ACNE VULGARIS A ROSACEA ACNE VULGARIS • chronic inflammatory disease of the pilosebaceous unit, usually begins in puberty and often lasts for several years, sometimes decades, mainly affects young people in puberty • several factors contribute to its formation - increased sebum production, hormonal influences, bacteria, genetics, lifestyle… • affects mainly areas rich in sebaceous glands, which is the face, upper back and upper torso ACNE – ETIOPATHOGENESIS • the etiopathogenetic basis is chronic inflammatory process of the pilosebaceous unit • excessive sebum production, retention of keratin in the follicles and colonization by the anaerobic microbe Cutibacterium acnes (new name, originally Propionibacterium) with the subsequent formation of inflammatory mediators in the follicle and surrounding tissue • hormonal effect - increased sebum production associated with higher levels of androgens stimulating the androgen receptors of the sebaceous glands • it is caused by clogging of the follicle opening, there are non-inflammatory (microcomedones, closed comedones, open comedones) and inflammatory lesions (papules, pustules, nodules, cysts) • hypekeratization causes the formation of closed comedo, which is clinically represented by a small white papule (up to 1 mm) • continued retention of keratin dilates the opening of the hair follicle and the closed comedo becomes an open comedo with a black dot in the centre caused by melanin • sebum accumulates in the follicle and bacterial saprophytic flora, especially Cutibacterium acnes and Staphylococcus epidermidis lead to overproduction of unsaturated fatty acids, which have comedogenic and chemotactic effects • the growing comedo increases pressure in the closed follicle, breaks its wall, attracts polymorphonuclear cells, causes inflammation and the formation of inflammatory papules, papulopustules, nodules, abscesses and fistula with scarring ACNE - CLINICAL REPRESENTATION 1. ACNE COMEDONICA • represents the mildest form of acne with predominantly open and closed comedones, only with isolated papulopustules 2. ACNE PAPULOPUSTULOSA • predominantly red papules, pustules and papulopustules, sometimes leaving small scars 3. ACNE NODULOCYSTICA • formation of painful bumps with fistulas and purulent secretion • there is prominent, sometimes keloid scarring (acne keloidea) and the formation of epidermoid cysts from repeated damage to the follicular epithelium, mostly with a prominent central pore, which rupture easily and cause inflammation • the chest and upper back are often also affected along with the face 4. ACNE CONGLOBATA • severe form of acne, which is found more often in men, is caused by merging of inflammatory bumps and abscesses - formation of fistulas and extensive atrophic and hypertrophic scars • mainly on the chest, back, shoulders, sometimes on the arms and buttocks, the face is less affected 4. ACNE CONGLOBATA • may also occur along with hidradenitis suppurativa, abscesses of the scalp and neck with scarring alopecia (perifolliculitis capitis abscedens et suffodiens, folliculitis dissecans) and inflammation of the pilonidal sinus - ACNE TETRADA • ACNE INVERSA also falls under this category - it affects intertriginous areas 5. ACNE FULMINANS • severe accute febrile ulcerative form of acne nodulocystica with fever, leukocytosis, swelling and joint pain, sometimes sterile osteomyelitis (most often sternoclavicular joint) • requires hospitalization, administration of total corticoids, antibiotics, followed by oral isotretinoin SPECIAL TYPES OF ACNE • acne mechanica: created by friction - headbands, hats, facemasks • acne medicamentosa: most often from corticosteroids acne steroidea, from halogenated hydrocarbons bromine acne, chloracne, vitamin B12, isoniazid; PUVA ap. • acne excoriata: in young women with excoriations from constant squeezing, psychotherapy is often required SPECIAL TYPES OF ACNE • acne cosmetica: caused by comedogenic ingredients in cosmetics • acne venenata: contact acne (from contact with mineral oils - acne oleosa, acne picea due to pix lithanthracis application • acne neonatorum: caused by androgens transmitted from the mother • acne aestivalis (so-called Mallorca-acne): caused by follicular hyperkeratosis induced by the sun LOCAL TREATMENT We use drugs with comedolytic, anti-inflammatory, antibacterial and antiseborrheic effects: • local retinoids - tretinoin (magistraliter), adapalen (Differine cream) • azelaic acid (Skinoren cream) • benzoyl peroxide (Akneroxid gel) • topical antibiotics - erythromycin (Zineryt solution), clindamycin (Dalacin T solution) • various combinations - adapalene + benzoyl peroxide (Epiduo gel), clindamycin + benzoyl peroxide (Duac gel), clindamycin + isotretinoin (Acnatac) .... • NEW DRUG clascoterone (Breezula) - the first topical antiandrogen to treat acne (so far only in the USA) SYSTEMIC TREATMENT • antibiotics (tetracycline, doxycycline): long-term use (months) in a dose sometimes lower than recommended for infections • hormonal contraception: in women, especially when there is worsening of acne symptoms during the menstrual cycle, antiseborrheic effect, most commonly used in combination , e.g. ethinyl estradiol and cyproterone acetate (Diane 35) • spironolactone: diuretic, acts as an antiandrogen, blocks androgen receptors and inhibits 5-alpha reductase, reduces sebum production and thus improves acne, the use in this indication is OFF-LABEL • retinoids - isotretinoin (13-cis-retinoic acid) • for more severe or unresponsive forms • most often at a dose of 0.5-1 mg / kg / day for several months to a year, depending on the tolerance of the daily dose, the total cumulative dose should be 120 mg/kg body weight • the effect of the treatment is usually long-lasting • causes a decrease in sebum production, sebaceous glands get smaller, increases the differentiation of keratinocytes with a consequent reduction in follicular hyperkeratosis and has a weak anti-inflammatory