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J.M. Azaña Defez, M.L. Martínez Martínez Doctors in Medicine and Surgery

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J.M. Azaña Defez, M.L. Martínez Martínez Doctors in Medicine and Surgery Acne J.M. Azaña Defez, M.L. Martínez Martínez Doctors in Medicine and Surgery. Consultant Physicians at the Dermatology Service. Pediatric Dermatology Unit. University Hospital Complex of Albacete Abstract Resumen Acne is a chronic inflammatory skin disease of El acné es una enfermedad cutánea inflamatoria the pilosebaceous unit of multifactorial etiology crónica del folículo pilosebáceo, de origen characterized by increased sebaceous secretion, multifactorial, caracterizada por: aumento de la comedone formation, inflammatory lesions and secreción sebácea, formación de comedones, lesiones risk of scarring sequelae. It is undoubtedly one inflamatorias y riesgo de secuelas cicatrizales. of the most frequent dermatological processes Es, sin duda, uno de los procesos dermatológicos in the daily clinical practice, especially in más frecuentes en la práctica clínica diaria, adolescence, although it can also appear in especialmente en la adolescencia, aunque también childhood and persist into adulthood. Adequate puede aparecer en niños y persistir en la edad management of this pathology is relevant, adulta. Es importante un manejo adecuado de esta as it can cause lower self-esteem and social patología, que puede producir una disminución de la dysfunction in patients, with the subsequent autoestima y disfunción social de los pacientes, con impact on quality of life. el consiguiente impacto en la calidad de vida. Key words: Cutibacterium acnes; Grading and classification of acne; Acne management; Isotretinoin. Palabras clave: Acné; Cutibacterium acnes; Graduación y clasificación del acné; Manejo del acné; Isotretinoina. Introduction Etiopathogenesis acne among the Spanish population Acne is a frequent inflammatory skin aged 12 to 18 years is 74%, without Acne is a multifactorial disease, produced disease of chronic course and polymor- significant differences regarding sex by: increased sebaceous secretion, follicu- phous in its clinical expression. and with a peak between 14 and 16 lar epidermal hyperproliferation, comedoge- years of age(2); therefore, it accounts nesis, bacterial colonization and induction for 25% of dermatological consul- of inflammation. cne is a chronic skin disease of tations. Acne is estimated to be of the pilosebaceous unit, of mul- moderate / severe intensity in about Acne is a disease of the piloseba- A tifactorial etiology, characteri- 20% of patients. ceous follicle, induced by androgens zed by its clinical polymorphism. It Its highest prevalence and intensity of adrenal and gonadal origin: its undoubtedly represents one of the occur around 14-15 years of age in onset correlates with the increase in dermatological processes of greatest females and somewhat later (16-18 sebaceous production triggered by interest in daily clinical practice. years) in males. Despite its prevalence this hormonal stimulus. The pilo- in adolescence, in 7-25% of patients it sebaceous unit is the target organ of Epidemiology will persist into adulthood. acne, explained by the distribution of In females, it can manifest a longer lesions in the areas with the highest Acne can appear in all stages of life, course; whilst in males, more serious concentration. although its prevalence is higher in ado- forms are identified(3). The factors involved in its deve- lescence and there seems to be a genetic There seems to be certain genetic lopment include: increased sebaceous predisposition. predisposition to develop acne: history secretion and follicular epidermal of acne is often found in parents, and hyperproliferation, which leads to Acne is one of the most frequent in addition, there is a high concor- the formation of: comedones (come- dermatological diseases, as it is dance in monozygotic twins(3,4). dogenesis), bacterial colonization by estimated that around 85% of the Seasonal variations in acne severity Cutibacterium acnes (formerly named population will present it throug- are observed, with a tendency to wor- Propionibacterium acnes) and induc- hout their lives(1). The prevalence of sen in winter(5). tion of inflammation(6). 