Acne and Acne related disorders
Disorders of sebaceous glands and Rosacea
Omar Abdulaziz Al-Sheikh, M.D.
College of Medicine
King Saud University
Objectives
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Acquiring knowledge of the etiology and pathogenesis of
acne and acne related disorders.
Understanding the disease spectrum and various types
of clinical presentations.
Knowing the differential diagnosis of acne and related
disorders.
Acquiring knowledge of the therapeutic options and their
indications.
to be familiar with the etiology, clinical types and
treatment of rosacea.
Definition:
Is a chronic inflammatory disorder of the
pilosebaceous apparatus of certain body area
(Face> Torso > rarely the Buttocks), 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
Etiology:
1.
2.
3.
4.
Genetic Aspect, (Acne runs in family) other
example: the case of severe acne that is
associated with XXY syndrome.
Occupation (Environmental, Mechanical) e.g.
exposure to acnegenic mineral oil (Pomade
acne), dioxin
Drugs Oral and topical Hydrocortison (Steroid
acne), Lithium, Hydantoin, contraceptives
Endocrine Factors (Recalcitrant Acne, POD/s,
MARSH Syndrome) .
Pathogenesis:
( three main steps recognized
and hypothesized)
1. Follicular Hyperkeratosis (the cause not fully
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understood) theory suggest:
deficiency in Linoleic acid,
the effect of 5-a reductase enzyme on
converting Androgen (Testosterone) hormone
to the active acnegenic and potent
(Dihydrotestosterone) DHT,
the direct effect of Interleukin-1 on follicular
hyperkeratosis
Fig 1
Fig 2
Fig 3
Perifollicular Hyperkeratosis
histology
Seborrhoea is a common feature between
patients with acne.
2. Abnormal production of abnormal sebum
increasing the ratio of wax ester to cholesterol
and cholesterol ester and is believed to be the
response of sebaceous glands to DHEA
3. Colonization of the affected unit with
bacteria Propionibacterium acne and
yeast named Malassezia furfur
Fig 4
Malassezia furfur
Fig 5
Propionibacterium acne
P
acne is a potent activator of complement via
classical pathway
Fig 6
Fig 7
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
Fig 8
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Hydrolytic enzymes released from the activated
complement antibodies complex together with
exoenzymes produced from P acne cause
rupture of follicular wall
Fig 9
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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:
(Acne and acne related
Disorders)
Acne Vulgaris:
Papules: (Less than 0.5 cm)
1.
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Comedones (Open “Blackheads” or closed
“Whiteheads”)
Open Comedones (Blackheads)
Fig 10
Fig 11
Open Comedones
Closed Comedones (Whitehead)
Fig 12
Fig 13
Closed Comedones
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Inflammatory papules
Fig 14
Fig 15
Inflammatory papules
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Pustules :
Fig 16
Fig 17
Pustules
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Nodule (more than 0.5 cm)
Fig 18
Fig 19
Nodule
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Cystic acne: the cysts are usually large 14cm
Fig 20
Fig 21
2. The nodules and cysts could be associated with
sinuses as in Acne inversa
 Acne inversea (Hidradenitis suppurativa “a misleading
name”) because it is considered by some to be a
disorder of apocrine gland (Sweat gland) but In my
opinion Acne inversa affects primarily the Pilo Seb. Unit
and affect secondarily the sweat gland, hence the
correct name Acne inversa rather than Hidradenitis
suppurativa is preferred.
Fig 22
3. Neonatal Acne and Infantile Acne
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Neonatal acne: cause unknown but some
believed is due to passing of Transplacental
androgen other suggest the role of Mlalassezia
furfur and sympodalis . affect 1 in 5 mainly
inflammatory comedones on nose and cheeks
affect new born between the 1st and 6th week of
age
Fig 23
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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 Endogenic androgen from
the infant’s gonads.
Fig 24
4. Recalcitrant Acne
Affect Women and associated with (Adrenal
hyperplasia "11-B- or 21-B hydroxlase
deficiencies) acne is usually nodulocystic
5. Acne Fulminans
Affect youngsters 13 – 17 years of age, very
severe with ulceration and puss discharge,
associated symptoms include (fever, malaise,
myalgia, arthritis and bone pain) laboratory
investigation shows ESR
Can be induced by starting the patient on high
dose of isotretinion (Roaccutane).
Fig 25
6. Acne Conglobata
Very severe Acne, Nodulocystic form with abscess
formation, affect Torso more than the face,
usually associated with XYY Syndrome.
Fig 26
Fig 27
7. Acne Agminata (Lupus Milliaris Disseminatus Faciei)
Some believe it is form of Rosacea
(Granulomatous type), diagnosis is made at
Histological base, Caseating Granulomata at the
dermal level.
Fig 28
8. Acne as part of other syndromes
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MARSH Syndrome (Melsma, Acne, Rosacea,
,Seborrhoeic eczema, and Hirsutism)
Acne Conglobata
Favre Racouchot syndrome elderly with elastosis as part
of Helioderma, sun exposure is a predisposing factor.
