalized.
Hyperthyroidism combined with leukocyte, granulocyte or thrombocytopenia
Some Graves’ hyperthyroidism is combined with a decrease in peripheral blood leukocytes, granulocytes or platelets. The mechanism of leukocyte, granulocyte or thrombocytopenia due to hyperthyroidism is unknown, and may be related to immune factors or combined viral infections. Occasionally, severe anemia, aplastic anemia, or splenomegaly and hypersplenism may occur.
The dose levels used to treat Graves’ hyperthyroidism do not result in leukocyte, granulocyte, or platelet reduction. For patients with leukocytopenia, granulocyte or plateletopenia, treatment should be actively administered, along with symptomatic, supportive and leukocyte-raising drugs and regular blood tests. If there is a clear cause of leukopenia, the cause should be treated at the same time. For patients with granulocyte deficiency, antithyroid drugs must be stopped immediately.
For hyperthyroidism combined with leukopenia, thrombocytopenia or thrombocytopenia and granulocyte deficiency, treatment is significantly better than antithyroid drugs or surgery.
Hyperthyroidism combined with muscle weakness and periodic paralysis