Acne vulgaris and Acne related disorders Dr. Mohammed A. Al-Shahwan M.D. College of Medicine King Saud University

Objectives Acquiring knowledge of the etiology and pathogenesis of acne vulgaris. Understanding the disease spectrum of acne vulgaris. Acquiring knowledge of the therapeutic options for acne vulgaris and their indications. To be familiar with the etiology, clinical types and treatment of rosacea.

Acne vulgaris Is a chronic inflammatory disorder of the pilosebaceous apparatus of certain body areas resulting in greasiness and polymorphic skin eruption.

Incidence Acne affects all skin types, the male and female ratio is virtually the same but tends to be more severe in males. 85% affects the age group 12 – 24 years 8% affects the age group 25 – 34 years 3% affects the age group 35 – 44 years

Pathogenesis ( three main steps recognized and hypothesized) 1. Follicular Hyperkeratosis (the cause not fully understood) theory suggest: deficiency in Linoleic acid the effect of Androgen (DHT) the effect of Interleukin-1 The effect of P.acne

Perifollicular Hyperkeratosis histology

2. Abnormal production of sebum which can increase further by the response of sebaceous glands to testosterone & DHT

3. Colonization of the affected unit with bacteria Propionibacterium acne and yeast named Malassezia furfur Malassezia furfur Propionibacterium acne

Propionobacterium acne lipases act on sebaceous fatty acid (Triglycrides) to release irritant free fatty acid and low-molecular- weight peptide an extra cellular factor that penetrate the follicular wall and stimulate Polymorphs and Lymphocytes initiating inflammation

Hydrolytic enzymes released from the activated complement antibodies complex together with exoenzymes produced from P acne cause rupture of follicular wall

Once the wall is damaged , Various agents (prostaglandin-like substance, amino acid, short chain fatty acids) that are produced by the inflammatory cells and P acne extrude to the dermis causing more inflammation

Clinical features polymorphic skin eruption composed of : Papules Comedones (Open “Blackheads” or closed “Whiteheads”) Inflammatory papules Pustule Nodule Cyst

Open Comedones (Blackheads)

Closed Comedones (Whitehead)

Inflammatory papules Inflammatory papules

Pustules Pustules

Nodules Nodule

Cysts

Neonatal Acne and Infantile Acne Neonatal acne: the cause is unknown but some believed is due to passing of Transplacental androgen while others suggest the role of Malassezia furfur . It present mainly with inflammatory papules on nose and cheeks affecting new borns between the 1st and 6th week of age

Infantile Acne: affect males more than females, usually between 3 and 6 months of age, and tend to be severer than the neonatal one and believed to be due to Endogenous androgen from the infants gonads.

Acne Fulminans Affect youngsters 13 – 17 years of age, very severe with ulceration and pus discharge, associated symptoms include (fever, malaise, myalgia, arthritis and bone pain) laboratory investigations shows elevation of ESR & WBC Can be induced by starting the patient on high dose of isotretinion (Roaccutane).

Acne Conglobata Very severe Nodulocystic form with abscess formation, affecting Torso more than the face. It usually affect males more that females.

Chloracne (Halogenated Hydrocarbons or Chlorinated Phenols (Dioxin) Other forms of acne Acne excoriee Acne Aestivalis Acneform eruption e.g. Chloracne (Halogenated Hydrocarbons or Chlorinated Phenols (Dioxin) Pomade acne ( Oil Folliculitis ) Steroid acne

TREATMENT

Topical Keratolytic ( anti-inflammatory & comedolytic) Retinoid ( Retinoic acid 0.025, 0.05, 0.1% & Adapalene 0.1%) Salicylic acid 2% (beta-hydroxy acid) Azelaic Acid 20 %

Topical antibiotic ( anti-inflammatory & anti-microbial) clindamycin Erythromycin Benzoyl peroxide Sodium Fusidic acid

Systemic therapy Systemic Antibiotic : Tetracycline Doxycycline Minocycline Azithromycine

