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Acne and Rosacea View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by eScholarship - University of California UC San Diego UC San Diego Previously Published Works Title Acne and Rosacea. Permalink https://escholarship.org/uc/item/5xs3g48j Journal Dermatology and therapy, 7(Suppl 1) ISSN 2193-8210 Authors Picardo, Mauro Eichenfield, Lawrence F Tan, Jerry Publication Date 2017 DOI 10.1007/s13555-016-0168-8 Peer reviewed eScholarship.org Powered by the California Digital Library University of California Dermatol Ther (Heidelb) (2017) 7 (Suppl 1):S43–S52 DOI 10.1007/s13555-016-0168-8 REVIEW Acne and Rosacea Mauro Picardo . Lawrence F. Eichenfield . Jerry Tan Received: August 11, 2016 Ó The Author(s) 2017. This article is published with open access at Springerlink.com ABSTRACT considered to be the underlying disease mechanisms in acne, while the multifactorial Acne, one of the most common skin diseases, pathology of rosacea is thought to involve both affects approximately 85% of the adolescent vasoactive and neurocutaneous mechanisms. population, and occurs most prominently at Several advances have taken place in the past skin sites with a high density of sebaceous decade in the research field of acne and rosacea, glands such as the face, back, and chest. encompassing pathogenesis and epidemiology, Although often considered a disease of as well as the development of new therapeutic teenagers, acne is occurring at an increasingly interventions. In this article, we provide an early age. Rosacea is a chronic facial overview of current perspectives on the inflammatory dermatosis characterized by pathogenesis and treatment of acne and flushing (or transient facial erythema), rosacea, including a summary of findings from persistent central facial erythema, inflammatory recent landmark pathophysiology studies papules/pustules, and telangiectasia. Both acne considered to have important implications for and rosacea have a multifactorial pathology that future clinical practice. The advancement of our is incompletely understood. Increased sebum knowledge of the different pathways and production, keratinocyte hyper-proliferation, regulatory mechanisms underlying acne and inflammation, and altered bacterial rosacea is thought to lead to further advances colonization with Propionibacterium acnes are in the therapeutic pipeline for both conditions, ultimately providing a greater array of treatments to address gaps in current management practices. Enhanced content To view enhanced content for this article go to http://www.medengine.com/Redeem/ 6C47F0600685C21C. Keywords: Acne; Acne vulgaris; Adolescent; M. Picardo (&) Pathogenesis; Pediatric; Pre-adolescent; San Gallicano Dermatologic Institute, Rome, Italy Rosacea; Therapy e-mail: [email protected] L. F. Eichenfield University of California, San Diego, CA, USA ACNE J. Tan Acne is a chronic inflammatory disease of University of Western Ontario, Windsor, ON, Canada the pilosebaceous unit and occurs most S44 Dermatol Ther (Heidelb) (2017) 7 (Suppl 1):S43–S52 prominently at skin sites with a high density of sebaceous glands [e.g., the face (99% of cases), back (60% of cases), and chest (15% of cases)] [1]. Although it predominantly affects the adolescent population (approximately 85%), it can also affect pre- and post-adolescents. The pathogenesis of acne is multifactorial and polymorphic, and several different grading systems have been developed to assess the severity of acne. Substantial acne is associated with social impairment, diminished quality of life, depression, and reduced global self-esteem [2, 3]. Fig. 1 Primary and secondary factors contributing to acne ACNE PATHOGENESIS: NEW pathogenesis HORIZONS Several primary and secondary factors are immunity and keratinocyte and sebocyte believed to contribute to the onset and function, leading to amplification of the three development of acne [4]. Specifically, the basic key pathologic processes implicated in acne disease mechanism is thought to involve development: inflammation, keratinization, increased sebum production, keratinocyte and sebogenesis [7]. hyperproliferation, inflammation, and altered Support for the development of therapies bacterial colonization, primarily with that target molecules implicated in the Propionibacterium acnes (Fig. 1). The exact activation of innate immunity is provided by sequence of these events is unclear, but the several research findings. These include a major pathophysiologic factor is likely to be confirmed association between sebaceous lipid an androgen-induced increase in sebum synthesis and inflammation [8] and evidence of production and secretion, coupled with elevated levels of CD3? and CD4? T cells and qualitative changes in sebum. Characteristic inflammatory markers in early subclinical