Rosacea - Dermatologyrounds.ca

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2 0 0 6 Volume 5, Issue 4
DERMATOLOGY
TM
AS PRESENTED IN THE ROUNDS OF
THE DIVISION OF DERMATOLOGY,
Rosacea
By IRINA TURCHIN, MD, and DENIS SASSEVILLE, MD, FRCPC
Rosacea is a common, chronic, cutaneous condition primarily affecting the central portion
of the face. This condition has a variety of clinical presentations and has been recently classified
into different subtypes. Therapeutic options largely depend on the subtype of the disease,
as well as its cutaneous morphology. This issue of Dermatology Rounds reviews the etiological
hypotheses, clinical subtypes, and therapeutic modalities of this often distressing condition.
Epidemiology
Rosacea is a common condition, accounting for approximately 1% of all visits to the
dermatologist’s office. 1 The exact incidence of rosacea is unknown; however, its prevalence is
highest among fair-skinned individuals and was 10% in one Swedish study. 2 It is more common
in people of Celtic, northern, and eastern European origin. 3 The majority of affected patients
are between 30 and 60 years of age, although it can occur in younger individuals. 2 Women are
affected more commonly then men; 2 however, the disease in men is known to progress to
advanced stages. An erythematotelangiectatic rosacea is the most common subtype and has
been reported to occur in 81% of patients in one study. 2 Phymatous rosacea is seen almost
exclusively in men aged >40 years of age. 1 Eye involvement occurs in about half of rosaceaaffected
patients, but is often not recognized. 4
Etiology and pathogenesis
Rounds®
The etiology of rosacea remains unknown. Its pathogenesis is thought to involve both
genetic and environmental factors. Crawford et al grouped proposed etiologic mechanisms into
the following categories: vasculature, climatic exposure, matrix degeneration, chemicals and
ingested agents, pilosebaceous unit abnormalities, and microbial organisms. 5
Facial flushing is one of the most prominent manifestations of rosacea; therefore, it is not
surprising that cutaneous vascular abnormalities are thought to be involved in its pathogenesis.
Flushing is controlled by humoral substances and neural stimuli and characterized by increased
blood flow in the superficial dermis. 6 Lesional blood flow in rosacea patients was found to be
increased 3- to 4-fold compared to control subjects. 7 It has been proposed that frequent flushing
may lead to the loss of vascular tone and dilatation of dermal vasculature. 8 In the long term,
these changes result in a deep red erythema and telangiectasia. 1 Berg and Liden found that
rosacea patients are prone to vasodilation since 27% of rosacea patients suffer from migraine
compared to 13% in a control group. 2
Rosacea patients display an abnormal response to thermal stimuli. Wilkin has demonstrated
that the temperature of the coffee and not caffeine triggers flushing. 9 Some studies have
shown that an abnormal cooling mechanism could be the culprit in rosacea flushing. Brinnel
and colleagues demonstrated that venous blood flow is impaired in rosacea, possibly due to
abnormal function of the facial angular veins. 10
Patients with rosacea may be more susceptible to environmental factors and sunlight than
the normal population. Sparing of sun-protected areas, an association with fair skin, and the
presence of solar elastosis are among the clues that implicate ultraviolet (UV) exposure in the
pathogenesis of rosacea. 11 However, an increase in UV sensitivity has not been demonstrated in
rosacea patients; 12 only 17% to 31% of patients report worsening of their symptoms with sun
exposure. 2 The causal role of environmental factors and sunlight in the pathogenesis of rosacea
remains to be elucidated.
MCGILL UNIVERSITY HEALTH CENTRE
Members of the
Division of Dermatology
Denis Sasseville, MD, Director
Editor, Dermatology Rounds
Alfred Balbul, MD
Alain Brassard, MD
Judith Cameron, MD
Wayne D. Carey, MD
Ari Demirjian, MD
Anna Doellinger, MD
Odette Fournier-Blake, MD
Roy R. Forsey, MD
William Gerstein, MD
David Gratton, MD
Miriam Hakim, MD
Manish Khanna, MD
Raynald Molinari, MD
Linda Moreau, MD
Brenda Moroz, MD
Khue Huu Nguyen, MD
Elizabeth A. O’Brien, MD
Wendy R. Sissons, MD
Marie St-Jacques, MD
Beatrice Wang, MD
Ralph D. Wilkinson, MD
Centre universitaire
de santé McGill
McGill University
Health Centre
McGill University Health Centre
Division of Dermatology
Royal Victoria Hospital
687 Pine Avenue West
Room A 4.17
Montreal, Quebec H3A 1A1
Tel.: (514) 934-1934, local 34648
Fax: (514) 843-1570
The editorial content of
Dermatology Rounds is determined
solely by the Division of Dermatology,
McGill University Health Centre.

