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Many hormonal diseases are accompanied by damage to the skin of the face, hands, feet, and head. If the cause of this lesion is a hormone-exchange defect (for example, a hormone deficiency), it will manifest itself in the early stages of the disease and may be a diagnostic sign of thyroid disease. Skin lesions can also develop as a complication of the underlying disease. Finally, skin lesions can be a complication as a result of treating the underlying disease (for example, insulin treatment causes atrophy of the fat layer of the skin in patients with type 1 diabetes).
A. Thyrotoxicosis (increased secretion of thyroid hormones)
1. With thyrotoxicosis, the skin becomes hot, smooth, and damp from sweat. The palms, face become red. In severe cases, enhanced pigmentation develops.
2. Hair and nails with thyrotoxicosis. Hair thinning, becoming soft, oily. Quite often, diffuse alopecia (baldness) develops. The nails are separated from the nail bed (onycholysis), the process begins with a ring finger (Plummer’s nail).
3. Local mucous edema due to the deposition of acid salts in the skin (for example, hyaluronic acid salts). They have the appearance of reddish brown or yellow plaques; normal location – the front surface of the legs (pretibial myxedema). The skin is similar to the peel of an orange, covered with coarse hair. Plaques are painless, cold to the touch, with no pressure on them. Itching is possible. Pretibial myxedema is a characteristic sign of diffuse toxic goiter. It can even be observed in treated patients with low or normal levels of thyroid hormones.
4. Limb changes. Diffuse toxic goiter is sometimes accompanied by deformation of the long tubular bones of the extremities (hypertrophic osteoarthropathy), as well as the phalanges of the toes and hands. The skin of the hands and feet is thickened, the fingers are like drumsticks, and the nails are on watch glasses. X-ray examination reveals spicules – ossification along the vessels from the periosteum to the bone. These changes are usually combined with the pretibial myxedema (described in
B. Hypothyroidism (reduced thyroid function, lowered hormone levels).
1. Congenital hypothyroidism – is characterized by a change in the structure and color of the skin, it becomes dry, cold, pale with a yellowish tinge. The changes are caused by slower blood flow, anemia, the deposition of acid salts in the skin, physiological jaundice and an increased content of carotene yellow pigment (carotenemia). The sweat compartment is lowered. Due to a violation of thermoregulation and a decrease in temperature, the child’s marbling of the skin manifests itself – the vessels shine through the skin and form a mesh pattern. This pathology is accompanied by an umbilical hernia, shortening of the proximal extremities (located closer to the body), a wide flattened nose, and a protruding tongue.
2. Acquired hypothyroidism (reduced thyroid function). The picture of the disease is in many ways similar to congenital hypothyroidism. But in adults and in children, dryness and peeling of the skin is stronger than with congenital abnormalities. The ducts of the sweat glands are atrophied, so sweat is practically not excreted. Due to the deposition of acid salts in the skin, mucous edema develops – myxedema. With acquired hypothyroidism, myxedema has a generalized character (multiple mucous edema, unlike local mucous edema with thyrotoxicosis). The skin is puffy, pale, edematous; a hole after pressure does not remain. These changes are especially visible on the skin of the face and eyelids.
3. Hair loss with hypothyroidism. Diffuse alopecia (alopecia) develops. The remaining hair is tight and dry. The third part of hair on the eyebrows falls outside. Poor hairiness in the armpits and pubic hair. Sometimes children develop enhanced hair growth on the arms, legs and back (hypertrichosis), which disappears after treatment.