acne changes in sebum composition reported in lesions (microcomedones) [9, 10]. Furthermore, acne patients include reduced levels of linoleic recent studies highlight the important acid, increased levels of squalene and lipid contributory role of Toll-like receptor peroxides, and an increased ratio of activation and subsequent interleukin-1 alpha saturated/mono-unsaturated fatty acids [4–6]. secretion by keratinocytes in comedogenesis Hormones, the environment, neurologic and [10, 11]. inflammatory mediators, and lipid metabolism The pilosebaceous unit and resident have all been implicated in the regulation of sebocytes also play an active role in skin sebum production [4]. endocrine function. Androgen hormones as The quantitative and qualitative changes in well as growth-promoting hormones and sebum production have also been implicated in growth factors control sebaceous gland colonization of the follicular duct by P. acnes. function, and recent attention has focused on Notably, sebum quality may influence skin insulin/insulin growth factor-1 signaling and its microbiome composition, particularly in terms ability to stimulate sebocyte proliferation and of the abundance and strains of P. acnes differentiation. Importantly, endocrine changes populating the pilosebaceous unit. P. acnes is closely related to pubertal rises in insulin thought to contribute to acne pathogenesis resistance have been reported to affect acne through several different mechanisms onset and development, leading to a including interaction with innate cutaneous re-evaluation of nutritional influences and Dermatol Ther (Heidelb) (2017) 7 (Suppl 1):S43–S52 S45 endocrine factors involved in the promotion of FOCUS ON PEDIATRIC ACNE acne development [12]. The Western diet, characterized by a high glycemic load, may be The Earlier Onset of Acne an environmental factor linking acne to hyperinsulinemia and may represent a Although often considered a teenage disease, targetable adjunctive aspect of acne acne is occurring at an increasingly early age, pathogenesis. A low-glycemic-load diet appears possibly because of earlier puberty and/or other to ameliorate the signs of acne, reducing factors. Twelve years of age is no longer the number of both inflammatory and considered the low end of the ‘normal’ range non-inflammatory lesions and affecting the for onset, and there has been an overall decrease fatty acid composition of sebum triglycerides in the average age of children seeking treatment through reduced fatty acid mono-unsaturation for acne. This earlier onset mirrors a downward [4, 12]. Consumption of milk can induce trend in age at the start of puberty and may mechanistic target of rapamycin-1 (mTORC1) represent the first sign of pubertal onset in signaling through several different pathways children aged 7–11 years [18–20]. Acne and [13]. A major mechanism is considered to be the acne-like conditions can also develop in stimulation of IGF-1 production by the liver neonates, infants, and young children, and following ingestion of specific amino acids may be associated with differential diagnoses found in milk. These include tryptophan-rich or systemic pathologies that differ from those of lactalbumin, relevant for the hepatic synthesis pre-teen and teenage acne vulgaris. The American of IGF-1, and the branched amino acids leucine, Acne and Rosacea Society/American Academy of isoleucine, and valine, involved in the Pediatrics guidelines promote recognition of early stimulation of insulin secretion [14]. Moreover, acne, pathologic acne (acne associated with milk proteins possess approximately twice the underlying endocrinologic or other pathologic amount of glutamine as beef, and glutamine in conditions), and scarring acne [21]. the sebaceous gland is required for cellular proliferation and lipogenesis, as a large amount is converted to the amino acids glutamate, Neonatal Acne alanine, serine, glycine, and aspartate [15]. A combination of these milk-derived metabolic Neonatal acne develops during the first 0–6 effects can explain the elevated insulinemic weeks of life and is characterized by index induced by the consumption of whole erythematous papulopustules affecting the and skimmed milk. Evidence also suggests that face, scalp, neck, and torso. Not considered peroxisome proliferator-activated receptors true acne, neonatal acne may be associated with (PPAR) expressed in sebaceous-gland cells and skin colonization by Malassezia species their ligands play an important role in the (M. sympodialis, M. globosa) and is usually a regulation of human sebum production and self-limiting condition, although symptom acne development [8, 16, 17]. resolution may be achieved more quickly with The clarification that sebum alterations and a topical anti-yeast
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