1. Rosacea

2. Maryam Ghasemi Daneshjooye Pezeshki Daneshgah Esfahan 901111521 DR Fatemi

3. epidemiology relatively common disease fair-skinned people
rarer in dark-skinned people
women are more often affected than men in earlier stages
Men more rhynophima
importance of sun-damaged skin

4. pathogenesis precise etiology of rosacea remains a mystery
hypothesis :degenerative changes of the perivascular, and possibly vascular, collagen and elastic tissues in inherently susceptible individuals exposed to climatic factors.
lead to small vessel dilatation resulting in flushing, telangiectases, and erythema.
the dilated vessels become incompetent with perivascular leakage of potentially inflammatory substances.

5. CLINICAL FINDINGS centrofacial disease
principally localized on the nose, cheeks, chin, forehead, and glabella
rosacea is classified into stages :
1- Episodic Erythema
2-Stage I
3-Stage II
4-Stage III

6. Episodic erythema
predisposed to flushing and blushing, evoked by numerous nonspecific stimuli such as ultraviolet radiation, heat, cold, chemical irritation, strong emotions, alcoholic beverages, hot drinks, and spices.
Eventually flushing and blushing lead to permanent erythema

7. Stage 1 erythema persists for hours and days
Telangiectases become progressively more prominent
complain of sensitive skin that stings and burns after application of a variety of cosmetics, fragrances, and certain sunscreen

9. Stage 2
inflammatory papules less than 0.5 to 1.0 mm in size, with or without pustules
persist for weeks
Some papules show a small pustule at the apex, justifying the term papulopustular.
lesions are always follicular in origin vellus and sebaceous follicles are involved
deeper inflammatory lesions may heal with scarring, but scars are small and tend to be shallow
pores become more prominent
papulopustular attacks become increasingly frequent

11. Stage 3 A small proportion of the patients
particularly on the cheeks and nose, less often on the chin, forehead, or ears
large inflammatory nodules, furunculoid infiltrations, and tissue hyperplasia.
Finally, the patient shows inflamed and thickened edematous skin with large pores, resembling the surface of an orange ( peau d'orange).
features are caused by inflammatory infiltration, connective tissue hypertrophy with masses of collagen deposition, diffuse sebaceous gland hyperplasia, and overgrowth of individual sebaceous glands
Ultimate deformity is rhinophyma

14. treatment
Treatment schedules are determined by the stage and severity of the disease
1. Control of inflammation:
Topical products:
1. Metronidazole
2. Sodium sulfacetamide-sulfur
3. Azelaic acid
4. Benzoyl peroxide
5. Erythromycin/ clindamycin
6. Tacrolimus
7. Tretinoin
Oral medications:
1. Tetracyclines
2. Macrolides
3. Metronidazole
4. Isotretinoin

15. treatment 2. Repair of structural damage: 1-Laser
2-Intense pulsed light
3-surgical techniques (rhinophyma)
3. Prevention of further damage:
1- Sunscreens
2- Cosmetics
3-Avoidanceof triggerfactors(flushing)

16. treatment Box 13-6 Treatment of rosacea by subset 1. All subsets:
Daily sunscreen
Sun avoidance strategies
Cosmetic coverage
Avoidance of specific factors that trigger flushing
Laser and intense pulsed light
2. Erythrotelangiectatic subset:
Morning:sodium sulfacetamide-sulfur cleanser
followed by a moisturizing sunscreen and/or
camouflaging cosmetic with sunscreen
Night: leave on metronidazole, azelaic acid or sodium
sulfacetamide-sulfur product

17. treatment 3. Papulopustular subset:
Morning:Topical metronidazole, azelaic acid, sodium
sulfacetamide-sulfur or benzoyl peroxide-antibiotic
combination + suncreens
Nightly:sodium sulfacetamide-sulfur cleanser +
different one of the above topical products forAM
usage
Oral antibiotics or isotretinoin depending on severity
4. Glandular subset:
1-Benzoyl peroxide-antibiotic combination most
effective, other topicals less so
2-Oral antibiotics or isotretinoin depending on severity
3-Surgical intervention as needed for phymatous
changes