acne

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Pilo-sebaceous follicle
Pilo-sebaceous follicle

Definition:

  • Acne is an inflammatory dermatosis of pilo-sebaceous follicles
  • Giving follicular lesions that occur in adolescence and are related to both:

Seborrhea

Anomaly of keratinization of the epithelium of the pilosebaceous follicle canal inducing the formation of comedone

Epidemiology:

  • Frequent condition, affects about 90% of adolescents
  • Affects both girls (14-16 years) and boys (16-17 years)

Pathophysiology:

4 mechanisms:

  • Anomaly in the functioning of the sebaceous gland:

Source and structurit's thef androgens:

In humans: Testosterone is secreted by leydig cells in the testicle and a small part by the adrenal gland

In Women:

50%: by the peripheral conversion of delta 4 androstenedione, this conversion requires the presence of the enzyme: 17-hydroxy-steroid dehydrogenase, it occurs at the level of liver cells and skin cells

Acne a125%: is produced by ovarian stroma

25%: by the fasciculated area of adrenals

Di-Hydro-Testosteroborn (DHT): a biologically active metabolite of testosterone. It is estimated that DHT is about 30 times more potent than testosterone because of its increased affinity for androgen receptors. Stimulates sebum synthesis in the sebaceous gland

  • Acne a2Cutinifortion Disorder:

Comedon formation: becauseatinocyte proliferation, differentiation, adhesion – folmovie obstruction – I knowbaceous retention

  • Proliferation of bacterial flowera:

Bacterial colOnization: Gram bacteria, anaerobic bacteria, follicular inflammation responsibilities (Propionibacterium acnes, P.Granulosum, P.Avidum)

P.Acnes Peptides scattering through the wall – polymorphonuclear chemotactism (IL1, 4, 6, 8 and IFN g) – inflammation

  • Acne a3Genetic field: Molecular biology studies have recently shown that the intracytoplasmic receptor of androgens in the sebaceous gland, on which DHT is fixed, has several functional sites leading to activation and transcription of these genes. The gene of this receptor is carried by the X chromosome in position q1-q12. The expression of this gene would vary depending on the development and age of the subject, and could intervene in the genetic transmission of acne

Clinical:

Withmy Acne (juvenile polymorphic acne): this is the most common form

  • Aspect:

Heper-seborrhea: this is the glossy appearance of the predominant skin on the face (middle-facial region), sometimes the anterior face of the thorax and the vetebro-dorsal gutter

acne a4RIn truthonal injuries:

Open Comewomen (blackheads): 1-3 mm diameter bodily caps, made of sebum and keratin that clogthe the infundibular orifice that will be oxidized by the contact of the air hence the black coloration hence the black coloration

Closed Comewomen (white dots): are whitish papules 2-3 mm in diameter due to the accumulation of sebum and keratin in the closed infundibulum

Inflammatory injuries:

Superficial injuries:

PApuLit is: small red eysys, farms,

sometimes painful

PFREEZE: small red yeasts with a purulent container at their tops, which may appear immediately or be secondary to papules

Deep injuries:

Nodules: painful and palpation-fluctuating inflammatory swellings that can develop into fistulas, inflammatory cysts or abscesses. They leave scars after healing

Scars: may be flat, depressed or keloid (in reliefs), they may be hypo- or hyper-chromic

  • Seat: face (midfacial region), side faces of the neck, neckline, shoulders, back in full or neck

Acne a5Clinical forms:

  • Severthe Acne:

Conglobata: large comedones and multiple and voluminous nodules. The evolution is towards unrepressed, depressed scars and sometimes strains, hence its severity

Acne a6Fulminans: male adolescent, is characterized by an ulcero-necrotic evolution of lesions with fever, alteration of general condition, arthralgias, hyperleucocytosis

