Myxedema can be divided into generalized myxedema, also known as true myxedema, and pretibial myxedema, also known as thyroid mucinosis.
Western Medicine Name
Myxedema
English name
myxedema
Affiliated Department
Internal Medicine-Endocrinology
Disease site
skin
The main symptoms
Edema
Main cause
Thyroid insufficiency
Multiple groups
Women, children
Contagious
Non-contagious
Myxedema
Overview of Myxedema
Systemic myxedema
Generalized myxedema is a metabolic disorder characterized by scattered or diffuse mucin deposition in the skin and collagen fragmentation under the microscope. Mucin exists in the matrix. It consists of proteoglycans and glucosaminoglycans. These acidic mucopolysaccharides produced by fibroblasts have strong hygroscopicity and can bind 1000 times its own volume of water. And maintain the volume and texture of the dermis. Under normal circumstances, chondroitin sulfate and heparin, which belong to mucopolysaccharide sulfate, are the basic dermal mucins. In some diseases, fibroblasts produce a large number of abnormal acidic mucopolysaccharides, which are usually hyaluronic acid. These acidic mucopolysaccharides (mucins) accumulate in the dermis in large quantities. Diseases that form various mucus states can be treated by plastic iron, Axin Blue toluidine blue and other special stains were confirmed. The presence of mucin can be confirmed by the disappearance of staining after tissue culture with hyaluronidase. Because the moisture in mucin is lost during the operation and is not visible under conventional HE staining, it is considered that there may be an increase in mucin when collagen gaps appear large. [1]
Myxedema Epidemiology
The incidence rate for adult women is about 1.4%, for men is about 0.1%, and for males and females is 1:10. Most onset is 30 to 60 years old.
Causes of myxedema
Thyroid insufficiency can be caused by abnormalities of the thyroid gland, pituitary gland, occasionally or hypothalamus, and certain drugs related to the thyroid gland (radioiodine, antithyroid agent, lithium, p-aminosalicylic acid); neck radiotherapy, thyroidectomy Surgery, Hashimoto's thyroiditis. [2]
Pathogenesis of Myxedema
Primary pituitary disease or injury, which results in reduced secretion of thyroid stimulating hormone (TSH), can also lead to secondary thyroid dysfunction, which is common in patients with pituitary tumors such as partial pituitary resection and postpartum pituitary necrosis (Sheehan syndrome). Similarly, hypothalamic dysfunction results in reduced secretion of thyroid-releasing hormones, and thus reduced secretion of pituitary TSH, which can also cause secondary thyroid dysfunction. [2]
Clinical manifestations of myxedema
1. Sickness (cretinism) Symptoms appear within weeks after birth. It is characterized by low basal metabolic rate, less activity, fear of cold appetite, slow response, and lower than normal body temperature. Physical retardation, short unevenness, retarded mental development, wide eyelids, widening of the distance between the eyes, flattened nose bridge, thick lips and large tongue, swollen eyelids, thick and brittle hair, dry and desquamated skin, non-depression edema The neck is short, the abdomen is swollen, the stubby muscles of the limbs are reduced, and the cry is hoarse.
2. The clinical manifestations of juvenile myxedema vary with the age of onset. The incidence of young children is generally similar to mild illness and mild. Older children or adolescents are mostly similar to adult myxedema, but with varying degrees of growth retardation.
3. Adult myxedema reduces sweating, fear of coldness, fatigue, poor appetite, weight gain, mental retardation, low body temperature, indifferent facial expression, cheek and eyelid edema, pale and anemia, skin is ivory, dry and rough, and desquamation increases Thick, especially in the arms and thighs, with non-concave mucus edema, sparse and thin shedding on the outside of the eyebrows, shedding of armpit hair and pubic hair, slow and easy growth of brittle nails with vertical and horizontal stripes, thin and fragile teeth, muscle weakness, weakness, and bradycardia , The heart enlarges, pericardial effusion, severe cases can cause coma. [3]
Myxedema complications
There may be muscle weakness, bradycardia, enlarged heart, and pericardial effusion. [4]
Myxedema Treatment
Used in thyroid powder (tablets) or levothyroxine sodium (L-thyroxine) or iodronin (L-triiodothyronine) have significant effects. It is advisable to start with a small dose and gradually increase it to a tolerated amount. [5]
