ABSTRACT
Objective To analyze the current clinic application of severe acne treatment, and to provide evidences to improve its treatment. Methods Using sampling survey, a total of 3 012 severe acne patients who visited the dermato-logical department of 35 hospitals over the country for the first time were selected for this study. Each patient filled a ques-tionnaire about their acknowledgement, history of medical intervention and drug therapy of severe acne. Results Among all 3 012 patients with severe acne, 76.6%believed acne is a kind of skin disease, but only 35.2%of the patients went to see doctors at early stage of disease, while others choose interventions such as self-extrudation , topical medication or skin care products, herbal tea/folk recipes, beauty salons and application of coverture cosmetics. Among all severe acne patients, 2 388 cases (79.3%)had taken oral medications, which included 1 161(48.6%) patients who took anti-biotics. 394 cases (33.9%) took roxithromycine and 173 cases(14.9%) took other kinds of anti-biotics. 55.5%of all these patients who took oral medication less than 4 weeks in duration. 2 081 cases (69.1%) applied external drugs, in which includes 90 cases (4.3%) of using glucocorticoid, and 437 cases (21.0%) of using other kinds of external products. The adverse effects of topical treat-ments were commonly observed, such as erythema (512 cases, 24.6%), desquamation (683 cases, 32.8%), scab (73 cases, 3.5%) and hypersensitive (281 cases, 13.5%). Conclusion Severe acne is a disease need systematic treatment. but only mi-nority of the patients went to see doctors at early stage of disease. The current problems in treatment of severe acne include lack of target in choosing drugs, not long enough treatment course, and adverse effects of cutaneous administration.Early , safe and targeted medical attention with sufficient treatment course is encouraged.
ABSTRACT
Objective To observe the effect of ultraviolet irradiation comparising 95％ ultraviolet A (UVA)and 5％ ultraviolet B(UVB)on the proliferation of human epidermal keratinocytes(HEKs),in hope to offer a basis for the construction of a photodamaged skin model induced by sunlight.Methods HEKs were isolated from foreskin tissue and cultured in vitro.After several passages,the HEKs were irradiated with different doses(0,2.5,5,10,20,30,40,60 J/cm2)of UV comprising 95％ UVA and 5％ UVB.Methyl thiazolyl tetrazolium(MTT)assay was used to evaluate cell viability after 24 hours of additional culture.SPSS 17.0 software was used to calculate the median lethal dose(LD50)of ultraviolet radiation in HEKs.Results The proliferation of HEKs was inhibited by 0,1.03％,6.60％,17.28％,31.28％,49.59％,59.67％ and 70.99％ respectively after irradiation with UV of 0,2.5,5,10,20,30,40 and 60 J/cm2.A significant inhibition of cell proliferation was observed in HEKs irradiated with UV at a dose of no lower than 10 J/cm2 compared with unirradiated HEKs(F =62.11,P ＜ 0.05).The LD50 of UV in HEKs was 31.31 J/cm2.Conclusions Aas the dose of UV irradiation increases,the proliferative activity of HEKs decreases,with the LD50 of UV being 31.31 J/cm2.
ABSTRACT
ObjectiveTo explore the effects of epidermal proteins and lamellar bodies on skin barrier in glucocorticoid-dependent dermatitis.MethodsTotally,60 patients with glucocorticoid-dependent dermatitis and 40 normal human controls were eligible for this study.A noninvasive method using TewameterTM was applied to determine transepidermal water loss (TEWL) value in these subjects.Tissue specimens were obtained from the lesions of 13 patients with glucocorticoid-dependent dermatitis and normal skin of 10 human controls.Subsequently,haematoxylin and eosin(HE) staining was performed to observe the histopathological changes,immunohistochemistry to detect the protein expressions of K6,K10,K14,K15,loricrin,filaggrin,involucrin in epidermis,and electron microscopy(EM) to estimate the density of lamellar bodies in tissue specimens.ResultsCompared with the normal controls,the patients displayed an elevated TEWL value (P ＜ 0.05),which suggested an impaired epidermal barrier.Histopathology of lesions revealed nonspecific inflammatorychanges withmarkeddifferencesbetweendifferentclinicaltypesofglucocorticoid-dependentdermatitis.Immunohistochemistry revealed an attenuated expression of K10,K14,loricrin,filaggrin,involucrin and abnormal expression of K15 in lesional epidermis compared with the normal epidermis (all P ＜ 0.05),hinting a suppression of epidermal differentiation and proliferation as well as an impairment of cornified envelope structure.The number and density of lamellar bodies were also reduced in lesional epidermis compared with the control epidermis.ConclusionsCompared with normal skin,the structure of skin barrier is impaired in lesions of glucocorticoid-dependent dermatitis,to restore skin barrier is essential for the treatment of this entity.