subclinical hyperthyroidism
Introduction
Introduction to subclinical hyperthyroidism Subclinical hyperthyroidism, referred to as subclinical hyperthyroidism, refers to no clinical symptoms, or symptoms are inaccurate and non-specific. Although serum FT3 and FT4 are within the normal range, serum TSH is below the reference range, and may cause serum TSH. Reduced other diseases, thyroid diseases diagnosed only by laboratory findings. According to the serum TSH level, it can be divided into two categories: 1 serum TSH is 0.1 ~ 0.45 mU / L, slightly decreased in the detectable range of serum TSH. 2 serum TSH significantly decreased, less than 0.1 mU / L. basic knowledge The proportion of illness: 0.0025% Susceptible people: no special people Mode of infection: non-infectious Complications: arrhythmia
Cause
Subclinical hyperthyroidism
The pathogenesis of subclinical hyperthyroidism is similar to that of hyperthyroidism.
1. Endogenous: In areas where food intake is sufficient, the most common cause of hyperthyroidism is Graves disease, while early Graves disease can be characterized by subclinical hyperthyroidism. In areas with insufficient iodine intake, multiple nodules Or single nodular toxic goiter is a common cause of subclinical hyperthyroidism. In the course of disease progression, subclinical hyperthyroidism first occurs, followed by obvious hyperthyroidism.
2. Exogenous : often caused by iatrogenic factors, such as excessive thyroid hormone replacement therapy for patients with hypothyroidism, or TSH inhibition therapy for patients with thyroid cancer, in elderly patients with autonomous nodules, Subclinical hyperthyroidism can also be induced by an increase in exogenous iodine load such as radioactive contrast agents, amiodarone or other iodine-containing drugs and seaweed.
Prevention
Subclinical prevention of hyperthyroidism
There is no effective preventive measure for this disease. Early detection and early treatment are the key to prevention. Usually pay attention to light nutrition and avoid stimulating spicy food. Pay attention to psychological adjustment and keep your mood comfortable.
Complication
Subclinical hyperthyroidism complications Complications arrhythmia
It can cause myocardial damage, arrhythmia, and can also affect bone metabolism. Some patients may have mild mental symptoms and signs.
Symptom
Subclinical hyperthyroidism Symptoms Common symptoms Goiter, osteoporosis, hypercalcemia, heart rate, arrhythmia, left ventricular hypertrophy
Subclinical hyperthyroidism is usually asymptomatic, but after long-term follow-up, subclinical hyperthyroidism can cause myocardial damage, arrhythmia, affecting bone metabolism, and some patients may have mild psychiatric symptoms and signs, subclinical hyperthyroidism that is inhibited at TSH levels. Among patients, the incidence of emotional disorders is more common than in patients with significant hyperthyroidism.
Heart damage
(1) At rest, the diastolic perfusion is impaired, the left ventricular ejection fraction increases, and the activity tolerance decreases significantly. After treatment with -adrenergic blockers, it may be improved.
(2) heart rate acceleration, atrial arrhythmia, contraction as expected.
(3) Echocardiographic examination revealed left ventricular hypertrophy.
2. Abnormal bone metabolism : In the early years after menopause, women are at high risk of loss of bone mineral density. Hyperthyroidism increases the activity of osteoblasts and osteoclasts, reflecting the urinary N-terminal binding peptide and osteocalcin of bone turnover. Increase, there is a net increase in bone resorption, therefore, whether it is subclinical hyperthyroidism or obvious hyperthyroidism, will increase postmenopausal osteoporosis, in patients with obvious hyperthyroidism, increased bone resorption may cause hypercalcemia, But more common is the decline in bone density, which is more severely affected than the trabecular bone.
At present, the influence of subclinical hyperthyroidism on bone is still inconclusive. Some studies have found that in subclinical hyperthyroidism patients with serum TSH levels ranging from 0.1 to 0.45 mU/L, the incidence of fractures has not increased, but at the age of 65, serum. The incidence of hip and vertebral fractures increased in patients with TSH levels below 0.1 mU/L.
There is no positive report on the effects of subclinical hyperthyroidism on skeletal metabolism in premenopausal women and men. Through large-scale statistical analysis, a similar conclusion is drawn that the amount of TSH inhibitor L-T4 makes postmenopausal rather than menopausal The bone density of former women has decreased.
Examine
Subclinical examination of hyperthyroidism
1. Serum TSH test: For patients with low serum TSH levels, follow-up examination should be conducted. When the TSH level is lower than the detectable lower limit level, the hyperthyroidism should be suspected. The TSH is lower than the normal range, but the patient can still be detected. Reexamination was performed after 3 months, and for those patients who did not receive serum TSH and did not receive thyroid hormone therapy, further examination was required.
2. Determination of serum thyroid hormone : serum FT4, FT4 (or index), TT3 or FT3, and thyroid peroxidase antibody (TPO-Ab, TMAb) and thyroglobulin antibody (TgAb) should be examined if any of the serum If the level of free thyroid hormone is elevated, it can be clearly diagnosed as hyperthyroidism. If the level of thyroid hormone in the blood is normal, it indicates subclinical hyperthyroidism. The serum TSH should be reviewed after several months to exclude the inhibition of transient TSH. If the thyroid autoantibodies are positive, then Prompt for the presence of autoimmune thyroid disease requires careful follow-up.
3. Others: When serum TSH is inhibited and serum thyroid hormone levels are normal, the following tests can help determine the presence of subclinical hyperthyroidism and its pathogenesis.
(1) TSH is slow or lack of response to thyroid stimulating hormone releasing hormone (TRH), suggesting subclinical hyperthyroidism.
(2) The 131I rate of thyroid gland is increased, and the diagnosis of thyroid autonomic nodules is helpful when scanning a high-function imaging area.
(3) Determination of serum thyroglobulin (Tg): If the serum Tg is above the normal upper limit or higher than normal, it indicates the presence of endogenous thyroid hyperfunction and secretion of excess Tg, if the serum Tg is at the normal low limit, then The high thyroid function is unlikely, and if the serum Tg is inhibited, the presence of hyperthyroidism can be ruled out.
According to the condition, choose ECG, echocardiography, X-ray examination and bone density examination.
Diagnosis
Diagnosis of subclinical hyperthyroidism
diagnosis
Exogenous subclinical hyperthyroidism can be diagnosed according to medical history and laboratory examination, but because of sub-clinical hyperthyroidism without obvious symptoms, when diagnosing endogenous subclinical hyperthyroidism, the thyroid should be carefully examined first, because the presence of goiter may suggest thyroid function. Abnormal; secondly, for suspected thyroid dysfunction, elderly patients, those with thyroid disease risk factors should be tested accordingly.
Differential diagnosis
It should be differentiated from decreased serum TSH levels caused by non-thyroid diseases, such as pregnancy, hypofunction of the pituitary or hypothalamus, etc., which can cause a decrease in serum TSH levels; use of glucocorticoids, dopamine, aspirin, furosemide, and fenflurine Acids such as fencolfenac can also cause a decrease in serum TSH levels, but the TSH inhibition caused by these factors is mostly temporary, and serum FT4 is also abnormal. Even if FT4 is in the normal range, it is often at a lower concentration. Clinical hyperthyroidism of FT4 tends to be in the high concentration region of the normal range.
