skin hardening
Introduction
Introduction Skin sclerosis is caused by inflammation or degeneration of collagen fibers or adipose tissue; siltation of lymph and blood; and symptoms caused by physical factors and metabolic disorders. Should pay attention to family history. Such as adult premature aging, sclerosing atrophy syndrome, the former autosomal recessive inheritance, the latter is autosomal dominant inheritance. There is also a phenomenon of family aggregation in patients with systemic hardness. It is common for fathers and sons to have problems with their daughters or sisters. Personal history should pay attention to the birthplace, such as living in the south of the Yellow River, there are many opportunities for filariasis. In the past history, if there is a history of surgical removal of local lymph nodes, it can cause local lymphatic deposition and lymphedema.
Cause
Cause
The first-phase treatment dose is too large, causing degeneration of collagen fibers and blood vessels. Homogenize and harden. Often see telangiectasia.
Neonatal sclerosis: As the content of unsaturated fatty acids in the subcutaneous fat of newborns is reduced, the proportion of saturated fatty acids is relatively high, and the latter has a high melting point, which causes fat to solidify when cold body temperature drops.
Lymphatic deposition and varicose syndrome
1. Lymphatic edema: Edema caused by defects in lymphatic growth during birth.
2. Secondary lymphedema: common in chronic recurrent erysipelas, filariasis, lymph node surgery.
3. Varicose syndrome: due to varicose veins caused by lower leg stasis dermatitis, embolic phlebitis, recurrent cellulitis, and finally lead to brown skin and fibrosis and hardening of the skin before the lower leg.
Tumor
1. Fibrotic basal cell carcinoma.
2. Carcinoid syndrome: Carcinoid tumor is an amine precursor uptake and depletion of cell tumors. It can produce small molecular peptide hormones and serotonin, histamine and vasopressin.
Metabolic factor
Sclerosant grade fluid edema. Its skin appears as abnormal globulin deposits. In recent years, it has been found that in some cases, there are monoclonal globulins in the serum.
Hereditary factor
1. into N premature aging: congenital hereditary, autosomal recessive inheritance. Also known as Weme syndrome.
2. Sclerosing atrophic syndrome: autosomal dominant inheritance. It occurs at birth and is characterized by a hard skin-like change in the fingers.
Examine
an examination
Related inspection
Reticulocyte count (RC) serum 1 antitrypsin assay (1-AT) immunopathological examination
Physical examination
It should be noted that skin sclerosis is a systemic symmetry, or a limited asymmetry; the former is mostly a systemic cause, while the latter is mostly a local factor. Such as systemic scleroderma is an autoimmune disease, the lesion can affect the skin and internal organs; and the lower leg repeated erysipelas infection, only cause lymphatic blockage of the lower leg and local lymphedema. Scleroderma can be divided into tumescent and hard, without pigmentation, smooth skin surface and certain elasticity, such as lymphedema, vascular deposition, metabolic protein deposition, etc.; and another hardness is as hard as wood, Accompanied by hyperpigmentation or atrophic systemic stiffness disease, varicose vein syndrome.
Experimental examination and pathology
Diagnostic filariasis can be found after taking a blood smear at 10 pm. Systemic scleroderma and syndrome check serum antibody 5cm. Positive for positive and centromere antibodies, 5cm-70 positive for the specific antibodies of the two diseases means that the systemic scleroderma is violated and the disease is serious. Histopathological changes in systemic scleroderma: early dermal collagen fiber swelling, perivascular lymphocytic infiltration. Late inflammation is not obvious, collagen bundle thickening has crane-like hyaline degeneration, vascular wall fibrosis hyperplasia, vascular endothelial cell proliferation, lumen narrowing, even embolism, skin sclerosis, epidermal atrophy pigment increased. Radioactive dermatitis is characterized by hyperkeratosis and atrophy of the epidermis, disordered arrangement of acanthocytes, visible keratotic cells, and obvious small vessel dilatation and collagen fiber homogenization. Nuclear atypia can also be seen, which can lead to cancer.
Diagnosis
Differential diagnosis
The diagnosis should be differentiated from the following symptoms:
Local skin tightening: Local skin tightens, most commonly in scleroderma. Scleroderma is also known as systemic sclerosis. As the name implies, it is a disease in which the skin becomes hard. Skin changes are a hallmark of systemic sclerosis. However, the degree of lesions varies greatly. The mild ones only have localized skin sclerosis and calcification. In severe cases, extensive skin hardening and thickening may occur throughout the body. Typical skin lesions in turn undergo three stages of swelling, infiltration, and atrophy. The lesions are symmetrical, and the lesions are gradually extended from the fingers to the proximal end, and the boundary between the lesioned skin and the normal skin is unclear.
