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Due to the irregular application of glucocorticoid external preparations and the misuse of cosmetics containing hormones, the incidence of hormone-dependent dermatitis has increased year by year. We reviewed relevant literature and reviewed the etiology, pathogenesis, clinical manifestations, diagnosis, histopathology, and treatment of glucocorticoid-dependent dermatitis.
Since external use of hydrocortisone in 1951, the clinical application of glucocorticoids has gradually become widespread, and its corresponding side effects have also attracted the attention of medical workers. In 1955, the first case reported the side effects of topical fludrocortisone, followed by related reports at home and abroad, especially the irregular use of domestic hormone preparations, which has caused the incidence of hormone-dependent dermatitis to continue to rise.
1. Cause of hormone-dependent dermatitis
1.1 Abuse or misuse of hormones
Physicians topical steroid preparations less standardized, can not be selected based on the effectiveness of the appropriate hormone correct the disease, medication site selection or improper use of steroids for too long, some patients are obtained from non-specialists and pharmacies, hormone poorly understood, in order to treat the primary disease Long-term use of hormones. Some beauty salons or hospital-made hormonal preparations have no ingredient description or no labeling of possible adverse reactions, which objectively caused patients to misuse hormones without their knowledge.
1.2 Cosmetic use of confusion
At present, the cosmetics market is relatively chaotic, although a large number of 1,614 restricted and banned substances are stipulated in the “Cosmetic Hygiene Regulations” (2007), and the total method coverage is 4.7%. Many of the substances added to cosmetics lack systematic components, toxicity, efficacy testing methods and evaluation requirements, including glucocorticoids, sex hormones, and antibiotics that are not routinely tested. After short-term application of hormone-containing cosmetics, many consumers have reduced pigment in the short-term, and the dilation of capillaries has caused the illusion of white tenderness. In the long-term application, dependence has occurred, leading to hormone-dependent dermatitis.
2. Pathogenesis of hormone-dependent dermatitis
2.1 Epidermis and dermis thinning
Local long-term topical hormones, which inhibit cellular DNA synthesis and mitosis, and inhibit the proliferation and differentiation of keratinocytes. By interfering with the differentiation of the epidermis, hormones cause reduced formation of transparent stratum corneum and eventually thin the stratum corneum. Zheng et al. Found that the epidermis became thinner after continuous encapsulation with potent hormones for 6 weeks. There were only 2 to 3 layers of epidermal cells. The epidermal cells had irregular morphology and structure, and the stratum corneum was almost completely missing. Meanwhile, on the anti-mitotic effect that the reduction of protein synthesis, the Kolbe found that three weeks after the topical application of clobetasol propionate cuticle protein, and inhibit the proliferation and differentiation of fibroblasts, collagen synthesis reduction, caused thinning of the dermis. Pan Weihua and other researchers established hormonal-dependent dermatitis models with fragrant pigs and found that external use of glucocorticoids of any strength may show varying degrees of epithelial atrophy and thinning after 35 days of administration. proportional to the degree of atrophy and hormone strength.
2.2 Impaired epidermal barrier function
Hormones inhibit the proliferation and differentiation of other skin cells. Kao Js et al. Found through electron microscopy that even short-term application of hormones for 3 days can lead to a decrease in the production and secretion of lamellar bodies, a corresponding decrease in secreted cholesterol, free fatty acids, and ceramide between epidermal cells, and a thin extracellular layer. The bilayer decreases, and these changes in the structure of the skin ultimately inhibit lipid synthesis and reduce the number of keratinized particles below the stratum corneum. The hormone-induced stratum corneum integrity and abnormalities in suction are related to the reduction of keratinocytes in the stratum corneum. The integrity of the stratum corneum and abnormal internal suction increase the sensitivity of the skin to the outside world. The stratum corneum is a barrier function provided by the stratum corneum cells and the abundant lipids between the cells. The thickness of the stratum corneum becomes thinner, the number of lamellar bodies and lipids in the stratum corneum decrease, which impairs the epidermal barrier function and increases the loss of percutaneous water.
