Abstract
ABSTRACTBackground : Acne vulgaris is acommon skin disease, affecting more than 85% ofadolescents and often continuing into adulthood.People between 11 and 30 years of age and up to5% of older adults. For most patients acne remainsa nuisance with occasional flares of unsightlycomedones, pustules and nodules. For other lessfortunate persons, the sever inflammatory responseto Propionibacterium acnes (P.acnes) results inpermanentMethods: Disfiguring scars. (1, 2) Stigmata of severacne cane lead to social ostracism, withdrawalfrom society and severe psychologicdepression (1-4).Result Pathogenesis of acne Traditionally, acnehas been thought of as a multifactorial disease ofthe folliculosebaceous unit, involving excesssebum production, abnormal follicularhyperkeratinization, overgrowth ofPropionibacterium acnes, and inflammation (Fig2). Recent laboratory and clinical investigationsinto the roles of the innate immune system andextracellular matrix remodeling proteins have shedadditional light on this pathogenetic process (5-7).Role of androgens: Activity of type 1 5areductaseenzyme was shown to predominate inhuman sebaceous glands and epidermis. Thisenzyme is responsible for the conversion oftestosterone to the more potent androgen,dihydrotestosterone (DHT). DHT in turn is thoughtto mediate androgen dependent skin diseases suchas acne, hirsutism and androgenetic alopecia (13)The enzyme 5a-reductase type 1 has been studiedin those with and without acne and it has beenhypothesized that those with acne might have moreactive 5a-reductase type 1 .(2)Conclusion : The prominent role of hormones inthe pathophysiology of acne has long beenrecognized and corroborated by clinical andexperimental observations and therapeuticexperience (14). Although acne is not considered aprimary endocrine disorder, androgens, such asdihydrotestosterone, dehydroepiandrosteronesulfate, and testosterone, and growth hormone andinsulin-like growth factors, have all beenimplicated in the pathogenesis of acne (15).Corresponding address to :Dr. Yasir Mansour Mohamed Al-AniIslam Mohammad Nabil El Helou
Highlights
Increase in sebum production: Adrenarche causes increased production of DHEAS from adrenal gland with subsequent rise in testosterone and DHT. This leads to sebaceous gland enlargement and increased sebum production.(23) Androgen stimulation drives the changes in both follicular keratinocytes and sebocytes that lead to the formation of microcomedones and subsequent development of inflammatory lesions and comedones(24) In acne patients, excess sebum production is mainly due to a difference in the response of the target organ, increased circulating androgens or both
Follicular hyperkeratnization: The cause of the hyperproliferation of keratinocytes and the abnormalities of differentiation and desquamation are unknown(27) Recent studies suggest that interleukin 1 alpha ( IL-la) and androgens may be involved in this process(28,29)
Inflammation: Toll-like receptors (TLRs) are ‘‘pathogenassociated pattern recognition receptors’’ that recognize particular pathogen-associated molecular patterns conserved among microorganisms and elicit specific immune responses (36) Expressed on many immune cells
Summary
Increase in sebum production: Adrenarche causes increased production of DHEAS from adrenal gland with subsequent rise in testosterone and DHT. This leads to sebaceous gland enlargement and increased sebum production.(23) Androgen stimulation drives the changes in both follicular keratinocytes and sebocytes that lead to the formation of microcomedones and subsequent development of inflammatory lesions and comedones(24) In acne patients, excess sebum production is mainly due to a difference in the response of the target organ (the pilosebaceous unit), increased circulating androgens or both. Recent studies have shown that P.acnes affects both the differentiation and viability of sebocytes.(32) Immune response to P. acnes includes humoral and cell-mediated immunity as well as complement activation.(31,33)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
