What Is Rhus Dermatitis?

Bullous skin disease refers to a group of skin diseases with bullous as the basic damage, such as pemphigoid and pemphigoid. The cause of these skins is an autoimmune response, they are all autoimmune diseases.

Bullous skin disease

Bullous skin disease refers to a group of skin diseases with bullous as the basic damage, such as pemphigoid and pemphigoid. The cause of these skins is an autoimmune response, they are all autoimmune diseases.

Causes of bullous skin disease

Pemphigus is an autoimmune disease. Its etiology and pathogenesis are not completely clear, but a lot of evidence shows that it is an autoimmune disease. Antibodies to keratinocytes or intercellular substances are present in the serum of patients with pemphigus. Patients with skin lesions and surrounding tissues also have similar antibody deposits. Skin lesions and surrounding tissues also have similar antibody deposits. The target antigen to which these antibodies are directed is autologous epidermal tissue. Pemphigus is the formation of blisters on the skin caused by the thorns of keratinocytes that are released by the reaction between antigens and antibodies. Pemphigus, especially erythematous pemphigus, often coexists with other autoimmune diseases, such as thymoma, myasthenia gravis, SLE, and psoriasis. Corticosteroids and immunosuppressants have a positive effect on the treatment of pemphigoid, and plasma exchange therapy can obtain clinical relief by removing autoantibodies in the serum.

1. Pemphigus antibody is a key factor in the onset of pemphigus

In patients with pemphigus, direct immunofluorescence examination showed that almost 100% of active patients could detect pemphigoid antibody deposition on the skin around the skin lesions. The main type of antibody was IgG with occasional IgA and IgM. Indirect immunofluorescence detection found that more than 85% of patients had pemphigoid antibodies in their serum, and the antibody titer was positively correlated with the severity of disease and activity. In clinical remission, antibody levels decreased.

Repeated injections of pemphigoid patient serum into animal skin have induced a variety of animal models of pemphigoid, and the range of skin lesions in animals is directly proportional to the injected antibody to pemphigoid serum. The pemphigoid patient serum was added to the artificially cultured skin mass tissue, and it was found that pemphigoid antibodies were deposited on the epidermal cell membrane, and the cell separation on the basal layer occurred after 1-2 days, and the spinous layer cells loosened after 3-4 days. ; The subsequent use confirmed that it was the IgG antibody in the pemphigoid serum that caused the spinous layer dissociation, and the titer of the added antibody was closely related to Chengdu of the spinous layer dissociation. Adding pemphigoid antibodies to the cultured keratinocytes, cell-cell contact separation can be seen within 20 minutes, causing the cells to fall off the wall of the culture dish. The above can see the importance of pemphigoid antibodies in the pathogenesis.

2. Pemphigus Antigen

Pemphigus antigen is produced during epidermal differentiation. It is a 130KD transmembrane desmoglycoprotein and is one of the calcium-dependent cell adhesion molecules.

3 The mechanism of spinous layer loosening

First recall the connection of epidermal keratinocytes (keratinocyte diagram, desmosome, blister diagram).

Adjacent keratinocytes are connected through desmosomes. Desmosomes are important adhesive connection structures between epidermal cells. Desmosomes include desmin and glycoprotein, which are calcium-dependent cell adhesion molecules. Cell adhesion plays a direct role.

Pemphigus pathology is characterized by the mutual release of blisters and spines in the epidermis. Transmission electron microscopy revealed that the intercellular adhesion material disintegrated in the early stage of the lesion, the intercellular space widened, and the desmosomes were destroyed and disappeared later. The tension filaments connected to the desmosomes were broken and arranged disorderly.

In pemphigoid organ culture model and spinous layer release model, plasminogen activator (PA), especially urokinase plasminogen activator (u-PA) activity was significantly increased, 48-72 hours It reached a peak within the time, which basically coincided with the time of skin lesions. It was found that urokinase can cause spinous layer-like release, and plasminogen activator can catalyze the conversion of plasminogen to active plasmin. The result is the hydrolysis of fibrin, fibronectin and laminin, which accelerates Formation of spinous layer release caused by pemphigoid antibodies.

In short, pemphigus antibody-induced spinous layer dissociation is a special type of immunological injury. It does not require complement or lymphocyte involvement. It is a special tissue injury induced by autoantibodies. The process of spinous layer loosening can be summarized as: Pemphigus antibody is generated due to the action of a certain initiating factor. The antibody binds to the corresponding antigen on the epidermal cell membrane, which causes the epidermal cells to release or activate proteases. The matrix destroys the adhesion between normal cells and cells, resulting in spinous layer dissolution.

Bullous skin disease check

1. Cytology

Spiny-released cells (also known as Tzank cells)

2. Histopathological examination

Blister or fissure formation in the epidermis, spinous release cells

3 Immunofluorescence

Review the content of immunological experiments

a) Direct Immunofluorescence (DIF): Principles and Performance-Fishing Net Fluorescence between Spines

b) Indirect immunofluorescence (IIF): Principles and performance-Pemphigus antibody

Types of bullous skin disease

Pemphigus is clinically divided into four types: common type, proliferative type, deciduous type, and erythema type.

1. Pemphigus vulgaris

1) Characteristics of skin lesions: loose bullae, easily ruptured, forming an erosion surface and difficult to heal

2) Skin lesions: they can spread throughout the body. 60% first oral involvement

3) Nissl disease: concept and meaning, which other diseases can also be found

4) Age of occurrence: middle-aged and elderly

5) Prognosis: worst

6) Clinical examples

2. Proliferative pemphigoid

1) It is an ordinary type of opposite sex. There are two types of Neumann type & Hallopeau type

2) Features: mushroom-like proliferation or papilloma-like hyperplasia

3) Location: Wrinkles such as groin and around the nose and mouth

3 Pemphigus decidum

1) Skin lesions: loose blister, extensive erosion, lobular crusts

2) Part: generalized, less oral involvement

3) Prognosis: poor

4 Erythematous pemphigus (Senear-Usher syn.)

1) benign type of deciduous type

2) Characteristics of skin lesions: erythema, crusts, similar to DLE or seborrheic dermatitis

3) Parts: head, face, chest, upper back

4) Prognosis: Good, can be converted to deciduous or ordinary

Bullous Dermatological Diseases Treatment

Dapsone is preferred. Available sulfadiazine, small doses of prednisone. Avoid gluten-containing foods and avoid iodine-containing preparations.

1. Supportive Therapy

2. Corticosteroids

First choice. Hormonal treatment principles

Hormonal side effects, hormonal sepsis have become major causes of death

3. Immunosuppressive

The purpose is to reduce the amount of hormones and side effects. Watch for side effects from immunosuppressants

4 Others: plasma exchange therapy, high-dose intravenous gamma globulin, etc.

5. Local treatment