Basedow Pathology

2021-01-27 12:00 AM

Genetically associated with 15% of patients with a loved one with the same disease and approximately 50% of a patient's relative with autoantibodies to the bloodstream.

Define

Basedow is one of the most common clinical hyperthyroidism diseases with the main manifestations: thyrotoxicosis with diffuse large goitre, bulging eyes and peripheral lesions.

Basedow disease has many different names of Graves' disease. Parry's disease. Diffuse toxic goitre. Autoimmune hyperthyroidism. Thanks to the advancement of immunology, more and more antibodies present in the patient's plasma have been detected, so it is now classified as an autoimmune-related disease.

Whole disease

The disease occurs at all ages, especially the age of 20-40 years, predominating in women, the ratio of male/female = 1/5 - 1/7 in the area without local goitre. However, in the epidemiological area, this rate is lower. According to VolpĂ©, it may be related to an inhibitory T-cell defect, which is a key factor in autoimmune thyroid disease. Some of the factors noted can cause an immune response in Basedow such as:

Pregnancy is most often the perinatal (postpartum) period.

Using a lot of iodine, especially people living in areas lacking in iodine, it is possible that iodine may trigger the underlying Basedow disease.

Using lithium modifies the immune response.

Infections and viral infections.

Stop corticosteroids suddenly.

People with HLA B8, DR3 (Caucase resident) HLA BW 46, B5 (China) and HLA B17 (black skin).

Stress role is not confirmed.

Genetically associated with 15% of patients with a loved one with the same disease and approximately 50% of a patient's relative with autoantibodies to the bloodstream.

Pathogenesis

There is a defect of inhibitory T-cells (Ts, T8), which allows helper T (TH) cells to stimulate B-lymphocytes to synthesize antibodies against the thyroid gland. Thyroid-stimulating immunoglobulin or TSH R Ab (Stim): an antibody that stimulates the TSH receptor) causes thyrotoxicosis. In addition, many types of antibodies to thyroglobulin, antibodies to the thyroid Peroxidase enzyme or antibodies were found. In addition, the inflammatory process of orbital muscle infections due to the sensitivity of cytotoxic T lymphocytes or killer cells to the orbit antigens in combination with antibodies. cytotoxic. The thyroid and eye glands may be related by a common antigen between the thyroid gland and orbit.

At the thyroid

T lymphocytes become sensitive to antigens in the thyroid gland and stimulate the B lymphocytes to synthesize antibodies against these antigens. The antibody is directed against the TSH receptor in the thyroid cell membrane and is capable of stimulating thyroid cell growth and activation (antibodies that stimulate the TSH receptor). This may have something to do with the underlying genetics, but the reason for this is how "acute" happens.

At the eye

Cytotoxic Lymphocytes (also called Killer cells) and cytotoxic Antibodies sensitive to common antigens (Commun - Antigen) in fibroblasts in the eye socket (Orbital fibroblast), muscle eye socket and thyroid organization. The cytokines from these lymphocytes have been susceptible to causing oropharyngeal fibroblasts and orbital myositis. The result is swelling of the eye socket, eyeball bulging, diplopia, redness, congestion and conjunctival oedema, swelling around the eye socket (protrusion of the thyroid gland).

Manifestations in the skin and extremities

Oedema of the anterior tibial plateau and periosteal lesions of the fingertips and the tips of the toes (thyroid disease) may also be cytokin-related by fibroblast-stimulating lymphocytes in these sites. .

In addition, the symptoms of thyrotoxicosis were previously thought to be the result of high levels of catecholamine in the blood such as tachycardia, shaking hands, sweating, eyelid twitching, and staring. The quantitative concentration of circulating epinephrine in the normal range so can explain in Basedow disease makes the body more sensitive to catecholamines.

This is partly due to an increase in catecholamine receptors in the heart and several other organs.

Clinical symptoms

Divided into 2 groups of major syndromes, which are manifestations of the thyroid and extra-thyroid.