166 EN - PEDIATRÍA INTEGRAL Pediatr Integral 2021; XXV (4): 166 – 175 ACNE The onset and persistence of the follicular channel and, later, by an due to a ductal hydration mechanism activity of the sebaceous glands is inflammatory reaction to a foreign that would favor the obstruction. This mainly due to the action of andro- body triggered by the rupture of the is the mechanism that explains the gens. After its activity in the postna- ductal wall. The cell wall of C. acnes exacerbation of acne lesions produced tal period, due to the maternal hor- contains a carbohydrate antigen that by the use of protective masks during monal influence, sebaceous glands stimulates the development of anti- the SARS-CoV-2 pandemic (“Mask remain minimized until puberty, bodies, which facilitate the inflam- acne”). when the size and number of lobes matory response. Various drugs, such as anabolic per gland increases, as a result of the There are multiple factors related steroids or contraceptives contai- androgenic stimulus (adrenarche). to acne exacerbation episodes. Various ning progestogens with androgenic The presence of this glandular acti- studies postulate that diet could be action, can exacerbate acne. In addi- vity is a necessary requirement for considered a stimulating factor for tion, there are numerous treatments the development of acne. There is acne, since foods that are high in such as: oral corticosteroids, isonia- a greater sebaceous secretion and, sugar and other carbohydrates, dairy zid, lithium or certain anti-cancer in addition, a qualitative alteration. products or proteins, would affect drugs, capable of inducing acneiform These events have been related to the serum insulin and insulin-like growth eruptions. development of hypercornification of factor (IGF-1), which would induce The use of high lipid-based cos- the sebaceous duct and changes in an increase in the production of avai- metic formulations, aggressive clea- surface microorganisms. The conse- lable androgens and the development ners or alkaline soaps can: alter the quence of hypercornification of the of acne(3). However, currently, there skin barrier, promote the formation sebaceous duct is microcomedone: is no scientific evidence with contro- of comedones and induce inflam- keratinocytes are grouped in dense lled studies to justify the restriction mation. clumps with monofilaments and of specific foods(10). The term exposome defines the lipid droplets, retaining the secreted The exacerbation of lesions in assorted environmental factors that sebum that distends the channel and stressful situations is a known fact, influence the development and seve- the gland. This microcomedone is the in relation to the neuroendocrine rity of a disease, in this case acne. primary acne lesion. regulation of sebocytes, the increase Identifying the negative exposome Acne is not an infectious process, in adrenal secretion and the manipu- factors can help reduce its impact and but there are microorganisms that lation of lesions. Conversely, acne has manage the disease(11). colonize and multiply in the folli- an undoubted psychosocial impact, cular duct, and that can play a role with consequent repercussions on Clinical manifestations in the pathogenesis. Cutibacterium quality of life. acnes (C. acnes), which predominates About 70% of patients report a Acne is an inflammatory skin disease with in areas rich in sebaceous glands, can premenstrual acne exacerbation. two main characteristics: lesional polymor- act as an opportunistic pathogen in This has been related to: increased phism and chronic course. acne. C. acnes is scantily present on hydration of the pilosebaceous duct, the skin surface, whereas it is the progressive decrease in estrogen levels In addition to seborrhea, open and/ dominant resident in the piloseba- with anti-inflammatory action and or closed comedones and inflamma- ceous unit; and the development of increased progesterone in this phase, tory lesions are observed such as: acne would be related, not with its with androgenic and pro-inflamma- papules, pustules and nodules, as well proliferation, but with the selection tory effects. as residual lesions (scars and pigmen- of certain types, especially the IA1 70% of patients show acne impro- tation alterations). phylotype, in a medium with increa- vement with sun exposure during the Regarding the distribution of the sed sebaceous secretion in addition summer months. This amelioration lesions, almost all the patients (99%) to balance alteration of the skin could be potentially explained by the present facial localization, accompa- microbiome(7,8). Also, the formation “camouflage” effect caused by tanning nied in more than half of the cases, of biofilm, an organized conglo- and an anti-inflammatory action of by involvement of the back (60%) and, merate of bacteria enhancing their the immune suppression induced by to a lesser extent, the pectoral area survival, could increase its pathoge- ultraviolet light(5). This is the theore- (15%). The majority of patients will nicity and resistance to antibiotics. tical foundation of phototherapy for refer to a gradual onset of the lesions These data open up new therapeutic acne. However, ultraviolet radiation around puberty, so that in cases in possibilities in the management of can also increase the comedogenic whom a sudden onset of these is acne (probiotics, anti-biofilm com- effect of sebaceous secretion and described, an underlying cause must pounds...)(9).
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