Rosacea

Seborrhoeic dermatitis,
Acne, Rosacea
Éva Remenyik
Sebaceous gland follicles
• Arnosan’s triangle, i.e. central parts of
chest and back, face – predilect. sites of
acne
• to a lesser extent: arms, neck, abdomen
• Genitoanal region
Sebum / product of sebaceous
glands/:
Pale yellow, fluid, viscous mixture of
glycerides + fatty acids / 65%
squalene / 10 %
waxesters / 25 %
glycerides
free fatty acids (bact.lipases)
production: high – after birth and for 3-5 months thereafter
low-childhood
pronounced – before and during puberty
less than normal = asteatosis / atopy, ichthyosis/
more than normal = seborrhea / acne, etc./
Seborrheic dermatitis
• papulosquamous disorder
• sebum-rich areas
• Pityrosporum ovale, l
– lipase activity—releasing inflammatory free
fatty acids (FFA)—
– activate the alternative complement pathway
• immunologic abnormalities, and activation
of complement.
Seborrheic dermatitis
• aggravated
–
–
–
–
changes in humidity,
trauma (eg, scratching),
seasonal changes,
emotional stress.
• severity
– varies from mild dandruff to exfoliative erythroderma.
– may worsen in Parkinson disease and in AIDS.
Seborrheic dermatitis
• Onset: puberty
• Peak 40 years
• In infants: cradle cap,
flexural eruption or
erythroderma
Course
• Intermittent, active phases: burning,
scaling, and itching, alternating with
inactive periods.
• Increased activity is seen in winter and
early spring, with remissions commonly
occurring in summer
Medication may flare or induce
seborrheic dermatitis
• auranofin, aurothioglucose, buspirone,
chlorpromazine, cimetidine, ethionamide,
gold, griseofulvin, haloperidol, interferon
alpha, lithium, methoxsalen, methyldopa,
phenothiazines, psoralens, stanozolol,
thiothixene, and trioxsalen
Differencial diagnosis
• Asteatotic Eczema
Atopic Dermatitis
Candidiasis, Cutaneous
Contact Dermatitis, Allergic
Contact Dermatitis, Irritant
Dermatologic
Manifestations of
Gastrointestinal Disease
Dermatomyositis
Drug Eruptions
Drug-Induced
Photosensitivity
Erythrasma
Extramammary Paget
Disease
Glucagonoma Syndrome
• Impetigo
Lichen Simplex Chronicus
Lupus Erythematosus,
Acute
Nummular Dermatitis
Pemphigus Erythematosus
Pemphigus Foliaceus
Perioral Dermatitis
Pityriasis Rosea
Rosacea
Tinea Capitis
Tinea Corporis
Tinea Cruris
Tinea Versicolor
Treatment
•
•
•
•
•
Topical corticosteroids ( creams, lotions, or solutions)
ketoconazole or naftifine creams.
sulfur or sulfonamide
Systemic ketoconazole (severe or unresponsive)
Topical calcineurin antagositák
• Dandruff
– Salicylic acid, tar, selenium, sulfur, and zinc in shampoos
– oil is especially helpful when widespread scalp plaques are
present.
Acne vulgaris
• Lesions:
comedones,
papules, pustules,
and nodules in a
sebaceous
distribution.
• Localisation:
face chest, back,
and the upper arms
Acne vulgaris
• Frequency: 85-100%
• Consequence:
– can cause physical pain and psychosocial
suffering
– scarring
– Acne fulminans, can be associated with fever,
arthritis, and other systemic symptoms.
Comedo -- Lesions may be "open" or "closed,"
depending on the presence of a visible black tip resulting
from defective keratinization.
Papule/pustule -- Inflammatory lesions that if large or
persistent may lead to permanent scarring.
Nodule -- A deep inflammation, >5 mm in size,
guaranteed to produce a scar. Lesions are erroneously
termed "cysts." In reality, they are abscesses with no
cyst wall present.
Conglobate lesions -- Grouped nodules connected by
sinus tracts present in the severest forms of acne.