At the thyroid

Goitre:

The goitre is large, usually diffuse, relatively even, soft, elastic or slightly stiff, there may be systolic fibrillation, systolic blowing at the tumour, and if the tumour is large, it can compress neighbouring organs. Some manifestations of vasomotor disorders of the neck (redness, hot skin, increased sweating), still a small proportion of patients do not have a large goiter (antibody-related).

Thyrotoxicosis syndrome:

These symptoms are usually proportional to the thyroid hormone concentration with many of the organs affected.

Cardiovascular: Thrill, tachycardia, dyspnoea, shortness of breath during exertion and at rest. In large arteries, pulse rapidly jumps and hear a systolic murmur, systolic blood pressure increases (increase in cardiac output) compared with diastolic blood pressure, increased pressure, severe case of arrhythmia, pulmonary oedema enlarged liver, oedema of the lower extremities.

Neuromuscular: Shivering in the hands is a recognizable and prominent symptom accompanied by muscle weakness. Patients are often tired, irritable to change moods, easily emotional, talkative, restless, not focused, sleepless.

Peripheral vasomotor disturbances, when the face is red when pale, increased sweating, the palms of the hands and feet are moist. The tendon reflex may be normal, increased or decreased. In particular, signs of muscle weakness, muscle atrophy, stools (Tabouret), respiratory muscle weakness cause difficulty breathing, oesophageal muscle weakness making it difficult to swallow or choke.

In the young, cardiovascular symptoms are usually prominent, while the elderly is dominant in neurological and cardiovascular symptoms.

Signs of increased metabolism: Increased body temperature, always feeling hot, bathing several times a day, thin quickly, drink plenty of water, uncomfortable hot, cold comfortably. In addition, there are manifestations of calcium metabolism disorders causing hypercalcemia or osteoporosis phenomenon in postmenopausal elderly complications, spondylolisthesis, spontaneous fracture, inflammation around the joints.

Gastrointestinal manifestations: eating a lot (still thin), diarrhoea with abdominal pain, vomiting, jaundice.

Genital urinary: Multiple urination, decreased sex drive, menstrual disorders, infertility, impotence, and male enlargement.

Skin and dependent organs: Pruritus, manifestations of skin pigmentation disorder, and white leprosy occur on the back of hands and extremities; dry, hoe hair, losing softness is easy to lose; hair loss; Brittle nails and brittle feet.

However, it is also necessary to clinically differentiate two groups of symptoms to indicate appropriate treatment.

Sympathetic nerves: Tachycardia, tremor, increased systolic blood pressure, increased reflexes, wide corners of the eyes, gaze, nervousness, depression, irritability, and anxiety.

Thyrotoxicosis: Increased oxygen consumption, overeating, weight loss, psychosis, tachycardia, increased myocardial contractility, decreased resistance to the vascular system.

Extra-thyroid manifestations

Eye damage:

Commonly seen is the bulge of the eye. There are two types: protrusion of the eye and the real bulge of the eye (endocrine bulge), which may not be related to the degree of thyrotoxicosis or to be independent of treatment. So, it can happen after treatment, especially surgery or radiation therapy.

False eye: Non-infiltrative damage related to functional abnormalities due to increased activity of the sympathetic nervous system, increased thyroxin, causing increased stretching of the lash lift muscles, making the eyes open.

True protrusion (endocrine bulge): Infiltrative damage related to orbit components causing endocrine eye disease in the context of autoimmune in Basedow disease, causing damage to the eye muscles and post-socket organization. Eye disease is often associated with increased levels of antibodies to TSH (stimulating) receptors. According to the American Thyroid Association classification, the ocular manifestations are classified as follows:

Grade 0: No signs and symptoms.

Grade I: Asymptomatic, signs of upper eyelid tugging, loss of agonism between eyeball and forehead, between the eyeball and upper eyelid (symptom predominance is related to thyrotoxicosis, recovery from euthyroidism) .