Recently, there has been a lot of interest in dermal
matrix degeneration in the pathogenesis of rosacea. It is
still uncertain whether endothelial damage precedes
degeneration of the dermal matrix or dermal matrix
degeneration is the primary event. In one animal study,
vascular abnormalities preceded dermal matrix degeneration
after exposure to UV light. 13 Alternatively, other
authors 11,14 support a matrix-centered theory, which
postulates that telangiectasia, flushing, and persistent
erythema are all caused by defective dermal matrix support,
resulting in a pooling of serum, metabolic waste,
and inflammatory mediators. These changes result in
prolonged inflammation and tissue damage.
Certain dietary factors (ie, spicy foods, alcohol, and
hot beverages) are known to trigger rosacea flushing;
however, there is no evidence to implicate these triggers
as the primary pathogenic factors. 5 Corticosteroids,
amiodarone, high doses of vitamins B 6 and B 12 and,
recently, epidermal growth factor receptor inhibitors,
have been reported to induce rosacea or rosacea-like
eruptions. 15-18
There is controversy about follicular involvement in
rosacea. Marks and Harcourt-Webster found pilosebaceous
unit abnormalities in 20% of rosacea papules, and
perifollicular inflammatory infiltrates in 51% of specimens.
11 However, follicular inflammation is characteristic
of the glandular type of phymatous rosacea. 19
The role of Demodex, a hair follicle mite, in the
pathogenesis of rosacea remains a subject of debate.
Although several studies have attempted to elucidate its
pathogenic role, 5,7,20-22 to date, there is not enough evidence
to implicate Demodex as a primary pathogenic
factor. The role of Helicobacter pylori in the pathogenesis
of rosacea has been another controversial subject.
Crawford et al 5 suggest that interest in its potential role
emerged from statistically unsupported associations
between rosacea and gastrointestinal diseases.
Eradication of H. pylori has been associated with an
improvement in rosacea. 23,24 However, a double-blind,
placebo-controlled study by Bamford et al 25 did not
support this association.
Definition and subtypes
The National Rosacea Society Expert Committee
proposed primary and secondary features for the diagnosis
of rosacea (Table 1) 26 . They suggest that the presence
of ≥1 of the following primary features, with a central
facial distribution, is indicative of rosacea: flushing (transient
erythema), nontransient erythema, papules and
pustules, and telangiectases. Crawford et al 5 believe that
persistent erythema on the central face that lasts for at
least 3 months is the most important clinical sign.
Secondary features, ie, burning or stinging, erythematous
dermal plaques, dry appearance, edema, ocular
manifestations, peripheral location, and phymatous
changes, often appear with ≥1 of the primary features,
but can also occur independently. 26 Crawford et al 5 also
point out that for the valid diagnosis of rosacea, several
Table 1: Primary and secondary features in the
diagnosis of rosacea 26
Clinical Diagnosis Clinical
features
characteristics
Primary Presence of ≥1 • Flushing
of the primary
features
(transient erythema)
• Nontransient erythema
• Papules and pustules
• Telangiectasia
Secondary May include • Burning or stinging
≥1 secondary • Plaque
features • Dry appearance
• Edema
• Ocular manifestations
• Peripheral location
• Phymatous changes
diseases must not be present, including polycythemia
rubra vera, connective tissue diseases (lupus erythematosus,
dermatomyositis, and mixed connective tissue
disease), carcinoid syndrome, and mastocytosis. Rosacea
is also excluded in patients with long-term steroid use on
the central facial convexities. 5
The Expert Committee has proposed a provisional
classification system that defines 4 rosacea subtypes and 1
variant, based on the primary disease features (Table 2) 26 .