Pathomechanism of acne
• Sebum production, sebocyte 5 alpha reductase (testosterondihydrotestosterone)
– Androgens ↑ estrogen↓
• Hyperkeratinization (follicular)
– Androgens (DHEAS)
– IL1alpha
• Propionibacterium acnes
– Proinlammatory cytokines (IL-12, IL-8, TNFa)
• Inflammation
– Primary or secondary
Patomechanizmus
Genetikai faktorok
Környezeti tényezők
androgének
Faggyútermelés
lipidek
Folliculáris keratinizáció
citokinek
Propionibacterium acnes
Gyulladás
IgG, lipáz, ROS,
kemotaktikus faktorok
Citokinek,TLR
Clinical findings
• primary noninflammatory lesions
closed (whitehead)
and open (blackhead)
comedones
• secondary inflammatory
lesions
papules pustules
 nodules  abscesses
• postinflammatory
lesions
cysts – scars
(atrophic, keloidal)
Causes:
• cosmetic agents, hair pomades
• medications:
– steroids, lithium, some antiepileptics, and
iodides.
• endocrine disorders with excess
androgens
– Congenital adrenal hyperplasia, polycystic
ovary syndrome,
• genetic factors
Clinical Variants of acne
Clinical Findings
Comments
Diagnosis
to Consider
Erythematous papules and pustules
on face of neonate without
comedones
Neonatal
acne
May be due to Pityrosporum
folliculitis, resolves in days to
weeks
Inflamed papules and pustules
starting 3-6 mo after birth
Infantile
acne
Attributed to early gonadal and
adrenal secretion of androgens,
especially in boys; may last to
age 5; may herald later severe
acne
Persistent mild acne associated with
use of greasy, occlusive cosmetics,
sunscreens, or moisturizers
Acne
cosmetica
More common in women
Acne associated with use of helmets,
shoulder pads, bras, chin rests (e.g.,
violins)
Acne
mechanica
Suggested by the history and
unusual location of skin lesions
Typical acne lesions near the
hairline; history of applying thick
oil to the hair
Pomade
acne
Most common in black women and
men
Acne associated with ulcers and
erosions that heal with scarring;
history of picking at the skin
Acne
excoriee
Typically a young woman
Large confluent draining nodules
and abscesses; severe scarring
Acne
conglobata
A severe scarring form that
requires aggressive management
An explosive onset of severe
widespread nodular lesions with
systemic symptoms (e.g., fever,
arthralgia, myalgia)
Acne
fulminans
Nodular lesions that contain large
quantities of necrotic material may
drain, leaving large eroded areas
over the face and back; exclusively
in males
An explosive onset of severe
facial nodules and edematous
plaques
Pyoderma
faciale
Severe nodular acne occurring
exclusively in females, also known
as rosacea fulminans
Acne associated with drug use
Druginduced
acne
Androgens, corticosteroids, and
halogenated medications (e.g.,
iodides, bromides, lithium, and
anticonvulsants)
intertiginous areas inversa / =
of males
a. triad = a.