Grade II: In addition to the signs of degree I, there are also feelings of foreign bodies in the eyes, photophobia (Photophobia), watery eyes, eyelid oedema, congestion and conjunctival swelling ... (muscle infiltrates and held eye socket, especially around eye socket).

Grade III: True protrusion, based on eyeball convexity due to post-socket laxative (3 to 4mm (light convex) laxative); 5-7mm (medium convex) and (8mm Clinical considerations should be based on racial factors because the normal convexity of the eyeball as assessed by the Hertel scale of yellow people is 16-18mm, white skin 18-20mm and black skin. 20-22mm

Grade IV: Damage to the motor muscle.

Grade V: Corneal damage.

Grade VI: Reduced or lost vision due to damage to the optic nerve.

To evaluate a relatively honestly about post-socket laxative as well as treatment evaluation, it is necessary to ultrasound the eyeball.

Oedema:

Occurrence 2-3%, usually located in the front of the legs, below the knee, is symmetrical. The thick (unable to pull up) lesion area is several centimeters in diameter, limited. Skin lesions are pink, shiny, infiltrated hard (pig's skin), raised pores, sparse, erect hair (orange), sweat excretion. Sometimes the damage spreads from the lower extremities to the feet.

To the extremities :

The tip of the fingers and toes are clubbed deformed, related to the periosteal, which may have a soft, pale, and temperature-normal organizational response that distinguishes chronic lung disease. There are also signs of onycholysis.

In addition to the above symptoms, some signs of other associated autoimmune diseases such as adrenocortical insufficiency, hypothyroidism, diabetes, severe myasthenia gravis were found in the context of autoimmune poly endocrine disease.

Subclinical

Immunoassay

Presence in the blood of the patient some antibodies against the thyroid gland such as:

Antibodies stimulate TSH receptors (specific to Basedow's disease).

Antibody to thyroid peroxydase (TPO).

Anti-thyroglobulin (Tg) antibody, is nonspecific because it can be found in Hashimoto's disease.

Antibacterial antibody (MIC) .

This implies a few cases of poor response to antithyroid drugs.

The presence of the above antibodies is also seen in some other autoimmune thyroid diseases such as Hashimoto, single goiter, nuclear goiter, thyroid tumour with the rate of change.

Test to assess hyperthyroid function

Increased concentration of thyroid hormone in plasma:

T3: (95-190 ng / dl = 1.5-2.9 nmol / l): increase.

FT3: (0.2- 0.52 ng / dl = 3- 8 pmol / l): increase.

T4: (5 - 12 (g / dl = 64 - 154 nmol / l): increase.

FT4: (0.9 - 2 ng / dl = 12 - 26 pmol / l): increase.

Ratio T3 (ng%) / T4 (microgram%): over 20 (assess the disease progression)

Hypersensitivity TSH (0.5 - 4.5 (U / ml): decreased.

I131 concentration in the thyroid gland after 24 hours is higher than normal. Note that some antithyroid drugs also cause this phenomenon (carbimazole group). It is recommended to evaluate at 4, 6 and 24 hours.

The Werner test is often used in the early stages, to distinguish it from cases with high radioactive iodine concentrations (iodine monotonic, toxic thyroid tumours). Rarely used at present because of the availability of hypersensitive TSH and thyroid scintigraphy.

TRH test and Querido test (TSH stimulation of the thyroid): currently rarely indicated.

Test thyroid morphology and structure

Thyroid ultrasound: Enlargement of the thyroid gland, thick waist, heterogeneous structure, hypersensitivity (false thyroiditis). Energy Doppler can reveal chaotic thyroid structures such as fires during systolic and diastolic periods with dilated blood vessels in the thyroid gland, most carotid artery, and a bouncing external carotid artery. (dancing carotid artery). In many atypical cases (initiation or treatment) it is difficult to distinguish from the image of Hashimoto.