• Erythematotelangiectatic rosacea (ETR), subtype 1, is
mainly characterized by flushing and persistent central
facial erythema. Telangiectases, central facial edema,
stinging and burning sensations, roughness or scaling
are common, but not essential, for diagnosis.
• Papulopustular rosacea (PPR), subtype 2, is characterized
by persistent erythema with transient papules
and/or pustules in a central facial distribution. 26
Papules and pustules may also occur in a perioral,
perinasal, and periocular distribution. PPR subtype is
often seen in combination with ETR or as a progression
of ETR. It may co-occur with acne or closely
resemble acne. 26
• Phymatous rosacea (PR), subtype 3, is characterized
by skin thickening, irregular surface nodularities, and
enlargement. Rhinophyma is the most common presentation;
however, phymatous changes may also
involve the chin, forehead, cheeks, and ears. Additional
stigmata of PR are patulous follicles in phymatous
distribution and telangiectases. 26
• Ocular rosacea (OR), subtype 4, is most frequently
diagnosed when cutaneous signs of rosacea are also
present. It is characterized by ≥1 of the following:
watery eyes or bloodshot appearance, foreign body
sensation, burning or stinging, dryness, itching, light
sensitivity, blurred vision, telangiectases of the
conjunctiva and lid margin, or lid and periocular
erythema. 26 Meibomian gland dysfunction, as chalazion
or hordeolum, is common. Blepharitis, conjunctivitis,
and irregularity of the eyelid margins may also
occur. 26 Patients with OR commonly present with
cutaneous signs, but OR may precede cutaneous
rosacea by many years. 5

Table 2: Classification of rosacea subtypes and
their clinical characteristics 26
Subtype
Variant
Classification
Granulomatous 26 or glandular 5 rosacea (GR) is a
variant characterized by hard, yellow, brown, or red
papules or nodules. These lesions tend to be less inflammatory
than the lesions in PPR and tend to appear on
relatively normal-appearing skin on the cheeks. In
women, the chin is more commonly affected. 5 This
phenotype is most common in men with thick, sebaceous
skin.
The Expert Committee also suggests that rosacea
fulminans, steroid-induced acneiform eruption, and
perioral dermatitis should not be considered as subtypes
or variants of rosacea, but rather as distinct clinical
entities. 26
Pathology
The pathologic findings of rosacea vary with the
stage of the disease. In the early stages, telangiectasia,
superficial perivascular, and perifollicular lymphocytic
and/or neutrophilic infiltrates are seen. 27 In the later
stages, there are intrafollicular collections of neutrophils
and perifollicular histiocytic and lymphocytic infiltrates.
The infiltrate contains perifollicular and perivascular
noncaseating epithelioid granulomas surrounded by
lymphocytes and plasma cells. 28 Solar elastosis is often
present. Sebaceous hyperplasia, dilated follicular infundibula,
telangiectases, and perifollicular infiltrates of
plasma cells, lymphocytes, and histiocytes are seen in
phymatous rosacea. Granulomas, suppuration, and fibroplasia
are common. 19
Treatment
Erythemato
telangiectatic
Papulopustular
Phymatous
Ocular
Granulomatous
Clinical characteristics
• Flushing
• Persistent central face erythema
• With/out telangiectasia
• Persistent central face erythema
• Transient central face papules
• and/or pustules
• Thickening skin
• Irregular surface nodularities
• and enlargement
• Location: nose, chin, forehead,
• cheeks, or ears
• Eye symptoms : dryness,
• burning, itching, stinging,
• foreign body sensation
• Ocular photosensitivity
• Blurred vision
• Telangiectasia of the sclera or
• other parts of the eye
• Periorbital edema
• Noninflammatory; hard,
• brown, yellow or red papules
• or nodules of uniform size
Despite recent advances in our understanding of the
pathogenesis of rosacea, treatment strategies focus
primarily on suppressing its signs and largely depend on
Table 3: Treatment options according to rosacea
29, 30
clinical subtype
Rosacea subtype
Erythemato
telangiectatic /
Papulopustular
Phymatous
Ocular
Glandular
variant
Treatment
• Lifestyle modifications: trigger
• avoidance, sun protection,
• barrier-protective emollients
• Topical metronidazole
• Topical sodium sulfacetamide
• Topical azelaic acid
• Topical tretinoin
• Oral antibiotics
• Oral isotretinoin (10-20mg qd)
• Laser and light therapy –
• PDL, IPL, KTP
• Oral isotretinoin
• Ablative laser therapy – CO2, Er: YAG
• Surgery – cryosurgery, heated
• scalpel, dermabrasion, tangential
• excision combined with scissor
• sculpturing, radio-frequency
• electrosurgery
• Lid hygiene, warm eye compresses
• Topical metronidazole gel to
• eyelid margins
• Oral antibiotics
• Topical benzoyl peroxide
• Topical antibiotics
• Topical tretinoin
• Oral antibiotics
• Oral isotretinoin
• Spironolactone (25-50 mg daily)
• Oral contraceptives
the subtype of the disease, as well as its cutaneous
morphology (Table 3).
