Rosacea
 Cause unknown
 Aggravated by anything giving vasodilatation eg heat
or caffeine
 Usually over 40yrs females, worse in males/Celts
 Onset gradual with papules and pustules on the
cheeks chin mid forehead and tip of nose
 Erythematous background, often with associated
telangiectasia
Distribution
Papules/pustules/erythema
Nasolabial sparing
Rhinophyma
Can be unilateral
Subtle
telangiectasiae
Opthalmological problems
 Up to 5% rosacea patients
 Blepharoconjunctivitis
 Lid hygeine, oral oxytetracycline for 6 wks if severe
 Dry eyes – ocular lubricants
 Chronic corneal inflammation and neovascularisation
respond to low dose topical steroid (but risk of perforation)
 Corneal perforation – keratoplasty
 Prominent telangiectasiae suggests topical steroid use
 Gross rosacea
 Rosacea may persist and worsen
 Exacerbated by anything causing flushing
 Persistent red face with flushing may prove resistant to
treatment
 Remember carcinoid, facial fluishing but absence of
other stigmata of rosacea.
 Treatment
 Mainstay broad spec antibiotics, mode of action
unknown
 Oxytetracycline 500 mgs bd
 Rule of 1/3rds
 1/3rd better after 8 wks
 1/3rd better after 2nd or 3rd 8 wks of oxytet
 1/3rd need long term due to persistent relapse on
cessation of treatment
 Can use erythromycin or doxycycline
 Antibiotics given for 2 months, should see
improvement by 16 wks
 Topicals
 0.75% metronidazole gel (Rosex) not as effective as
oral antibiotics
 Useful if get a flare of rosacea
 Helpful to women candidiasis on antibiotics
 Azaleic acid gel 15%
 Clindamycin gel
58 trials, 6633 participants
Doxycycline better than placebo
40mgs as effective as 100mgs
Topical metronidazole
Topical alazaic acid
Further well-designed, adequatelypowered randomised controlled trials
are required
Cochrane link
 Treatment failure?
 Most will have erythema/telangiectasiae ‘red face’
 Telangiectasiae can be treated by laser
 Cosmetic camouflage
 Referral for
 classical rosacea not responding to treatment
?roaccutane
 Significant rhinophyma – laser recontouring
 Opthalmological rosacea
Seborrhoeic Eczema
 Overgrowth of P. ovale (malassesia) in hair follicles
giving a secondary eczematous response.
 >30 yrs
 males > females
 Immunocompromised (HIV)
 Gradual onset with erythema then scale usually in
nasolabial folds
 Often have scalp involvement – dandruff
 Pink or red scaly ill defined patches, may become more
acute with exudates.
 Typical distribution
 nasolabial folds,
 eyebrows,
 eyelashes (blepharitis),
 ext auditory meatus
 Scalp
 Chest
Treatment
 Tends to be persistent, fluctuating with weather, stress
 Need to know how to look after the problem
Pityrosporum ovale
Inflammation
antifungals
topical steroids
Treatment
 Treat yeast with imidazole eg ketoconazole
 Nizoral shampoo twice weekly and cream bd
 Maintainance shampoo once every 2 wks and cream in
bursts every 2 weeks
 1% Hydrocortisone cream
 2% salicylic acid, 2% sulphur in aq. Cream
 Lithium (ethalith) may be effective
SLE
 A syndrome
 Idiopathic or drug induced associated with
autoantibodies
 General symptoms
 Fatigue
 Fever
 Weight loss
 Malaise
SLE malar rash
 Diagnosis: SLE requires 4 of 11 criteria
 Malar rash
 Discoid rash
 Photosensitivity
 Oral Ulcers
 Polyarthritis involving more than 2 joints
 Pleuritis or Pericarditis
 Antinuclear antibody titer positive (1:40 or higher)

Titer over 1:320 is very suggestive
 Renal disease
 Neurologic disorder (e.g. Seizures, Psychosis)
 Anaemia, neutropenia or thrombocytopenia
 Anti-dsDNA, Anti-Sm positive, syphilis false positive
CDLE
 Probably autoimmune
affecting skin only not assoc
with circulating antibodies
 Precipitated and aggravated
by sun
 Middle aged and above
 Gradual onset, patients
notice scaly patches on the
face
 Absence of systemic
symptoms
 Prognosis, tends to persist until burnt out
 Treatment
 Potent top steroids – ie dermovate regularly
 High factor sunscreens
 Antimalarials – hydroxychloroquine if extensive or
doesn’t respond
 Retinoids
 Immunosuppressants if severe and extensive
Light induced problems
 Light sensitivity
Juvenile Spring Eruption
PLE
 Sun damaged
Solar elastosis
AKs
 DLE
 SLE
 Melasma
Actinic keratoses
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Malignant potential
0.1 – 10%
> 40yrs up to 40% population
May regress, remain static or undergo malignant
transformation
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Cryotherapy
Diclofenac
5-fluouracil
Imiquimod
PDT
Treatment
 Cryotherapy 5-15 secs freeze time
 3% Diclofenac (Solaraze) gel
BNF: Apply thinly twice daily for 60–90 days; max. 8 g daily
(carry on up the…………)
• Imiquimod (Aldara).
BNF: apply to lesion 3 times a week for 4 weeks; assess
response after a 4 week treatment-free interval; repeat 4week course if lesions persist; max. 2 courses
Local reactions common on this regime – erythema,
burning, ulceration, headache, flu symptoms
 Field change actinic damage
 Imiquimod weekly for 24 wks
 20 patients 28 wk trial once weekly for 24 wks assessed
at 28 wks
 46.7% marked improvement
 6.7% improved on placebo
 5-FU (BNF)
Apply thinly to the affected area once or twice daily; if
possible, cover malignant lesions with occlusive
dressing; max. area of skin treated at one time,
500 cm2 (23x23cm); usual duration of initial therapy, 3–4
weeks
• Local irritation, severe discomfort (top steroid)