Haggard face

Introduction Apathetic hyperthyroidism: contrary to the typical symptoms of hyperthyroidism, the mood is indifferent and not easy to be excited. Features are: 1 older women than men. 2 daze, lethargy, depression. 3 weight loss, fatigue, face and old age. 4 The skin is dry, rough and less sweaty. 5 eyelid edema drooping, but obvious eye is less common. 6 The thyroid gland showed more nodular or adenoma or cystadenoma. 7 muscle atrophy, body size and a number of cachexia state. 8 arrhythmia are many, with atrial fibrillation or sinus arrhythmia, the general heart rate is 90 ~ 120 times / min, with heart enlargement, insufficient blood supply or chronic heart failure. 9 The condition is heavier and the performance is atypical. It is easy to be misdiagnosed and cannot be properly treated. It can cause hyperthyroidism crisis; more than 10 cases of anemia, stomach disease, hypertension, hyperlipidemia, hyperviscosity and immune dysfunction.

Cause

1. Immune factors: In 1956, Adams et al found that long-acting thyroid stimulating hormone (LATS) acts similarly to TSH. It is an immunoglobulin (IgG) produced by B lymphocytes, an autoantibody against the thyroid gland. It can be combined with thyroid subcellular components to stimulate thyroid follicle epithelium to secrete thyroid hormone and cause hyperthyroidism. 60% to 90% of patients with hyperthyroidism have increased LATS. Later, it was discovered that LATS-P substance is also an IgG, which only excites human thyroid tissue, also known as human thyroid stimulating immunoglobulin (HTSI). More than 90% of patients with hyperthyroidism are positive.

2. Genetic factors: It is not uncommon to find familial Graves' disease in clinical practice. The same twins have Graves' disease up to 30%-60%, and ectopic eggs only 3%-9%. In addition to hyperthyroidism, family history surveys can also suffer from other types of thyroid diseases such as hypothyroidism, or TSI positive in family members, indicating that Graves disease has a family genetic predisposition. This genetic pattern may be autosomal recessive, autosomal dominant, or polygenic.

3. Other causes of illness

(1) hyperactive nodular goiter or adenoma. In the past, it was considered that this disease was not an autoimmune disease, and no immunological evidence such as IgG, TSI or IATS was detected in the blood. In 1988, serum thyroglobulin antibodies and microsomal antibodies were detected in single nodules in China, with a positive rate of 16.9% (62/383) and a multi-nodular positive rate of 54.7% (104/190). The hyperplastic thyroid tissue in these nodules is not regulated by TSI and becomes a hyperactive or hyperactive thyroid nodule or adenoma. At present, the incidence of thyroid adenoma and cancer is also believed to be due to tumor genes.

(2) The secretion of TSH from pituitary tumors increases, causing pituitary hyperthyroidism, such as hyperthyroidism associated with TSH secretory tumor or acromegaly.

(3) subacute thyroiditis, chronic lymphocytic thyroiditis, painless thyroiditis, etc. can be associated with hyperthyroidism.

(4) Hyperthyroidism caused by hyperthyroidism, called hyperthyroidism. If the thyroid gland patients take too much iodine, taking thyroid tablets or excessive levothyroxine sodium (L-T4) can cause hyperthyroidism, and a small number of patients taking amiodarone drugs can also cause hyperthyroidism.

(5) ectopic endocrine tumors can cause hyperthyroidism, such as ovarian tumors, choriocarcinoma, digestive system tumors, respiratory tumors and breast cancer and other secretory thyroid stimulating hormone can cause clinical hyperthyroidism.

(6) Albright syndrome is clinically characterized by multiple fibrous dysplasia, skin pigmentation, elevated blood AKP, and may be associated with hyperthyroidism.

(7) Familial hyperglobulinemia (TBG) can cause hyperthyroidism, which may be due to familial genetic defects or medication.

an examination

Related inspection

Skin color arterial blood gas analysis

1. Basal metabolic rate (BMR) measurement: hyperthyroidism increased, >15%, and increased and decreased with hyperthyroidism. It can be determined by instrument or by calculation. Calculation formula: quiet pulse pulse pressure -111-BMR%.

2. Blood cholesterol is reduced.

3.24h Increase in muscle uric acid>100mg/L (760mmol/L). Intramuscular creatine phosphokinase (CRK), lactate dehydrogenase (LDH), and aspartate aminotransferase (SGOT) were elevated.

4. Peripheral blood cells should be > 4.5 × 109 / L, neutral multinucleated white blood cells should be > 50%, anti-thyroid drugs can be used.

5. The rate of thyroid uptake 131I increased, and the female 6h was 9% to 55%. Males are 9% to 50%, and 24h are 20% to 45%. 3h is 5% to 25%. This test is affected by many drugs and iodine-containing foods, so these factors should be avoided 2 to 3 weeks before the test.

