subacute cutaneous lupus erythematosus
Introduction
Introduction to subacute cutaneous lupus erythematosus Subacute cutaneous lupus erythematosus (SCLE) is also known as superficial disseminated lupus, subacute disseminated lupus, psoriasis lupus, disseminated verrucous and the like. The lesion is different from discoid lupus erythematosus and is different from pan-type scarring discoid lupus. The skin lesions of this disease are characterized by symmetry, superficiality, generalization and no scar formation. basic knowledge The proportion of the disease: the probability of the population is 0.064% Susceptible people: no special people Mode of infection: non-infectious Complications: reticular bluish
Cause
Subacute cutaneous lupus erythematosus
(1) Causes of the disease
The etiology of this disease is unknown, the incidence of this disease is significantly higher in the family, and the incidence of hypergammaglobulinemia is higher in family members, suggesting that the pathogenesis of this disease is related to genetic factors. Based on genetic factors, some external factors Under the action of (daylight, ultraviolet radiation) and internal factors (spiritual stimulation, psychological severe disorder), through the neuroimmunoendocrine network, the antigenicity of the self-organized cells is changed, and finally the immune reaction occurs and the disease occurs.
(two) pathogenesis
1. The pathogenesis of subacute cutaneous lupus erythematosus is caused by multiple factors causing abnormalities in the human body, causing skin limitation or disseminated pathological damage.
2. Histopathology: The pathological changes of the lesions and the discoid lupus erythematosus have many similarities, but few hair follicle plug formation and hyperkeratosis, the depth of cell infiltration is also light, mononuclear infiltration is usually limited to 2/3 of the perivascular and periorbital around the dermis, the most characteristic change is located in the basal layer of the epidermis, which shows that the basal cells lose their normal structure and normal alignment, form edema and vacuoles between the basal cells or cells, and the epidermis - The dermal junction is partially occluded by mononuclear cell infiltration. This vacuolar degeneration of the epidermal basal cell layer is very obvious, sometimes causing subcutaneous vacuolization, increased melanin production and impaired pigmentation, leading to subepidermal macrophages. Internal melanin, 90% of patients with discoid lupus erythematosus biopsy immunofluorescence found that there is immunoglobulin deposition at the epidermal-dermal junction, and subacute cutaneous lupus patients with immunoglobulin at the epidermal-dermal junction The depositors only account for 40%.
Prevention
Subacute skin lupus erythematosus prevention
1. Avoid drinking and excessive fatigue.
2. If you are allergic to sunlight, you can use a light-proofing agent (such as 5% Ning Ointment), an umbrella or a wide-brimmed hat, and wear long-sleeved clothes and trousers when you go out to avoid exposure in the hot sun.
3. Avoid cold, colds or other infections.
Complication
Subacute cutaneous lupus erythematosus Complications
Soft mucosal mucosal damage can occur in about 40% of patients. This change is particularly common in patients with obvious systemic manifestations; reticular leukoplakia and periorbital capillary changes occur in about 1/5 cases; the most common have joint pain, the cause Unknown fever and general malaise.
Symptom
Subacute cutaneous lupus symptoms Common symptoms Chest papules erythema scaly mucosa damage papular joint pain reticular leukoplakia
The skin lesions of this disease are extensive, symmetric distribution, often involving the shoulder joint, the upper limb extension side, upper back and neck, the skin lesions begin with small erythema, mild desquamation papules, two skin lesions of the same shape can be Blended into a large lesion, this erythematous papule can develop into a scaly scaly lesion of surface desquamation, or it can spread to the surrounding to form an annular rash, and then merge into a multiple annular shape, occasionally the same patient The above two types of skin lesions may occur, but most of them are mainly one type, and often merge to form a large skin lesion. In the center of the annular lesion, there is a gray pigmentation loss, telangiectasia and superficial scales. The erythema surrounds the erythema. Occasionally, small blisters appear on the edge of these lesions. This is due to the epidermal separation caused by severe epidermal basal cell layer lesions. After the lesions subsided, there may still be pigmentation and telangiectasia. It lasts for several months and finally disappears, and telangiectasia can persist for a long time.
In short, the disease and discoid lupus erythematosus have common clinical features and significant differences, the disease is non-scarring, its desquamation and hair follicle plug formation is lighter, shorter duration, wider distribution, skin lesions have The tendency of fusion can form a large lesion area, and the pigmentation change is sometimes prominent. After the acute inflammation subsides, the pigment disappears for several months, but it is not accompanied by dermal atrophy, which is a reversible change. More than half of the cases are diffuse. Scar formation hair loss, and sensitivity to light is more common than discoid lupus erythematosus, about 40% of patients can develop soft palate mucosal damage, this change is particularly common in patients with obvious systemic manifestations; about 1/5 cases appear Variegated leukoplakia and periorbital capillary changes; about 1 in 5 cases of scarring lesions of discoid lupus erythematosus, which are often located in the scalp and can occur many years before the onset of SCLE, almost all patients There are mild systemic manifestations, the most common of which are joint pain, unexplained fever and general malaise, and few severe central nervous system damage.
Examine
Subacute cutaneous lupus erythematosus examination
1. Blood routine and erythrocyte sedimentation rate: generally no anemia, leukopenia can occur, and erythrocyte sedimentation rate increases.
2. Urine routine: a small number of patients have only mild proteinuria and hematuria.
3. Immunological examination: LE cells and antinuclear antibodies are positive in most cases, anti-SSA, SSB antibody positive, about 1/3 of cases have low titer anti-dsDNA antibody positive, 80% of cases are fluorescent ANA positive, of which 60 % of cases are above 1:160.
4. Normal skin biopsy, with immune complex deposition at the epidermal-dermal junction.
Diagnosis
Diagnosis and diagnosis of subacute cutaneous lupus erythematosus
diagnosis
According to the disease, the lesions are characterized by non-fixation, superficial, non-scarring, and alternating exacerbations and remissions. There is no characteristic of fixed and chronic scar formation characteristic of chronic discoid lupus erythematosus, and there is no serious systemic lupus erythematosus. The characteristics of multiple systemic damage, such as central nervous system lesions, renal lesions, combined with characteristic pathological changes of the epidermal basal cell layer, can be basically diagnosed clinically, and then refer to relevant laboratory tests, such as fluorescent ANA positive, anti-SSA, SSB Positive for antibodies, as well as HLA-DR3 or HLA-B8 positive, can be diagnosed as SCIE.
Differential diagnosis
The disease to be identified is basically the same as discoid lupus erythematosus, but other rheumatisms that are confused with lupus erythematosus, such as rheumatoid arthritis, dermatomyositis and mixed connective tissue disease, need to be excluded.
