Corticosteroid dependence

Introduction Glucocorticoid dermatitis refers to dermatitis caused by long-term topical glucocorticoids and is characterized by dependence on hormones. This is a side effect caused by inappropriate topical glucocorticoids. The glucocorticoid-dependent dermatitis is characterized by skin flushing, papules, skin atrophy, telangiectasia, acne-like and rosacea-like rash, with burning sensation, pain, itching. Dry, tight feeling, after the topical glucocorticoids are stopped, the skin disease recurs and there is a rebound phenomenon. The disease is extremely common, and more than 500 cases have been reported in various parts of China.

Cause

Topical glucocorticoids cause glucocorticoid-dependent dermatitis.

1. Failure to master the indications: patients do not understand the application range and adverse reactions of hormones, can not accurately grasp the indications of topical hormones, and use hormones for diseases that should not be treated with hormones such as hemorrhoids, rosacea, body lice, etc. There are also long-term and erroneous use of hormone-containing cosmetics for cosmetic freckle, whitening and skin rejuvenation.

2. Inappropriate selection of hormones: The varieties of topical hormones cannot be correctly selected. Facial skin is relatively thin and tender, blood vessels are rich, and the penetrating power of hormones is much larger than that in other parts. It should be treated with moderate or weak hormones instead of potent hormones. The data show that the topical hormones used by the patients are all potent hormonal preparations containing fluorine.

3. The dosage is large/time is too long: It is reported that the average dosage time of the patient's medication is 60g, and the average medication time is 6 months. The other reported symptoms are as short as 6 weeks and the longest is 6 months. The average duration of use is 2 months. Lead to dependence on hormones. The patient has long-term use of hormones for the treatment of primary diseases such as seborrheic dermatitis, eczema, psoriasis, lupus erythematosus and the like. The more potent the hormone is, the longer it will be used, and the more likely it is to develop the disease.

Second, the pathogenesis

1. Epidermal and dermal thinning: Local long-term topical hormones, hormones interfere with the differentiation of the epidermis, induce changes in skin structure and function, and inhibit the proliferation of keratinocytes. This leads to a reduction in the formation of transparent stratum corneum particles, which ultimately thins the stratum corneum. Thinning of the dermis is due to the change in viscoelastic properties of glycoproteins and proteoglycans which weakens the adhesion between fibrils of collagen and reduces collagen synthesis.

2. Hypigmentation/sinking: As the number of layers in the stratum corneum decreases, melanin that migrates to keratinocytes decreases, causing hypopigmentation. Pigmentation may be associated with glucocorticoid-activated melanocyte regeneration pigments. 3. Vascular exposure The weakening of the adhesion between the collagen fibers of the blood vessel wall may cause the blood vessels to widen, and the disappearance of the dermal collagen causes the blood vessels on the surface to be revealed.

4. Alcohol-like acne-like acne-like dermatitis: In the hormone-induced rosacea-like skin lesions, the density of the hair follicles is significantly increased, and the Demodex sputum seals the hair follicle sebaceous gland outlet, acting as a carrier, causing an inflammatory reaction or an allergic reaction. Potent hormones can also cause sebaceous glands to proliferate, resulting in a characteristic rosacea-like rash. Hormones can degenerate the hair follicle epithelium, causing the outlet to become clogged, acne-like rashes or exacerbating the original acne.

5. Folliculitis infection: due to the immunosuppressive effect of hormones, local infection of hair follicles and primary folliculitis can be aggravated.

6. Hormone dependence: Hormones have strong anti-inflammatory properties, can inhibit many skin disease symptoms, such as inhibiting the development of papules and reducing itching, vasoconstriction, erythema disappearing, however, hormones can not eliminate the cause of the disease, often can cause the original after discontinuation Aggravation of the disease, visible inflammatory edema, redness, burning sensation, discomfort and acute pustules and other rebound phenomenon. This phenomenon often occurs 2 to 10 days after the hormone is stopped, and lasts for a few days or 3 weeks. Due to the rebound phenomenon, patients continue to use hormones for external use, resulting in hormone dependence.

an examination

Related inspection

Blood routine skin test

Skin damage

It is characterized by flushing, erythema, papules, pustules, atrophy of the epidermis, shininess, wrinkling, hypopigmentation or hyperpigmentation, telangiectasia, hairy, acne-like and rosacea-like lesions.

2. Facial damage typing

The face is a high incidence area of glucocorticoid dermatitis. Its damage can be divided into:

1-portal type: moderately scattered erythema, papules, and pustules in a clear area about 3 to 5 mm from the lower lip around the mouth.

2 facial central type: double cheeks, lower eyelids, nose, forehead involvement, usually around the lips is normal skin.

3 diffuse type: refurbishment of the face, forehead and neck are involved.

Differential diagnosis

It needs to be differentiated from facial paralysis, hemorrhoids, rosacea, seborrheic dermatitis, frostbite-like lupus, and facial disseminated miliary lupus.

Point-like acne: Point-like acne Blackhead acne is the main damage of acne. It is a cheese-like semi-solid embedded in the hair follicle of the hair follicle. It is black at the outer end of the hair follicle. If it is squeezed, the head is black and visible. The part is yellow-white translucent fat plug.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.