effect • TERATOGENIC - hormonal contraception has to be given one month before the start and three months after the end of treatment to women with childbearing potential • side effects - cheilitis sicca (peeling and cracking of the lips), dryness of the skin and mucous membranes, increased levels of lipids (especially triacylglycerol), sometimes elevation of liver tests, rarely musculoskeletal problems • corticoids in acne fulminans due to the acute inflammatory response at the beginning, after the acute phase is over isotretinoin therapy is used ADDITIONAL TREATMENT • surgical treatment - excision, incision • intralesional application of corticoids - to epidermoid cysts • dermabrasion, C02 laser, chemical peeling - scar treatment • dermatocosmetics, skin cleansing, hydration, maintaining a healthy epidermal barrier • stress elimination, psychotherapy • adjustment of diet and lifestyle • still requires a lot of research, but it should no longer be believed that the link between diet and acne is a myth • zinc, vitamin A, probiotics, omega-3-MK can have a positive effect... • industrially processed foods with a high GI, dairy products... can have a negative effect • patients should keep a food diary to find out which dietary factors cause acne flare-ups ROSACEA ROSACEA • chronic inflammatory disease of the follicles with localization on the face (centrofacially) • characterized by initial erythema with telangiectasia, progressing to papulopustules and later to hyperplasia of fibrous tissue and sebaceous glands of the nose (rhinophyma) • affects people between the ages of 30 and 60, the highest frequency is after the age of 50, more in women, the population is affected by 5–22% ROSACEA – ETIOPATHOGENESIS • multifactorial - external and internal factors • genetic predisposition - especially a disorder of innate immunity, congenital vasomotor lability of the face - vascular hyperreactivity • role of Demodex folliculorum • gastrointestinal diseases - Helicobacter pylori • the disease is exacerbated by a number of external factors, especially those causing facial redness (hot drinks, spirits, temperature changes), niacin, local corticoids and especially ultraviolet radiation! ROSACEA – CLINICAL PRESENTATION • typically affects the nose, cheeks, center of the forehead and chin, exceptionally occurs on the neck, retroauricularly, in the neckline • usually omits periorbital and periorbital skin • initially inconspicuous manifestations - transient erythema of the center of the face after provocation by emotions, hot drinks, the sun, etc. • persistent erythema develops gradually with telangiectasia (stage 1) • later red papules and papulopustules form (2nd stage)), unlike in acne, comedones are missing • in addition, inflammatory nodules and infiltrates may form accompanied by hyperplasia of the sebaceous glands and fibrosis leading to thickening and thickening of the skin - phyma (stage 3) 1. SUBTYPE – ROSACEA TELEANGIECTATICA • first, early stage, synonyms: erythrosis, rubeosis, couperosis • vascular form - erythematoteleangiectatic rosacea • transient erythema (flushing) • later permanent centrofacial redness accompanied by telangiectasias, centrofacial edema, burning and stinging 2. SUBTYPE – ROSACEA PAPULOPUSTULOSA • second stage • inflammatory form - papulopustular rosacea • papules to papulopustules on permanently reddened skin • papules and pustules in the central part of the face, both periorbital, perinasally and periorally 3. SUBTYPE – ROSACEA HYPERPLASTICA • third stage • severe, hyperplastic form - phymatous rosacea • formation of large, inflammatory lesions, bumps, abscesses and oedematous skin with large pores • enlargement of the fibrous tissue and the sebaceous glands • the result is seborrhea, thickening of the skin to a cauliflower-like swelling: • Rhinophyma - on the nose • Gnatophyma - on the chin • Metophyma - on the forehead • Otophyma - on the earlobes • Blepharophyma - on the eyelids 4. SUBTYPE - OCULAR ROSACEA • up to 60% of patients with rosacea have ocular complications - most often manifested by red conjunctiva • in about 20% of cases it precedes skin symptomatology • clinically there is conjunctival hyperemia, telangiectasia, eyelid edema, periorbital edema, blepharitis, blepharoconjunctivitis, keratitis, chalazion, hordeolum • sight disturbances may occur due to corneal complications such as keratitis punctata, marginal keratitis and ulcus cornee SPECIAL TYPES • rosacea fulminans (facial pyoderma) • rosacea conglobata - picture 1 • steroid rosacea - papular rosacea: picture 2, often formed after steroids, typical small red papules to nodules • gram-negative rosacea • halogen rosacea • persistent edematous rosacea • lymphedematous rosacea (persistent solid facial edema - morbus Morbihan) ROSACEA – LOCAL TREATMENT • metronidazole (Rosalox cream, Rozex gel, magistraliter preparations), ivermectin (Soolantra cream), preparations with sulfur - anti-inflammatory effect, reduce Demodex folliculorum • erythromycin, TTC paste - anti-inflammatory effect • topical retinoids - for papulopustular forms, use according to tolerance, risk of greater redness • azelaic acid - anti-inflammatory effect, antioxidant effect • brimonidine (alpha receptor agonist, Mirvaso gel) - reduces redness, the effect after application is temporary ROSACEA – SYSTEMIC TREATMENT • antibiotics - TTC, azithromycin, metronidazole - for several weeks in a dose similar to acne • isotretinoin - in severe cases or resistance to treatment, at a dose of 0.2-1 mg /kg/day given for 3-4 months • eradication of Helicobacter pylori (with current gastrointestinal problems) and demodicosis Corticosteroids are contraindicated! / except for Rosacea fulminans / ROSACEA – ADDITIONAL TREATMENT • laser therapy (pulsed dye laser, intense pulsed light) in telengictasia • dermabrasion, CO2 laser in rhinophyma • photoprotection and elimination of aggravating factors! THANK YOU FOR YOUR ATTENTION :)