  • NeonAtal ACNe: stimulation of the sebaceous glands of the newborn by maternal androgens. Most often, these are closed comedones, the evolution is favorable after 2-3 months
  • Hererogenic Acborn: Some medications may cause acne flare-ups: local or general corticosteroids, antiepileptic, anti-TB, antidepressants, vitamin B12, oral contraceptives containing an androgenic progestin
  • Exogenous acne: mineral oils, cosmetics (presence of comedogenic products), repeated rubbing occlusion (e.g. backpack)
  • ACNe and pregnancy: the evolution is unpredictable, we note the appearance or worsening of acne lesions , inflammatory acnes mainly affecting the face.
  • Women's Acne: In women over the age of 25, we should look for signs of hyperandrogenism (hirsutism, alopecia, weight gain, amenorrhea…). In the absence of signs of hyperandrogenism a hormonal check-up is not indicated.

Predominant lesions in the lower part of the face.

The number is moderate, but deep nodules in small numbers

The mechanism of this acne of the adult woman is still unknown

The role of cosmetics is suspected without being demonstrated

If even minimal clinical signs of hirsutism are associated with tests to clarify etiology (an ovarian ultrasound, a hormonal check-up in the first part of the cycle including: free and bound testosterone dosage, delta-4 androstenedidiodio 17-hydroxy-progesterone for abnormalities in previous dosages)

Acne a7Positive diagnosis:

It is clinical, based on the appearance of the lesions, seat, age of onset

Differential diagnosis:

  • Rosacis: a condition that begins in his forties, it is a disease of the skin microcirculation, evolves in 4 stages:

Freadh: feeling red and warm on the face.

Terastaectasic (onrmanent)

Papplepustleuse phase

Skin infiltration phase (thickened skin): more in men than in women (rhinophyma)

  • Peri-Oral thereMtitis: Only inflammatory lesions are located around the mouth.

In wifen: Withe most often related to cosmetic abuse or repeated use of local corticosteroids.

  • Acne a8Gram-denyingive germ fOlinenculitis: it is a follicular pyodermite, complication of too long-term antibiotic treatment, especially with cyclines
  • Pillar Keratosis:

Due to a thickening of the surface part of the skin,

epidermis, women, appears as early as pre-adolescence

Due to the obstruction of the pores of the skin, it reaches the arms more often, but sometimes also the thighs, buttocks and more rarely the face

Complications:

  • Acne develops through flare-ups, then stabilization and disappearance around the age of 25
  • These flare-ups may be influenced by a number of factors:

Hormonals: there is an improvement in the woman in the middle of the cycle and worsening at the end.

Food: chocolate, candy, which are the most incriminated

Sthrees: promotes acne flare-ups in acne cases

SYou can: the sun aggravates facial damage

Tbothcco

  • Indelible scars: are the main complication of acne. These may include: depressed, hypertrophic scars, bridles, sequelae cysts, keloid scars requiring surgical repair
  • Youal edemaa: this is a rare complication of facial acne, it is a firm, indolent edema, orbital-nasal regions, which can extend to the forehead and cheeks, its mechanism remains unknown
  • Osteos: they correspond to a calcification of acne scarring, they occur on the face and are seen mostly in severe forms of acne.

Treatment: is extirpation with a vaccineostyle or a tip of bistouri

Thirdtment:

  • Treatment targets:

Reduce the number of lesions

Decrease the formation of new lesions

Avoid inflammation

Prevention of after-effects

Decrease sebum production

Decrease follicular hyperkeratosis

Avoid the proliferation of P. acnes

Avoid inflammation

  • Therapeutic means:

Local treatments:

Local Antibiotics: Topical erythromycin

Gpublicc Form: Eryacne® 4% in the form of a gel.

Action: antimicrobial and anti-inflammatory.