6. Plasma protein-bound iodine (PRI) normal value is 0.3 ~ 0.63pmol / L, hyperthyroidism increased, > 0.63pmol / L.

7. Thyroid hormone: T3 normal value is 950-205 g/L, T4 normal value is 60-14.8 g/L, and resin uptake ratio (RUR) is 0.8-1.1. The free T4 index (FT4I) is 9.6 to 16.3. FT3I 6.0~11.4pmol/L, FT4 is 32.5±6.0pmol/L. Hyperthyroidism is increasing. The normal value of rT3 is 0.2-0.8 mol/L, and the hyperthyroidism is also increased, and sometimes changes earlier than T3 and T4.

8. The normal value of TSH radioimmunoassay is 3~10mU/L, and the pituitary hyperthyroidism is elevated. Generally, the hyperthyroidism TSH is at normal level or decreased.

9. T3 inhibition test: used to identify the nature of thyroid absorption 131I. The method is to measure the 131I value first, then take T3 60g/d (3 times/d) orally, and then measure the 131I rate after 6 days, compare the results, or take oral thyroxine tablets 60mg, 3 times / d, 8 days later The 131I value was measured and the results were compared. In normal people and simple goiter, the 131I inhibition rate of T3 inhibition test is >50%. It is not suitable for patients with coronary heart disease to inhibit arrhythmia in patients with coronary heart disease because it can cause arrhythmia.

10.TRH (thyroid stimulating hormone releasing hormone) test: T3, T4 increased in hyperthyroidism, feedback inhibited TRH, stimulated TSH secretion, so after intravenous injection of TRH 300mg, the pituitary still does not secrete TSH or rarely secretes TSH, the TSH of hyperthyroidism patients does not Raise. The level of TSH in patients with hypothyroidism is elevated.

11. Thyroid antibody test: thyroglobulin antibody (TGA), thyroid microsomal antibody (TMA) and other antibodies such as anti-nuclear antibody (ANA), anti-smooth muscle antibody (SMA), anti-mitochondrial antibody (AMA) are commonly used clinically. , anti-myocardial antibody (CMA), anti-parietal cell antibody (PCA), and the like.

>90% of hyperthyroidism patients with the highest positive rate of thyroid stimulating antibody (TSAb) or thyroid stimulating immunoglobulin (TSI) may be positive.

1. Tendon reflex relaxation time: commonly used Achilles tendon reflex, normal person Achilles tendon reflex relaxation time 250 ~ 3380ms. About 40% of patients with hyperthyroidism

2. B-ultrasound can be found in the degree of thyroid enlargement, nature, single nodules or multiple nodules. Provide diagnostic assistance.

3. Thyroid scanning and radionuclide computed tomography can understand the thyroid enlargement, single nodules or multiple nodules, thyroid metabolic function, meaningful for differential diagnosis.

Differential diagnosis

Consideration must be given to the differential diagnosis:

1 simple goiter. Except for thyroid enlargement, there are no symptoms and signs mentioned above. Although the 131I uptake rate is sometimes increased, the T3 inhibition test mostly shows inhibition. Serum T3, rT3 were normal.

2 neurosis.

3 autonomic hyperfunctional thyroid nodules, radioactivity concentrated in the nodules during scanning: repeated scans after TSH stimulation, showing increased radioactivity of nodules.

4 other. Tuberculosis and rheumatism often have low fever, hyperhidrosis and tachycardia. People with diarrhea as the main manifestation are often misdiagnosed as chronic colitis. The performance of senile hyperthyroidism is atypical, often with apathy, anorexia, and obvious weight loss, which is easily misdiagnosed as cancer. Unilateral invasive exophthalmos need to be differentiated from intraorbital and cranial low tumors. Hyperthyroidism with muscle disease needs to be differentiated from familial cycle paralysis and myasthenia gravis.

Typical hyperthyroidism has high metabolic symptoms, thyroid enlargement, and ocular protrusion. The diagnosis is not difficult, but about 20% of patients with hyperthyroidism have atypical clinical manifestations, more common in the elderly, older patients, patients with chronic diseases. Or early hyperthyroidism and mild hyperthyroidism patients, symptoms and signs are not typical, often no eyeballs prominent, thyroid enlargement is not obvious, especially some patients with hyperthyroidism symptoms concealed, and some symptoms are more prominent, easily misdiagnosed as another system Diseases, common atypical manifestations have the following:

1. Cardiovascular type: with cardiovascular symptoms as prominent symptoms, tachycardia, arrhythmia, angina or heart failure. More common in women or older patients and patients with toxic nodular hyperthyroidism, clinically often diagnosed as coronary heart disease, hypertensive heart disease, arrhythmia and other diseases. In this type of hyperthyroidism patients, cardiovascular symptoms can be alleviated with anti-thyroid drugs, and treatment with cardiovascular drugs alone is not effective.

2. Neurological type: The neuropsychiatric symptoms are prominent, the patient's nervousness, inattention, emotional irritability, restlessness, insomnia, hallucinations, more common in women, easily misdiagnosed as neurosis or menopausal syndrome.