Systemic Retinoids : Isotretinoin caps (Roaccutane): 0.5 – 1 mg/kg Indicated for severe forms (nodulocystic , fulminant and conglobate) but also for milder forms associated with scarring or with significant psychological impact. Relapse is minimal with cumulative dose of 120 – 150 mg/kg. Side effects include: cheilitis, dryness, alopecia , photosensitivity, xerophthalmia, decreased night vision, keratitis, benign intracranial hypertension (incresed risk with concomitant use of tetracyclines), photosensitivity, hypertriglyceridemia, hypercholesterolemia, elevated liver enzymes, depression (controversial), skeletal hyperostosis, myalgias. Teratogenicity (category X) so, Pregnancy must be prevented during treatment and for at least 1 month after discontinuing the drug.

Other forms of therapy Oral steroid for acne fulminans and Intralesional steriods for cystic acne. Photodynamic therapy and Laser therapy (pulse dye laser) Hormonal therapy (Anti-androgen) e.g. OCP , flutamide and Spironolactone in treatment of acne associated with hyperandrogenism e.g. PCOS (Polycystic Ovary Syndrome).

Rosacea A controversial topic in dermatology largely because of its uncertain pathophysiology and clinical variation. Primary features of rosacea is flushing, papules, pustules and telangiectasia that affect the central face sp. Convex areas like nose , cheek ,chin and forehead

Epidemiology Common in Caucasian population women>men Onset typically begins after age 30

Etiology and pathogenesis 1.Vascular reactivity: Which usually induced by chronic repeated exposure to certain triggers e.g.: Hot or cold temperature Sunlight Hot drinks, Spicy foods and Alcohol Emotional distress Certain medications and cosmetics e.g. calcium channel blockers, nicotinic acid, morphine, amyl and butyl nitrite, cholinergic drugs, bromocriptine, tamoxifen, cyproterone acetate, systemic steroids and cyclosporine.

Etiology and pathogenesis 2. Dermal matrix degeneration and endothelial damage: due to Inherent problems with vessels permeability and Delayed clearance of inflammatory mediators and waste products Photodamaged connective tissue (solar elastosis is a common background on which rosacea histologic features are superimposed

Etiology and pathogenesis 3. Microbe – induced folliclular inflammation: Commensal organisms e.g. Demodex folliculorum (mite) or bacillus oleronius (bacteria) which reside in hair follicles and sebaceous glands may trigger folliculocentric inflammatory process .

Sub-type classification Sub types were defined by the National Rosacea Society (NRS) expert committee in 2002. 1) Erythematotelangiectatic : persistent erythema and telangiectasias on the central face. 2) Papulopustular: papules and pustules predominate on convex areas on a background of persistent erythema 3) Phymatous: prominent follicular orifices, thickened skin and nodularity which is due to sebaceous gland hyperplasia Most often affect the nose (rhinophyma) Almost exclusively affecting men 4) Ocular: Blepharitis is the most common feature It can present also by Conjuctivitis, iritis, scleritis, keratitis

Erythematotelangiectatic Rosacea

Papulopustular Rosacea

Rhinophyma

Rosacea variants Granulomatous rosacea: Rosacea variant characterised by monomorphic yellow- brown or red-brown papules/ nodules located on the face Histology shows granuloma

Treatment Sunscreens Avoidance of aggravating factors. Topical therapy include: Metronidazole Azelaic acid Benzoyl peroxide Tretinoin Erythromycin and Clindamycin Oral therapy include: Oral Tetracyclines e.g. Doxycycline and minocycline Oral Isotretinoin

Laser and light therapy Laser and Intense Pulsed light IPL is useful in treating persistent erythema and telangiectasias. Superficial small telangiectasias require short wavelengths: Pulsed dye laser (585 or 595 nm) KTP laser (532nm) Deep facial vessels require longer wavelengths : Diode laser (810) Alexandrite laser (755nm) ND:YAG (1064nm)

Treatment of Phymatous Rosacea Early Phymatous changes could be treated with Isotretinoin. Advanced changes is treated with surgery Scalpel tangential excision Electrosurgery CO2 laser ablation.