tetrad/
laboratory findings:
elevated ESR,
leukocytosis
Differential diagnosis
Clinical Findings
Comments
Diagnosis
to Consider
Perifollicular pustules, which may
involve unusual sites for acne
(e.g., extremities)
Folliculitis
Usually bacterial; diagnosed by
Gram stain and culture of
pustules; if Malassezia folliculitis,
Gram stain reveals Gram-positive
budding yeast
Patient on long-term antibiotics
develops pustules and nodules at
the anterior nares, followed by
outward spread on face
Gramnegative
folliculitis
Emergence of antibiotic-resistant
bacterial strain; requires switching
antibiotics
Onset at age >30; history of
flushing; erythematous papules,
pustules, and telangiectases
Rosacea
Close exam reveals lack of
comedones, the hallmark lesions
of acne vulgaris
Flat, skin-colored, elevated facial
papules
Verrucae
plana
Lack of pustules and comedones
helps identify warts
Differencial diagnosis
Rosacea
Pityrosporum
folliculitis
Perioralis dermatitis
Folliculitis
Perioralis dermatitis
Rosacea
Fleshy red papules over the central
face
Adenoma
sebaceum
Other skin and central nervous
system findings (e.g., seizures)
of tuberous sclerosis; lack of
comedones and pustules
White pinpoint cysts resembling
closed comedones on the face
Milia
Usually around the eyes; not
associated with other acne
lesions
Erythematous, inflamed papules on
chin and cheeks; history of longterm use of topical fluorinated
corticosteroids on face
Perioral
dermatitis
Periocular lesions may occur
concurrently
Closed comedones and nodules;
history of exposure to halogenated
hydrocarbons
Chloracne
A sensitive indicator of systemic
toxicity
Inflamed nodules in the axilla and
groin with draining sinus tracts
Hidradenitis
suppurativa
Diagnosis suggested by old
scars or sinus tracts and sterile
cultures
Numerous open and closed
comedones around the eyes of an
elderly person
FavreRacouchot
disease
Most common in men who
worked outside for many years;
attributed to cumulative sun
Differencal diagnosis
Cysts (epidermal,
trichilemmal)
Milia
Verruca plana
Hydradenitis suppurativa
Favre-Racouchot
Adenoma sebaceum
Consequence
– physical pain and psychosocial suffering
– Scarring, pigmentation
– Acne fulminans, can be associated with fever,
arthritis, and other systemic symptoms
Treatment
Drug
Dosage
Special considerations
Apply to affected area once
or twice a day, usually after
washing
Few side effects, but resistance to
erythromycin and clindamycin is
becoming a problem
Benzoyl peroxide, erythromycin, and
clindamycin available in less
expensive generic formulations
Benzoyl peroxide bleaches clothing
and bedding
Topical agents
Antibiotics
Erythromycin
Clindamycin
topical solution,
gel, or lotion
Sodium
sulfacetamide
(Klaron) lotion
Benzoyl
peroxide
Topical therapy
Antibiotics
Comedolytic agents
Azelaic acid (Azelex)
cream
Retinoids
Tretinoin (Retin-A,Avita)
cream, gel, microgel, or
solution (0.01%-0.1%)
Apply twice daily
Apply nightly; often
used with benzoyl
peroxide or an
antibiotic
Dryness or irritation common;
patients may worsen initially; not
photosensitizing
Skin irritation and photosensitivity
are main adverse effects;
oxidized if used at the same time
as benzyl peroxide; microgel
(slow-release) formulation less
irritating
Adapalene (Differin) gel or Apply twice daily
cream
Less irritation than with tretinoin
or tazarotene; unlike tretinoin; sun
precautions as with tretinoin
Tazarotene (Tazorac) gel
or cream (0.1%)
Often quite irritating
Apply nightly
Antibacterial agent combinations
Benzoyl peroxide and
erythromycin(Benzamycin)
Apply once
Effects are synergistic; must be
or twice daily refrigerated to retain potency
Benzoyl peroxide and clindamycin
(BenzaClin)
Apply once
Must be refrigerated to retain
or twice daily potency
Benzoyl peroxide with zinc and
glycolic acid (Triaz 6% and 10% gels)
Apply nightly
Oral antibiotics
Minocycline
(Minocin,Dynaci
n)
50, 75, or 100 mg b.i.d.
Highly effective, but expensive; early and
late severe hypersensitivity reactions,
lupus-like syndromes and hepatitis;
reversible pigmentation of the skin;
irreversible tooth staining with long-term
use
Tetracycline
(Sumycin)
250-500 mg b.i.d.
Inexpensive (generic), but compliance a
problem because must be taken on an
empty stomach to be absorbed
Doxycycline
(Monodox)
50-100 mg b.i.d.
Inexpensive (generic), well tolerated, but
is often photosensitizing
Erythromycin
(PCE and
E.E.S.)