Prior to initiating any therapy, patients with rosacea
should be instructed about triggering factors and avoidance
strategies. Common triggers include hot or cold temperature,
wind, hot drinks, alcohol, exercise, emotion,
topical products, medications that induce flushing, and
menopausal flushing. 29 There are several foods known to
aggravate rosacea including liver, dairy products (yogurt,
sour cream, cheese), vegetables (eggplant, tomatoes,
spinach, peas, lima and navy beans), fruits (avocados,
bananas, red plums, raisins, figs, and citrus fruit), condiments
and flavouring (chocolate and vanilla, soya sauce,
and vinegar), yeast extraction, hot and spicy foods. 30
Patient education should emphasize sun protective
measures, including broad-spectrum, non-irritating sunscreens,
avoidance of midday sun, and the use of protective
clothing. 29
Many rosacea patients have increased sensitivity to
certain components of commonly used topical products.
Common skin irritants in rosacea include solvents
(acetone, alcohol), penetrants (propylene glycol, alphahydroxy
acids), surfactants (sodium lauryl sulfate), biocides
(formaldehyde releasers, sorbic acid), sunscreens
(para-aminobenzoic acid, cinnamates, benzophenones),
and aromatics (menthol, benzyl alcohol, camphor).
Patients should be advised to use gentle cleansers
(Cetaphil ® bar, Dove ® moisturizing bar) and silicone-

containing moisturizers (dimethicone, cyclomethicone)
to prevent irritation. 31 Jappe et al 32 investigated
allergic contact reactions in rosacea patients.
The number of allergic contact reactions did not
appear to be significantly increased in rosacea
patients; however, a few of the observed allergens
were likely related to morbidity-specific exposures
and were potentially relevant. The authors concluded
that diagnostic allergy tests are recommended in
cases of doubt (eg, when there is an apparent deterioration
of rosacea following the use of cosmetics
or topical medications). 32
Camouflage cosmetics are important adjuncts
in rosacea management and should be incorporated
into the initial discussion with the patient. A review
by Gupta et al 30 outlines effective camouflage techniques.
Therapeutic options for rosacea management
include topical therapies, oral therapies, laser
and light treatments, and surgical procedures.
Topical therapies
The 3 main agents for topical rosacea management
are metronidazole, azelaic acid, and sodium
sulfacetamide-sulfur. Topical metronidazole is the
most widely-used topical agent and is available as a
gel, cream, or lotion. 30, 34 A recent systematic review
of rosacea treatments demonstrated its efficacy and
safety. 33 It has been shown to be effective when
applied twice daily for 8 to 12 weeks 30 and demonstrated
to reduce the inflammatory lesion count by
20% to 50% compared to a vehicle. 34 After discontinuation
of therapy, one-quarter of patients relapse
after 1 month, and two-thirds after 6 months; therefore,
maintenance therapy is essential. 34 A recent
study by Tan et al reported that metronidazole 1%
cream with sunscreen SPF-15 significantly decreased
facial telangiectases. 35 One small study reported
a significant improvement in OR when topical
metronidazole gel is applied to the eyelid margins. 36
Azelaic acid 20% cream has been proven effective
in the treatment of rosacea. When used twice
daily, it has been demonstrated to reduce the
inflammatory papule count from 30.8 to 8.3 and
erythema by 50% after 3 months of treatment. 37 A
study by Maddin compared twice-daily azelaic acid
20% cream to twice-daily metronidazole 0.75%
cream for the treatment of inflammatory rosacea
lesions and demonstrated no significant difference
between the 2 agents. 38 Azelaic acid 15% gel, used
twice-daily, has also been shown to be an effective
(51% to 58% reduction in inflammatory lesion
count) and safe topical therapy. 30 Unfortunately, it
is not yet available in Canada.