Application: The average durationn of treatment should be< 2 month, the topical antibiotic therapy should not be associated with a general antibiotic treatment (promotes resistance). 2 =&quot;" month,=&quot;" antibiotics = & quot;" by = & quot;" path = & quot;" locale=&quot;" ne=&quot;" must = & quot;" = no & quot;" be = & quot;" associated = & quot;" to = & quot;" un=&quot;" Treatment = & quot;" antibiotic = & quot;" General = & quot;" (promotes = & quot;" la=&quot;&quot;></ 2 month, the topical antibiotic therapy should not be associated with a general antibiotic treatment (promotes resistance).>

BenzoYl Peroxide:

Galenic shape: gel, cream with 2.5-10%

Action: anti-inflammatory and slightly keratolytic: Soluger, Ec / aran®, Cutecnyt®

Shere effects:

Irritatieffectss: At the beginning of treatment, this involves the use of low doses or the spacing of applications

Phototoxicity: this justifies an application in the evening, away from the light

Contact e, What: sometimes this means permanently outlawing the treatment, then treating eczema to other molecules

Topical Retinoids:

Gpublicc form: come in the form of cream, gel and lotion: Isotrex®, Locacid®, nities A®, Rétisol A® (0.025-0.05-0.1%).

Action: they have a predominant keratolytic effect, they are sometimes associated with topical erythromycin (Stievamycin®)

Shere effects:

andritation: at the beginning of treatment

Phototoxicicompanies or photosensitivity: apply in the evening and use sunscreen during periods of high sun

Drying effect: use emollients

Systemic treatments:

Antibiotics:

These are the cyclines:

1st generation: Tetracyclines 500 mg

2nd generationn: Doxycycline: Vibramycin®, Dotur

Action: antibacterial and anti-inflammatory

Galenic Shape: 100 mg tablets

Posology: prescribed at a rate of 100 mg/d for 15 days and then increased to 50 mg/d, the minimum duration of treatment is 3 months.

Sgo effects: photsensitivity, digestive disorders

Contraindications: Pregnant fern, child< 8 ans 8=&quot;&quot;></ 8 years>

Isotr-tinoin: Roaccutene®, Cureacn®

Action: the only curative treatment of acne, works by causing atrophy of the sebaceous glands, by reducing sebaceous secretion, keratolytic effect, anti-inflammatory action

Galenic Shape: capsules with 5-10-20 mg

Posology: 0.5-1 mg/kg/d until reaching a total cumulative dose of 120-150 mg/kg (duration: 6-8 months)

Shere effects:

Chedita: dryness of the mucous membranes, sign of impregnation

Skin xeroded

Teratogivenic effect: which explains contraception 1 month before, during the duration of treatment and 2-3 months after stopping

Absolute Contraindication: pregnancy.

Hormone therapy: it is the use of cyprotéroone acetate that has an anti-androgenic effect (DIANE®35)

Action: Blocks peripheral DHT receptors in sebaceous glands

Hormone therapy may be associated with local treatment

Additional treatments:

Morning aEvening toilet with to itsperfat sOUp or cleansing gel: Dermagor® – cleaning gel, Hyseac® – cleaning gel, Saforelle® dermatological bath

proscribebing the soap and make-up (or removing your make-up)

DermatolOgical Cleansing Of the Skin: Involves extracting closed and open comedones

Scar Treatment: which can be:

Surgical: bridles, keloid and depressed lesions.

Chemical peeling: application on the skin of fruit acids that cause stripping of the surface layer of the skin, acts on fine lines and pigmentations (is done in several sessions with good photoprotection)

Correct PhotOprotection: During periods of strong sunshine

Use of emollient/hydrating creams

  • Indications:

Mfire to againsteoutte acne: local treatment is enough

▪ If predominance of inflammatory lesions: local antibiotics, benzoyl peroxide

▪ If Predominance of Retentional Lesions: Topical Retinoids

More severe or extensive acne: general antibiotic therapy, combined with topical retinoid or benzoyl peroxide

NodulO-cystic acne or ftolure Of a wit-leadscted gebornoutl or local treatment: Isotretinoin®

Morayou Acne with Contrathisption Request: Diane® 35 associated with local treatment (benzoyl peroxide, local antibiotic, Retinoid)Acne a9