250-500 mg b.i.d. (taken
with food to reduce GI
symptoms)
Inexpensive (generic); stomach cramps,
diarrhea common, so compliance often
poor; bacteria may become resistant
Oral hormonal
Contraceptives
Diane-35
Estrogen
Cyproteron acetate
Retinoids
Isotretinoin
0.5 to 2 mg/kg/day for 4-6 mo
(Accutane)
Side effects:
Teratogenic
Mucocutaneous dryness
Hyperlipidaemy
Arthralgy
Liver funciton abnormalities
. cumulative
dose of 120150 mg/kg
Procedural treatments
• manual extraction of comedones and
intralesional steroid injections.
• superficial peels
• Phototherapy
– red light
– blue light
– photodynamic therapy
• laser treatments
Terapeutic steps in acne
Primary lesions
Forms
Mild
comedonica
papulopustulosa
Moderate
papulopustulosa
Sevre
congloblt
Teratment
Comedo
Papula,
pustula
Heg
L
BPO
L
Ret
L
AB
Sz
Antiandrogén
Sz
AB
Sz
Ret
+++
+
-
++++
++++
-
+/-
-
-
++
+
-
++++
++++
++
+/-
+
-
+
++
-
++++
++++
++++
++
++
-
+
+++
+
++++
++++
+/-
++++
++++
++
+
+
++++
++++
+++
++++
++++
-
++++
-
+/-
+/++++
femal
++++
++++
Rosacea
• facial flushing
• spectrum of clinical signs,
–
–
–
–
erythema, (transient, permanent)
telangiectasia,
coarseness of skin,
inflammatory papulopustular eruption resembling
acne – no comedones, blepharitis, conjunctivitis
– rhinopyhyma: sebaceous gland and connective tissue
hyperplasia / bulbous livid-red nose of males/
• central flush/blush areas of the face (ie,
forehead, nose, cheeks, chin),
– ocular disease and extrafacial
• Vascular lability, manifested clinically as
intermittent facial flushing,
Pathogenesis
no definite causative factors
• genetic disposition
• relationship to systemic diseases /
stomach, gut, cholecystopathia,
hypertension, etc./
• triggers:
– Dietary (eg, hot drinks, alcohol, spicy foods)
– environmental triggers (eg, sunlight,
temperature changes)
Pathomechanism
• UV light
• Demodex
• Innate immunity
• Vascular
• ROS
K. Yamasaki, R.L. Gallo / Journal of Dermatological Science 55 (2009) 77–81
differential diagnosis
•
•
•
•
•
•
•
•
acne vulgaris /comedones/
perioral dermatitis /no telangiect./
boils /solitary/
drug eruptions /widespread/
seborrheic dermatitis /pustules cammon/
rosacea like tuberculid /histology/
LE
PLE
Treatment
topical
• metronidazole
• Topical keratolytics (eg, benzoyl peroxide,
azelaic acid)
• shake lotion /sulfur, tetracycline, erythromycin/
• never: steorids!
• sun protection
• diathermy needle /telangiect./
• surgery /rhinopyma/
Treatment
systemic
• Systemic antibiotic
(Erythema responds poorly.)
– tetracycline (250 mg daily to 500 mg)
– metronidazole
– erythromycin 500 mg bid,
– minocycline 50-100 mg,
– doxycycline 50-100 mg daily to bid.
• Retinoid- isotretinoid
• Short course of steroid
Perioral dermatitis
• Gender: women (The vast majority of patients are
aged 20-45 years. )
• Skin lesions:
- grouped follicular reddish papules,
- papulovesicles, and papulopustules on
an erythematous base with a possible
confluent aspect
- mainly in perioral locations
Causes
• Drugs: abuse topical steroid
• Cosmetics: Fluorinated toothpaste; skin care
ointments and creams, especially those with a
petrolatum or paraffin base, and the vehicle
isopropyl myristate.
• Physical factors: UV light, heat, and wind
worsen POD.
• Microbiologic factors: bacteria, Candida
species, Their presence has no clear clinical
relevance.
• Miscellaneous factors: Hormonal factors. Oral
contraceptives. Gastrointestinal disturbances.
Treatment
• Antiacne drugs
• Zero-therapy
– initial worsening of the symptoms may occur
with treatment