Myxedema prevention
1. The cause of iodine-deficiency endemic cretinism is mainly iodine-deficiency.
2. Reasonable malnutrition can cause thyroid shrinkage and hypothyroidism, which affects children's physical strength and Chile's level
3. Early diagnosis and early treatment. [6]
Myxedema
Overview of Myxedema
Anterior tibial myxedema
Pretibial myxedema is a metabolic disorder characterized by scattered or diffuse mucin deposition in the skin and collagen fragmentation under the microscope. Mucin exists in the matrix and is composed of proteoglycans and glucosaminoglycans. These acidic mucopolysaccharides produced by fibroblasts have strong hygroscopicity and can bind 1000 times their own volume of water, which is essential for maintaining dermal moisture And maintain the volume and texture of the dermis. Under normal circumstances, chondroitin sulfate and heparin, which belong to mucopolysaccharide sulfate, are the basic dermal mucins. In some diseases, fibroblasts produce a large number of abnormal acidic mucopolysaccharides, usually hyaluronic acid, and these acidic mucopolysaccharides (mucins) accumulate in the dermis to form various mucus states. It can be confirmed by special dyeing such as colloidal iron, toluidine blue of Asoxan. Hyaluronidase staining disappears after tissue culture can confirm the presence of mucin. Because the moisture in mucin is lost during operation and is not visible under conventional HE staining, it may be considered when there are large gaps in collagen bundles. There are increased mucin. [7]
Causes of myxedema
At present, this disease is considered to be a manifestation of autoimmune diseases like exophthalmos in hyperthyroidism. The evidence is as follows:
1. The disease is almost always accompanied by diffuse hyperthyroidism, which has been considered an autoimmune disease.
2. In patients with diffuse hyperthyroidism, LATS (long-acting thyroid stimulating factor) may be found in the serum of hyperthyroidism, exophthalmos, and anterior tibial mucus edema.
3. LATS was also present in anterior tibial myxedema and biopsy specimens.
4. LATS is involved in activating lymphocytes and promoting fibroblast proliferation to produce a large amount of mucin. [8]
Clinical manifestations of myxedema
Skin lesions are most common in the anterior tibial area, which can start on one side, and then expand and involve the extension of the two lower legs. Most of them are symmetrically distributed. A few can also be found in the hands, arms, and face, and occasionally in the trunk. The lesions were round, oblong, or irregularly round, swollen and firm, and the boundaries of the plaques without depression were clear. Wax-like translucent to rose or light red, sometimes with brown or brownish black. The surface is uneven. Large pores can be searched for orange peel health. Partial sweating and thick black hair are common. Self-perception can be accompanied by pruritus or antagonism. [9]
Myxedema complications
Often accompanied by hyperthyroidism and exophthalmia.
Myxedema Treatment
1. Intralesional injection of triamcinolone (triamcinolone) therapy. Triamcinolone suspension diluted with physiological saline to a solution of 5mg / ml is intramuscularly injected. 1ml is injected into each part, and the total amount does not exceed 40mg, every 3 Once every 4 weeks; there are also claims that intra-injury injection of triamcinolone suspension and equal amount of hyaluronidase (1500U / ml physiological saline) can completely eliminate the damage, but the drug is stopped for several months, often relapses, and re-use in relapse cases This therapy is still effective.
2. Antitumor drug therapy
(1) Nitrophenyl butyrate (CB1248), 0.1 to 0.3 mg / kg per day, divided into 2 to 4 times, the total amount is 400 to 500 mg;
(2) Cyclophosphamide started to take 200mg / d, and gradually reduced to 50mg / d, the total amount was about 8g.
3. The traditional Chinese medicine method should be Jianpi Chushi Huoxue Huayu Decoction. [10]
Systemic myxedema