Sodium sulfacetamide 10% and sulfur 5%
combination therapy has been successfully used for
rosacea management. Sauder et al demonstrated a
42% reduction in the inflammatory lesion count
and a 52% reduction in erythema compared to a
vehicle group. 39 Unfortunately, this combination
therapy is limited by poor patient compliance due
to the unpleasant odour of sulfur.
Topical alternatives for rosacea management
include clindamycin phosphate 1% lotion, benzoyl
peroxide, topical tretinoin, topical calcineurin
inhibitors, and permethrin 5% cream. Although all
have demonstrated efficacy in reducing the inflammatory
lesion count and/or erythema, data on their
efficacy are still limited. 34 A few publications have
reported the occurrence of rosacea-like eruptions
triggered by calcineurin inhibitors. 40-43
Oral therapies
DERMATOLOGY
Rounds
Several oral agents have been used in rosacea
management. Oral antibiotics have been effectively
used for inflammatory lesion control with minimal
improvement in erythema and telangiectasia. 30
Tetracycline has been the oral treatment of choice,
with initial total daily doses of 1000 mg divided
BID or QID for up to 4 weeks and then reduced by
half for at least a total of 6 months. A study by
Sneddon was the first to demonstrate the efficacy of
tetracycline. In this study, 78% of patients treated
with tetracycline 250 mg BID for 1 month had
disappearance of pustules, flattening of papules, and
a reduction in erythema. 44 Upon discontinuation of
tetracyclines, relapses are frequent with 25% of
patients relapsing at 1 month and 60% at 1 year. 34
These relapses can be attenuated or prevented by
concomitant use of topical therapies.
Other tetracyclines shown to be as effective in
rosacea management are minocycline (50 mg to
100 mg QD or BID) and doxycycline. The standard
dose of doxycycline is 100 mg QD or BID, but
the subantimicrobial dose of 20 mg BID has been
described as being equally effective. They are suitable,
but more costly, alternatives to tetracycline.
Side effects of tetracyclines include candidal vulvovaginitis,
gastrointestinal distress, and pseudotumour
cerebri. Photosensitivity may be significant
with doxycycline. Vertigo, blue dyspigmentation,
lupus-like syndrome, and hypersensitivity reactions
have been reported with minocycline. 34
Macrolide antibiotics are effective alternatives
in pregnant rosacea patients or those intolerant
of tetracyclines. Trials comparing azithromycin and
clarithromycin (250 mg BID) to doxycycline
demonstrated a faster reduction of erythema and
inflammatory lesions; 45, 46 however, the cost of these
agents prohibits their widespread use.