2.3 Telangiectasia
The weakened adhesion between collagen fibers of the blood vessel wall can cause blood vessels to widen, and the decrease of dermal collagen causes the surface blood vessels to be exposed. It is also possible that local metabolites such as (NO) accumulate due to steroid contraction of blood vessels, and capillary dilatation occurs after discontinuation. The stronger the hormone, the stronger the effect of constricting blood vessels. Long-term use will cause dysfunction of small blood vessels and dilation of capillaries.
3. Clinical manifestation of hormone-dependent dermatitis
It manifests as erythema, pimples, flushing, telangiectasias, dry desquamation, swelling, pigmentation changes, acne-like or rosacea-like skin lesions, polymorphic damage such as hairiness, conscious itching, burning and discomfort.
Ljubojeviae et al. Divided facial steroid dermatitis into 3 types according to the site:
① Around the mouth. A clear area around 35 mm from the lower lip around the mouth has moderately scattered erythema, pimples and pustules.
② Central facial type. Both cheeks, lower eyelids, nose, and forehead are affected. Normally, the skin around the lips is normal skin.
③ diffuse type. The entire face, forehead and neck are affected.
He Li is divided into 5 types according to the characteristics of his skin lesions:
① Facial Dermatitis. Facial erythema and pimples with diffuse flushing of the skin and dilated capillaries;
② Acne-like skin lesion type; densely distributed acne, pimples, pustules; ③ skin aging type: skin aging, dry desquamation, increased wrinkles;
④Pigmentation type: Facial skin is dark, and it can be accompanied by flakes or diffuse light brown to dark brown pigmentation spots;
⑤Pairy hairs become thicker and longer: Facial hairs become thicker and longer, often accompanied by capillary dilatation and pigmentation.
4. Diagnosis and differential diagnosis of hormone-dependent dermatitis
It has been reported that its diagnostic criteria are:
① The use time of hormone is ≥1 month;
② Dependence of skin lesions on hormones: the original disease or skin lesions relapse and aggravate 2 to 10 days after hormone withdrawal;
③ subjective symptoms: burning, itching, pain, dryness, desquamation and tension;
④Objective signs: microvascular dilatation, erythema or flushing, edema, pimples, pustules or acne, pigmentation or skin atrophy.
To diagnose hormone-dependent dermatitis, you must have ① and ②, plus ① or ② of ③④. At the same time, hormone allergies, adverse hormone reactions, and recurrence or rebound of the primary disease must be ruled out. Some experts pointed out during the discussion that some of the above diagnostic criteria need further discussion: ① Regarding the use time of hormones, some experts believe that it should be more than 3 months, and some believe that it should be based on the strength of the hormone used and the cumulative dose. ② Regarding the clinical manifestations such as telangiectasia, which are classified as side effects of hormones, or one of the manifestations of hormone-dependent dermatitis, it remains to be determined: ③ Some experts believe that subjective symptoms are only reference in the diagnostic criteria.
It is not difficult to make a diagnosis based on the above diagnostic criteria, skin lesion characteristics and morphological distribution. Diseases such as rash are identified.
5. Histopathology of hormone-dependent dermatitis
Histopathology varies with the stage and severity of the disease. Eczema-like changes in the epidermis, slight thickening of the spinous layer, intercellular edema and keratosis, dilation of the small veins, infiltration of lymphocytes around the blood vessels, edema around the hair follicles with infiltration of inflammatory cells, sometimes abscesses and ulcers of the hair follicles, and a large amount in the cavity Polymorphonuclear leukocytes. Elastic fibers degenerate, occasionally demodex, and diffuse hypertrophic connective tissue, accompanied by hyperplasia of sebaceous glands.
6. Treatment of hormone-dependent dermatitis
6.1 Common treatment
Patients who stop using hormonal ointments are likely to cause irritating hormonal cosmetics, pay attention to sun protection, wash their faces with warm and cold water, and eat less spicy and irritating foods, and try to avoid external physical or chemical stimulation. People with pruritus can use antihistamines to reduce inflammation; those with light sensitivity can take hydroxychloroquine for a short time; those with hair follicle microbial infection should be treated with sensitive antibiotics.