Thyroid scintigraphy (thyroid scintigraphy) helps to partially determine the morphology and function of the thyroid with I123 or Tc 99m: radioactive material concentrates evenly on the entire two lobes of the thyroid - enlarged thyroid - helps stool differentiation of lesions of other hyperthyroidism diseases (multinuclear toxic goitre, toxic goitre, thyroiditis ...).

Thyroid tomography (CT Scanner) and MRI are less commonly used in diagnosis and are less structurally different from some inflammatory thyroid diseases.

Anatomical images of disease: The large thyroid gland has both lobes, diffuse, soft and neoplastic properties. The parenchyma of the thyroid is enlarged and hyperplasia, increasing the height of the epidermal cells and the excess to the follicular wall, creating papillary folds reflecting cell activity. Such dysplasia is often accompanied by lymphocytic infiltrates, which reflects the immune nature of the disease and is related to the concentration of antithyroid antibodies in the blood.

Probe eye damage

Measuring eyeball convexity with HERTEL ruler (going from the outer surface of the eye socket to the tangential plane of the front of the eyeball): simple method, many times, variable value. The drawback of this method is that it is not possible to directly assess the posterior sockets of the laxative lesion.

Look for keratitis.

Fundus examination; measurement of eyeball tonicity.

Ocular tomography to detect eye socket abnormalities, ocular motor, optic nerve in the absence of clinical manifestations (preclinical stage) and help distinguish other causes of protrusion.

Eye ultrasound: for evaluation of ophthalmic and posterior ocular muscle abnormalities (the thickness of the posterior sockets of the laxative can be measured).

Skin lesion test

Biopsy of soft oedema before tibial plateau, stained.

PAS (+) has a deposition of glycosaminoglycan.

X-ray of the limb bone

The bone membrane is thick

Diagnose

Typical body

Meet in young women with all the above clinical signs.

Symptomatic form

Advantages of several agencies:

Heart manifestation.

Neurological manifestations.

Muscle manifestation.

Severe Myasthenia gravis and Basedow. Thyrotoxic bone disease. Gastrointestinal manifestations.

Basedow and vomiting. Haematological manifestations. Big Breasts and Basedow. Basedow and weight gain.

May be related to the cause

Coordination with other autoimmune diseases.

Adrenocortical insufficiency and Basedow.

Diabetes and Basedow.

Biological organisms

Majorly increased T3.

Increase mainly T4.

Progressive forms

Typical type: Return to the equilibrium after treatment. Spontaneous regression: 10-20%

Acute and subacute: In subacute often associated with weight loss, diarrheal, arrhythmia, fever and psychotic manifestations; The acute episode often occurs due to treatment mistakes, especially poor medical preparation in patients with surgical indications.

Apathies: Common in the elderly, predominant muscle weakness, paralysis, anorexia and swallowing disorder. Often difficult diagnosis.

Differential diagnosis

Muscle atrophy in severe myopathy should distinguish primary myopathy.

Thyroid cyclic paralysis usually occurs in Asian women, causes sudden paralysis and hypokalaemia, sometimes spontaneous, can be prevented with potassium and β inhibitors.

Cardiac in hyperthyroidism: reversible onset of arrhythmias, not responding to digoxin, with increased cardiac output.

About 50% have no underlying heart disease, which responds to antithyroid drugs.

Elderly people exhibit weight loss, no large goitre, slow atrial fibrillation and depression (severe, called apathic hyperthyroidism).

Young women sometimes start with amenorrhea, infertility.

Hyperthyroxin syndromes caused by familial albumin disorders: due to an abnormality of albumin that is mainly associated with T4, poorly bound to T3, an increase in T4, FT4I but normal FT4, FT3 and TSH, it is necessary to differentiate the normal status. armour in hyperthyroidism.

Symptoms

Due to the pathogenesis associated with autoimmune disease it is possible to recover spontaneously or with therapy. During the course of the disease often encountered two complications as follows:

Thyrotoxic cardiomyopathy

Often manifested in two forms

Heart rhythm disturbances. varied with sinus tachycardia, extrasystole, paroxysmal supraventricular tachycardia ...