Oral metronidazole (200 mg BID) is another
alternative to the oral tetracyclines. It has been
shown to be as effective as oxytetracycline 250 mg
BID and can be used in pregnant women. 30,34
Isotretinoin (0.5 to 1 mg/kg/day) has been effectively
used in recalcitrant rosacea; it has a quick
onset of action and improves blepharitis and
T

conjunctivitis. The number and extent of side
effects, suboptimal effectiveness, and teratogenicity
are the main factors limiting its use. 30, 34 Dapsone
has been successfully used in severe, recalcitrant
rosacea in patients unable to use isotretinoin. 34
Flaxseed oil (1000 mg BID) has been advocated for
ocular rosacea. 34 A recent paper by Wu reviews the
use of topical and oral herbal supplements in
rosacea treatment. 47
Clonidine, beta-blockers, naloxone, ondansetron,
and selective serotonin reuptake inhibitors are all
variably successful in suppressing rosacea flushing;
however, at present, there is not enough evidence to
recommend their widespread use. 29 Saline injections
were not successful at preventing facial flushing. 29
Laser and light therapies
The main focus of laser therapy for rosacea is a
reduction in erythema and telangiectases. Lightbased
therapy appears to be most beneficial for
the ETR subtype of rosacea. 48 Several studies have
demonstrated a reduction in erythema, telangiectases,
and flushing in patients treated with 585 to
595 nm pulsed dye laser (PDL). On average,
patients require 2 to 6 treatments with maintenance
treatments every 4 to 6 months. 48,49 Main side
effects include post-treatment purpura (less likely
with 595 nm PDL), post-inflammatory hyperpigmentation,
and atrophic scarring. 49 Other vascular
lasers demonstrated to be effective for the treatment
of telangiectases are potassium titanyl-phosphate
lasers (KTP) and diode-pumped frequency-doubled
lasers (532 nm) and, for the treatment of deeper
and larger blue facial vessels, the 810 nm diode
laser, the long-pulsed Alexandrite, and the longpulsed
1064 nm neodymium:yttrium-aluminumgarnet
laser (Nd-YAG). 49
Intense pulsed light (IPL) therapy was shown to
be efficacious in rosacea patients with concurrent
photodamage. On average, patients require 2 to 5
sessions, spaced 3 weeks apart. Complications are
uncommon and include purpura, persistent edema,
and transient hypopigmentation. 49 Photodynamic
therapy with IPL preceded by application of topical
aminolevulinic acid for 15 to 60 minutes, is currently
under investigation; preliminary studies appear to
show promising results. 49
Phymatous rosacea does not respond to PDL or
IPL modalities and is best managed by ablative
lasers such as CO 2 or Erbium: YAG lasers. 48
Surgical therapies
Surgical treatment is mainly reserved for
patients with phymatous rosacea and is focused on
restoration of normal anatomical contours. Surgical
methods are divided into 2 main groups: complete
and incomplete excision. Complete excision utilizes
primary closure for small lesions and skin grafting
for large lesions. Better cosmetic results have been
reported with incomplete excision techniques that
include cryosurgery, dermabrasion, electrosurgery,
sharp blade excision, and shaving with a razor. 30
Conclusion
Rosacea is a common, but still poorly understood,
condition that associates vascular and pilosebaceous
abnormalities. Recent classification schemes
have expanded our knowledge of this emotionally
distressing disease. Therapeutic options are numerous
and must be adapted to each rosacea subtype.
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Upcoming Scientific Meetings
13-16 September 2006
European Society of Contact Dermatitis – 8 th Congress
Berlin, Germany
CONTACT: www.escd.org
4-7 October 2006
European Academy of Dermatology and Venereology
15 th Congress
Rhodes, Greece
CONTACT: info@eadv2006.com
4-7 October 2006
2 nd Annual Coastal Dermatology Symposium
Silverado Country Club & Resort, Napa, California
CONTACT: www.coastalderm.org
6-9 October 2006
Fall Clinical Dermatology Conference – 25 th Anniversary
MGM Grand Hotel, Las Vegas, Nevada
CONTACT: www.cbcbiomed.com
9-12 November 2006
7 th Las Vegas Dermatology Seminar
Skin Disease Education Foundation
Venetian Resort & Casino, Las Vegas, Nevada
CONTACT: www.sdefderm.com
sdef@sdefderm.com
Disclosure statement: Dr. Turchin and Dr. Sasseville have stated
that they have no disclosures to announce in association with the
contents of this issue.
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This publication is made possible by an unrestricted educational grant from
Astellas Pharma Canada, Inc.
© 2006 Division of Dermatology, McGill University Health Centre, Montreal, which is solely responsible for the contents. The opinions expressed in this publication do not
necessarily reflect those of the publisher or sponsor, but rather are those of the authoring institution based on the available scientific literature. Publisher: SNELL Medical
Communication Inc. in cooperation with the Division of Dermatology, McGill University Health Centre. ® Dermatology Rounds is a registered trade mark of SNELL Medical
Communication Inc. All rights reserved. The administration of any therapies discussed or referred to in Dermatology Rounds should always be consistent with the recognized
prescribing information in Canada. SNELL Medical Communication Inc. is committed to the development of superior Continuing Medical Education.
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