3. Gastrointestinal type: often with diarrhea as a prominent symptom of stool, a few days or even dozens of watery diarrhea. No pus and blood, often misdiagnosed as enteritis, chronic colitis. Some patients with abdominal pain as the main symptom, diffuse or localized abdominal pain, can be similar to biliary colic, renal colic, ulcer disease, pancreatitis, appendicitis, often diagnosed as acute abdomen and surgical treatment. Occasionally, a small number of patients with severe vomiting as the main symptom, even intractable vomiting and misdiagnosed as gastroenteritis. This type is more common in young and middle-aged people.

4. Muscle type: with muscle weakness, physical weakness and periodic paralysis as prominent performance, often without exophthalmos, no goiter and other symptoms of hyperthyroidism, or symptoms appear later, more common in middle-aged men, mostly after patients eat and Ingestion of large amounts of sugary foods occurs.

5. Cachexia type: with weight loss as a prominent symptom, rapid weight loss, muscle atrophy, subcutaneous fat reduction or disappearance, and even cachexia, often misdiagnosed as malignant tumor, more common in elderly patients.

6. Low-heat type: About half of patients with hyperthyroidism have low fever, general symptoms such as palpitations, and are easily misdiagnosed as rheumatic fever, typhoid fever, tuberculosis, and acute bacterial endocarditis. They are mainly found in young people. The characteristics of this type of low fever, the increase in body temperature is not proportional to the acceleration of heart rate, the heart rate is faster and more significant, the application of antipyretic drugs is not effective, and the anti-thyroid drug treatment effect is obvious.

7. Liver type: jaundice, upper abdominal pain, liver, elevated transaminase, leukopenia as the main symptom, often misdiagnosed as liver disease.

In addition to the atypical symptoms mentioned above, there are some atypical signs, such as hyperthyroidism, male gynecomastia, vitiligo, nail and nail bed separation (Plummer A), local hyperpigmentation, hyperglycemia, and more. Drink more urine, liver palm, hypercalcemia and so on. These need to be further understood to avoid misdiagnosis. General hyperthyroidism also needs to be differentiated from simple goiter (endemic goiter), acute thyroiditis, acute thyroiditis, Hashimoto's disease, thyroid tumor, thyroid cancer, autonomic dysfunction.

Differential diagnosis

1. Determination of total thyroxine (total T4). In the normal case of thyroid hormone-binding globulin (TBG), the increase in T4 (over 12 ng/dl) suggests hyperthyroidism. If TBG is suspected to be abnormal, the I125-T3 binding ratio (0.99±0.1 for normal and 0.74±0.12 for hyperthyroidism) should be determined and multiplied by T4 to correct the abnormality of TBG and calculate the free thyroid index (FT4I). The patient's results have increased. If it is normal, it should strive for further inspection.

2. The total blood T3 normal value is 100 ~ 150mg / dl, the disease is increased, the amplitude is often greater than the total T4.

3. Determination of anti-T3 (rT3), the normal mean value of blood rT3 was 50 ng.dl, and the hyperthyroidism was significantly increased.

4. Free T4 (FT4) and free T3 (FT3) The results of FT4 and FT3 are not affected by the aforementioned TBG, and can more accurately reflect the T4 functional state than the total T4 and T3 results. Normal values: FT4 is 10.3 to 25.7 pmol/L, and FT3 is 2.2 to 6.8 pmol/L. The outcome of patients with hyperthyroidism was significantly higher than the normal high limit.

5. 131I rate of thyroid, such as increased iodine rate, 3 hours greater than 25%, or 24 hours greater than 45% (close-range method), peak advance can be consistent with the disease, but should be used for T3 inhibition test to distinguish between simpleness Goiter.

6. The T3 inhibition test method is as described above. In the normal and simple goiter, the second 131I rate decreased significantly, reaching more than 50%. In patients with this disease and invasive exophthalmos, the stimulation of thyroid by TSH has been replaced by TSAb and is not inhibited by T3 and T4. Therefore, after one week of T320g in ophthalmology, the second time is 131I. Inhibit or less than 50%. This method is not suitable for elderly patients with coronary heart disease, so as not to cause heart rhythm disorder or angina pectoris.

7. Thyroid stimulating hormone releasing hormone (TRH) stimulation test is normal in patients with excitatory reactions, such as TSH close to zero, or immunometric asay results with higher sensitivity, the TSH is lower than normal, and is not excited by TRH. May be prompted for hyperthyroidism (including T3 hyperthyroidism). The significance of this test is similar to the T3 inhibition test, and it can avoid the disadvantages of ingestion of T3 affecting the heart and aggravating symptoms, and the supply of reagents has not yet become popular.

8. TSAb or TSI The positive rate of patients with this disease is about 80% to 90%. After the treatment of the disease, the activity of TSAb is obviously decreased or turned normal, which is beneficial to follow-up efficacy and identification of recurrence after treatment. It is also often used clinically to estimate the appropriate time for antithyroid drugs to stop taking.

9. Anti-thyroglobulin antibody (TGA) and anti-thyroid microsomal antibody (MCA) TGA and MCA can be positive in this disease, but its titer is far less than Hashimoto's thyroiditis.

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