I believe many of my friends are not clear about what disease TSH positivity is, mainly because many people misunderstand the professional terminology. In fact, TSH positivity refers to the increase of thyroid-stimulating hormone. The increase of this hormone can cause us to have metabolic dysfunction and myocardial sympathetic symptoms, so we still need to pay special attention to it. For the introduction of TSH positivity, we recommend that you read the following article. TSH (thyrotropin, thyroid stimulating hormone, TSH) is the Chinese name for thyroid stimulating hormone. TSH is a hormone secreted by the pituitary gland that promotes the growth and function of the thyroid gland. Human TSH is a glycoprotein containing 211 amino acids, with carbohydrates accounting for approximately 15% of the entire molecule. The entire molecule consists of two peptide chains - the α chain and the β chain. TSH comprehensively promotes the function of the thyroid gland. The earlier effect is to promote the release of thyroid hormones, and the later effect is to promote the synthesis of T4 and T3, including strengthening the activity of the iodine pump, enhancing the activity of peroxidase, promoting the synthesis of thyroglobulin and tyrosine iodination, etc. TSH promotes the metabolism of thyroid epithelial cells and the synthesis of intracellular nucleic acids and proteins, causing the cells to proliferate in a tall columnar shape, thereby enlarging the gland. Thyroid hormones can promote diuresis, potassium excretion and magnesium excretion. Therefore, water-salt metabolism and vitamin metabolism disorders are prone to occur in hyperthyroidism, such as hypokalemic periodic paralysis and hypomagnesemia. Because thyroid hormones excite the myocardial sympathetic nerves and enhance the effects of catecholamines, patients may experience tachycardia, arrhythmia, increased heart sounds, increased pulse pressure, and even heart enlargement and apical systolic murmur. The elderly are prone to atrial fibrillation, angina pectoris and even hyperthyroidism heart disease, which can cause heart failure when they occur simultaneously with coronary heart disease. The mental and nervous systems are prone to mental tension, such as impatience, excitement, insomnia, dizziness, worry, irritability, talkativeness, hand tremors, hyperreflexia and in severe cases, hyperthyroidism psychosis and autonomic dysfunction may occur. Because thyroid hormones can increase intestinal motility, the digestive system is affected and hunger, increased appetite, increased frequency of bowel movements, indigestion diarrhea, poor nutrition and absorption may occur easily. In severe cases, hypoproteinemia and ascites may occur, leading to a cachectic state and even bedriddenness, which is more common in the elderly. Hyperthyroidism causes dysfunction of the endocrine system, the most common of which is the involvement of gonadal function, amenorrhea and irregular menstruation in women, and impotence in men. However, female pregnancy is not affected. During delivery, care should be taken to prevent hyperthyroid crisis and heart failure. There is also protrusion of the eyeball (exophthalmos exceeding 16mm). In severe cases, the upper and lower eyelids cannot close, the eyeball's adjustment function is poor, and the convergence reflex is disordered. Hyperactivity of the sympathetic nervous system causes upper eyelid retraction, widening of the palpebral fissure and staring. In malignant exophthalmos, intraocular pressure increases, and corneal ulcers, perforations, conjunctival congestion, edema, and even blindness may occur. In severe cases, hyperthyroid crisis may occur; complications include anemia, stomach disease, hypertension, hyperlipidemia, hyperviscosity syndrome and immune dysfunction. 2. Clinical manifestations of kidney damage: In hyperthyroidism, excessive secretion of thyroid hormones leads to increased glomerular filtration rate, increased tubular reabsorption rate and excretion capacity, increased renal medullary blood flow, decreased solute concentration in the medulla, lowered osmotic pressure, and impaired urine concentration function. Patients may experience polydipsia and polyuria, and obvious thirst. There may be mild proteinuria, which may be related to increased renal blood flow. There are also reports of patients with nephrotic syndrome. Corresponding clinical manifestations may occur in case of renal insufficiency. A small number of patients may have renal tubular acidosis. The diagnosis of this disease must be based on the confirmation of hyperthyroidism. If the patient is accompanied by the above-mentioned clinical manifestations of kidney damage and clear laboratory test indicators, kidney disease caused by hyperthyroidism should be considered. Diagnosis of hyperthyroidism: The diagnosis is not difficult based on the clinical manifestations of hyperthyroidism hypermetabolism and the typical signs of diffuse thyroid enlargement and laboratory tests. In hyperthyroidism, the diagnosis can be established if serum thyroid stimulating hormone (TSH) is reduced, while serum total thyroxine (TT4), total triiodothyronine (TT3), serum free triiodothyronine (FT3) and serum free thyroxine (FT4) are all increased. Positive thyroid stimulating antibodies (TS-Ab) or TSH receptor antibodies (TR-Ab) can further confirm that the disease is autoimmune hyperthyroidism (Graves' disease). Because Graves' disease is a type of autoimmune thyroid disease, thyroid peroxidase antibodies (TPO-Ab) and thyroglobulin antibodies (TG-Ab) may also be positive at the same time. In a small number of patients, TSH is decreased, FT4 is normal, but serum free triiodothyronine (FT3) is increased, and they can be diagnosed with T3 hyperthyroidism. Total thyroxine (TT4) and total triiodothyronine (TT3) are less important than FT4 and FT3 in the diagnosis of hyperthyroidism because they are affected by the level of thyroid hormone-binding globulin. |
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