Hyperthyroidism heart failure.

It is necessary to distinguish 2 phases: (1) The first stage of heart failure increases supply (tachycardia, increased blood pressure, myocardial contractility ...) and (2) The later stage is myocardial disease (oedema shortness of breath, enlarged heart, arrhythmia, heart failure, decreased blood pressure, decreased cardiac contractility ...).

Hyperthyroidism level

Usually occurs in untreated or poorly treated patients.

Onset after a trauma (surgery, respiratory infections, trauma, cardiovascular accident, postpartum ...).

When radical treatment (surgery, radiation therapy) is not well prepared. Clinical manifestations with symptoms:

High fever 40-41 (, sweating, dehydration.

Very fast heart rate, arrhythmia, heart failure, pulse collapse.

Tremor, irritation, muscle damage (swallowing disorder), delirium, coma.

Diarrheal, abdominal pain, nausea, vomiting, jaundice.

An apathetic storm may be encountered with characteristic weakness, emotionlessness, and psychosis. Diagnosis is based on the suggested clinical data. Should be treated aggressively immediately, do not wait for test results.

Malignant bulging.

Treatment

There are many methods and means of treating Bassedow's disease today. The choice of treatment method depends on the physician's experience, underlying medical conditions, and patient tolerance and compliance during treatment. Here are some methods and means of treatment:

Internally medical treatment

The group of drugs that inhibit thyroid hormone synthesis:

Presentation: Often used clinically divided into 2 types Carbimazole (neomercazole) 5mg, Methimazole 5mg Propylthiouracil (PTU) 50mg, Benzyl thiouracil (BTU) 25mg

Mechanism of action:

Inhibits most stages of thyroid hormone synthesis

Carbimazole inhibits thyroid deodorization.

PTU inhibits the transformation of T4 into peripheral T3.

High dose carbimazole (> 60mg / day) inhibits antithyroid antibodies (reduces the presentation of thyroid antigens, reduces the release of prostaglandins and cytokines from thyroid cells, inhibits the production of free radicals from T cells and Special B cells present antigens thus reducing antibodies).

Effectiveness: Hormone quantification relative to the half-life of T4 and to the amount of hormone stored in the thyroid gland. Effective after 1-2 weeks, apparent after 3-6 weeks.

Dosage of synthetic antithyroid drugs:

For the Thiouracil group, a half-life of about 90 minutes, can start with high doses in divided doses, when reaching a single dose in the morning. PTU 100-150mg / 6 hours / day. After 4-8 weeks, reduce 50-200mg / once or twice / day.

For the imidazole group: half-life is about 6 hours, due to the anti-thyroid effect over 24 hours, the single dose in the morning starts 40mg / day for 1-2 months, then reduce the dose gradually 5-20mg. Follow FT4 and TSH.

Duration of treatment: (depending on etiology and purpose).

The duration of treatment for antithyroid drugs ranges from 6 months to 15 years or 20 years.

Side effects of the drug: side effects are relatively diverse in about 5% of cases.

Mild: gastrointestinal disturbances, rash, urticaria, fever, joint pain, loss of appetite (agneusie), obstructive jaundice (drug discontinuation), increased alkaline phosphatase.

Severe side effects such as Lupus, Lyeel's syndrome, alopecia, nephrotic syndrome, anemia, polyarthritis pain, multiple nerve root pain, loss of taste.

Neutropenia: when the neutrophil count <1200 / mm3 - must stop the drug if there is a threat of agranulocytosis, so close monitoring is required.

Agranulocytosis: 0.1% (methimazole) and 0.5% (PTU) of cases, determined when the white blood cell count is less than 200 / mm3, clinically unrecognizable. , it is necessary to inform patients of this risk in advance for timely detection and treatment. Stop mandatory antithyroid drugs and use antibiotics as soon as these symptoms appear, especially infection and sore throat.