6.2 Substitute or reduce the intensity and / or frequency of hormone use and gradually discontinue hormone replacement hormone therapy
topical tacrolimus ointment, once / day for the first 3 days, and twice / day after 3 days, continued for 1 week, It was changed to 1 time / day for 20 days, and finally changed to the next day for 30 days. Tacrolimus ointment is a new type of immunosuppressive drug that can avoid hormone rebound phenomenon. Use weak hormones instead of strong hormones, replace fluorine-containing hormones without fluorine, slowly withdraw the drug, and then use emollients instead. Clinical studies have shown that this method is suitable for patients who have used hormone preparations for a long time, such as those who have continuously used hormone drugs for more than 3 months or intermittently used hormone drugs for more than six months.
6.3 Improve skin barrier function
Promote the synthesis of epidermal lipid barrier and build a mixture of palmitic acid, cholesterol, ceramide for external use, and vitamin C can significantly improve impaired barrier function and the integrity of the stratum corneum. Emollient moisturizers are essential, and Liang Jianping reported that the application of moisturizers can significantly improve patient symptoms and increase compliance with treatment.
6.4 Laser Treatment
Weiwei Wang et al. Used dual-wavelength low-energy high-pulse laser to treat 104 patients with facial sensitivity diseases, with a cure rate of 75.3% (58/77). Zhou Dong et al. Treated 46 patients with facial hormone-dependent dermatitis after acute inflammation with total pulsed light therapy with a total effective rate of 93.5%. The strong pulsed light (500 ~ 1200nm) acted on the skin tissue to produce a photothermal effect, which can close capillaries. Clear spots, shrink large pores, enhance skin elasticity, and have a positive impact on the recovery of multiple effects of patients’ skin. At home and abroad, strong pulsed light has been reported to increase the expression of heat shock protein 70 in dendritic cells of the dermal papilla and the dermal layer, inhibit the skin inflammatory response, and reduce the dermal inflammatory cell infiltration.
To restore the skin’s normal barrier function, photoelectric synchronization technology (strong pulsed light + radio frequency) can be used. The lower light energy combined with radio frequency has a stronger heating and stimulating effect on the dermis, with less side effects and better efficacy.
6.5 Chinese treatment
Hormone-dependent dermatitis belongs to the category of “heat poisoning” in Chinese medicine. All the symptoms it produces are related to external wind, heat, humidity, and poisonous evils. Therefore, the principle of treatment is to cool the blood and detoxify, and to clear away heat, dryness, and dampness, and expelling wind. Supplement itching. In addition, psychotherapy can help patients get rid of their psychological dependence on external hormones and enhance compliance. Hu Weibin reported that psychological therapy was used for comprehensive treatment at the same time as the application of the drug. It was found that the clinical efficacy of patients was improved with psychological intervention on the basis of drug treatment, and their mental health and quality of life were also significantly improved.
6.6 Prognosis
The prognosis of this disease is affected by a variety of factors, including age, gender, skin thickness, medication site, duration of medication, strength of hormone potency, type of skin lesions, and individual response. Clinical practice confirms that hair follicle pimples, hair follicle pustules, and acne-like skin lesions and swelling are relatively easy to eliminate, which usually takes about 3 months; diffuse redness, vasodilation, skin atrophy, dryness, and pigmentation changes are difficult to treat It takes a long time, at least 6 months of treatment, and some even several years; and severe skin atrophy is permanent damage, especially the elderly, can not be cured. In summary, glucocorticoid dermatitis has been extremely common in China for more than 10 years, but its pathogenesis has not been fully understood, and there are few related basic studies. At present, no unified naming, concept, diagnostic criteria, and efficacy have been formulated. Judging criteria and clinical classification, treatment is mostly integrated with traditional Chinese and western medicine, comprehensive treatment.