Monitor when using antithyroid drugs:

Check the white blood cell formula periodically.

FT4 and TSH us.

Check liver function

Some standards can stop antithyroid drugs:

Using a very small dose of anti-thyroid after a period of time does not come back.

The volume of the thyroid is smaller (ultrasonic survey of the volume of the thyroid gland (normal 18 - 20cm3).

Antibodies to TSH (stimulating) receptors were not found in serum, after several tests.

Test Werner (+): Thyroid I131 concentration was inhibited with Liothyronine administration

(T3).

Other means of treatment

Inhibition of iodine transport:

Thiocyanate and perchlorate inhibit iodine transport but the use is often unfavourable, only in exceptional cases.

Inorganic Iodine:

When using Lugol, it is necessary to use antithyroid drugs 1-2 hours earlier.

Just 6mg of Iodur is enough to suppress the thyroid. Do not use inorganic iodine alone, but need to coordinate with anti-thyroid drugs to prevent inhibitory escape.

Current designations for inorganic iodides are mainly:

Prepare short days before thyroidectomy and surgery

Treat thyroid storm.

Previously, people used iodine for many months (over 8 months with 62%). Currently, the course uses an average of 10 -15 days.

Iopanoic acid and ipodate sodium (ipodate 500 mg/day, orally) have the effect of inhibiting T4 to T3 and inhibiting the release of T4, after 24 hours of inhibiting T3.

Lithium:

Caution should be exercised in patients with cardiovascular disease and metabolic disorders, especially dehydration at a dose of 300-450 mg / 8m hours and maintaining a concentration of 1 mEq / l. Use only when patients are allergic to Thionamide or iodine.

Glucocorticoid:

Dexamethasone 2 mg / 6 hours may inhibit thyroid hormone release.

Inhibitors of beta (propranolol, atenolol, esmolol) :

The average dose of propranolol is 20-80 mg / 6-8 hours.

Anticoagulants:

Atrial fibrillation accounts for 10-25% of Basedow patients, especially elderly patients. Warfarin easily causes bleeding after radiation therapy. Aspirin is indicated but with caution in high doses (aspirin increases FT3 and T4 due to decreased protein binding).

Sedation:

It is advisable to choose a group of barbiturates that reduce the amount of thyroxine due to increased degradation.

Cholestyramine:

Taking 4 mg, 4 times a day can reduce T4.

Near-total thyroidectomy

Point:

The disease recurs after many treatments.

The thyroid is too large.

Hyperthyroidism in pregnant women has a poor response to medical treatment.

Preparation before surgery:

Ideally, medical treatment to achieve equilibrium is achieved prior to surgery.

Postoperative monitoring:

Follow up every 4-6 weeks to detect hypothyroidism or return of hyperthyroidism. Note that there may be mild hypothyroidism that recovers spontaneously within 4-6 weeks. Hypothyroidism about 3%, reversible nerve paralysis so requires experienced surgeons.

Radioactive Iodine treatment

Using I131 concentrated in the thyroid gland to destroy the thyroid parenchyma in place, is currently the treatment of choice due to its high efficiency, economy and no serious side effects, there is no evidence to support treatment. Radioactive iodine affects eye diseases in Basedow or increases the risk of malignancy.

Point:

Maybe 35 years or older.

The disease recurs many times - no surgery.

Difficulty in monitoring (for the elderly).

Heart failure.

Allergy to antithyroid drugs.

In case of heart failure, severe thyrotoxicosis, and a large volume of the thyroid gland (over 100 grams), it is advisable to achieve an equilibrium before radioiodine therapy.

Contraindications:

Absolutely in pregnancy, but there is no evidence that radioactive iodine treatment can cause some negative uterine consequences (risk of fetal abnormalities in women after radiation therapy. ) and the ovaries (very low radiation entering the ovaries is equivalent to a probe dose X-ray).

Treat some special situations

Eye treatment in Basedow's disease:

Mild: C evil measures in place, use artificial tears for dry eye cases., Head elevation evening, small methylcellulose (0.5%) during sleep to protect the cornea.

Heavy type: Wear glasses or eye patches., Moisten spot., Antibiotic., Cartilage suture surgery,

Malignant form: Prednisolone 1.5 mg/kg / day divided equally, 4-6 weeks, then reduce the maintenance dose by 5-10 mg/day. Methyl prednisone 15 mg/kg every 2 weeks, azathioprine or cyclophosphamide or cyclosporine A can be used when corticosteroids fail. Extraction of plasma (currently not used method). External radiotherapy in the posterior socket of the 2000 C. Gy dose is given for 10 doses over two weeks. Drainage intervention reduces intraocular pressure, motor surgery of the eye. The above measures can reduce eyeball convexity from 5 to 7 mm.

Recently, people use Colchicine and Pentoxifylline

Treatment of oedema in Basedow :

Topically apply 1mg betamethasone (Celestoderm) or fluocinolone (Synalar).

Treatment of thyroid storm:

This is an endocrine emergency and requires active treatment, care and monitoring.

Antithyroid drugs: Propylthiouracil (PTU) 250-300mg / 6 hours or MĂ©thimazole 25mg / 6 hours orally or rectally (if not). In severe cases, PTU can be increased by 100 mg / 2 hours.

Iodine: Use two hours after using antithyroid drugs, add Sodium - Iodide 1g / IV / 24 hours or saturated solution of potassium - Iodide 10 drops / 12 hours or Ipodate Sodium 1g / day orally or intravenously.

Propranolol 40 mg orally or 1-2 mg intravenously every 6 hours, in the case of associated coronary artery disease. Or Verapamil 5-10mg / 6 hours / slow IV (in case of contraindicated β inhibition).

Hydrocortisone - hemisuccinate 50 mg / 6 hours intravenously (due to reduced cortisol storage and increased need for cortisol during stress).

Cold blanket.

Reduce fever with paracetamol (do not use aspirin).

Rehabilitation, electrolytes and nutrition are important.

Sedation and Phenobarbital.

Oxygen, diuretic and Digitalis are indicated in the presence of heart failure.

Treating or preventing the trigger.

Antibiotics, anti-allergy, postoperative care.

In severe cases, ineffective medical treatment requires blood extraction or peritoneal dialysis to reduce circulating thyroid hormone levels.

Regularly check the concentration of thyroid hormone every 3 - 4 days to adjust the drug. The combination of PTU, iodine, and Dexamethasone can return T3 levels to normal after 24 - 48 hours.

Treatment of heart failure:

This is a very delicate issue to consider before choosing a drug treatment.

Cardiac failure increases production: Mainly synthetic antithyroid drugs combined with beta inhibition if not contraindicated.

Heart failure to reduce output: Besides synthetic antithyroid drugs, it is necessary to coordinate with heart-boosting drugs, diuretics, and beta-blockers with caution.

Basedow Treatment in pregnant women:

Contraindications to I131 treatment.

Do not use iodine during treatment, causing hypothyroidism in the newborn.

Internally medical treatment.

Synthetic resistance: The first three months of using PTU and the second three months can be operated.

Propranolol can be used (note respiratory failure and fetal developmental failure if used in high doses and prolonged).

During breastfeeding can use PTU because the drug through breast milk is insignificant. The fetus should be closely monitored while using antithyroid drugs.

Treatment of reduction - agranulocytosis:

During the treatment of compromised antithyroid drugs, regularly check the leukocyte formula if the number of granulocytes below 1200 mm3 is detected, it is necessary to closely monitor because of the risk of agranulocytosis if the leukocyte is below 200 / mm3. Stop antithyroid drugs and depending on the level and use more Neupogen (Filgrrstim) or Leucomax (Molgramostim)

Prognosis

The patient's prognosis depends on the type of disease, the means of treatment, and the monitoring.