Polycystic ovarian syndrome
Atrophoderma vermiculatum as part of so called
Ulerythema ophryogenes, in Noonan Syndrome, de
Lange Syndrome, and Rubinstein-Taybi Syndrome Not
considered acne
9. Occupational
I Environmental
Chloracne rare forms of acne affect patients
exposed to Halogenated Hydrocarbons or who
ingested Chlorinated Phenols (Dioxin)
 Pomade acne or known as Oil Folliculitis
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Acne Aestivalis or so called Mallorca Acne
Occupational
II mechanical acne
Folicullitis Nuchae or so called Acne Keloidalis
 Pseudofollicultis barbae
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Acne excoriee as part of Psychodermatosis
TREATMENT
Note: All medications used for the treatment of acne act
as:
1. Anti comedonal
2. Anti inflammatory
3. Anti microbial
Topical Keratolytic
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Retinoid ( Retinoic acid 0.025, 0.05, 0.1%)
Adapalene (Differin 0.1%)
Salicylic acid
Benzoyl peroxide (peeling agent and
antimicrobial)
Azelaic Acid (10, 15, 20 %)
Topical Antibiotic
Topical clindamycin (Dalacin T)
 Erythromycin
 Mupirocin (Bactroban)
 Sodium Fusidic acid (less significant in the
treatment)
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Systemic therapy
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1.
2.
3.
4.
Antibiotic (Macrolides and Tetracylines)
Tetracycline
Doxycycline
Minocycline (blue grey discoloration and drug
induced LE)
Azithromycin
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Systemic Retinoids :
Isotretinoin caps (Roaccutane): 0.5 – 1 mg/kg
The most effective drug for acne.
Indicated for severe forms (nodulocystic and fulminant) 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 (less frequent than with
acitretin), 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 : Retinoid - induced embryopathy. Pregnancy category X.
Pregnancy must be prevented during treatment and for at least 1 month
after discontinuing the drug.
Other forms of therapy
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Systemic steroid (Prednisolone): for acne fulminans and
intralesional steriods for cystic acne.
Photodynamic therapy i.e. Laser therapy and phototherapy (Less
significant)
SMT D002 is a new promising and potentially safe medication
(Oxybutynin chloride), it has successfully completed two Phase I
trials in healthy volunteers and believed to treat seborrhoea, a
symptom of Parkinson's disease and the primary cause of acne.
Topical formulation of the drug is currently being developed by
Summit company.
Hormonal therapy (Anti-androgen)
Spironolacton (Potassium sparing agent) and Metformin as
(Hypogylcemic agent) in treatment of PCOS (Polycystic Ovary
Syndrome) have good results on acne
Rosacea
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A controversial topic in dermatology largely because of
its uncertain pathophysiology and clinical variation.
Erythema of the central face that has persisted for
months or more.
Primary features: flushing, papules pustules and
telangiectases.
Secondary features: burning, stinging, edema, plaques,
dry appearance, phyma, peripheral flushing and ocular
manifestations.
Epidemiology
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Common in caucasian population
Fair skinned individuals
women>men
Onset typically begins after age 30
Etiology and pathogenesis
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1) Vascular reactivity:
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Rosacea is induced by chronic repeated triggers of flushing
exposure, they include:
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1)
2)
3)
4)
5)
6)
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Hot or cold temperature
Hot drinks
Spicy foods
Alcohol
Certain cosmetics
Medications
7) Sunlight
8) Emotional disteress
9) Topical irritants
Etiology and pathogenesis
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2) Dermal matrix degeneration and endothelial damage
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Inherent problems with vessels permeability
Delayed clearance of inflammatory mediators and waste
products
Photodamaged connective tissue (solar elastosis is a
common background on which rosacea histologic
features are superimposed
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Etiology and pathogenesis
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The role of microbe – induced follicle based inflammation
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Commensal organisms which reside in hair follicles and
sebaceous glands may trigger folliculocentric
inflammatory papules.
Demodex folliculorum (mite) or associated bacteria
(bacillus oleronius).
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Sub-type classification
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Sub types were defined by the National Rosacea Society
(NRS) expert committee in 2002.
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1) Erythematotelangiectatic : persistent erythema and
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telangiectasias on the central face.
2) Papulopustular: papules and pustules predominate on convex
areas on a background of persistent erythema
3) Phymatous: patulous follicular orifices, thickened skin and
nodularity
Most often affect the nose (rhinophyma)
Almost exclusively in men
4) Ocular: Blepharitis is the most common feature (mebomian gland
dysfunction)
Conjuctivitis, iritis, scleritis, keratitis
Fig 29
Erythematotelangiectatic Rosacea
Fig 30
Papulopustular Rosacea
Fig 31
Rhinophyma
Rosacea variants
Granulomatous rosacea: Rosacea variant
characterised by monomorphic yellow
brown or red papules/ nodules located on
the cheeks and periorificial skin.
 Granulomas on histology
 The background facial skin is otherwise
normal
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Differential Diagnosis
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Full and detailed history (including medications)is required,
Medications that induce flushing include : all vasodilators,
calcium channel blockers, nicotinic acid, morphine, amyl
and butyl nitrite, cholinergic drugs, bromocriptine,
tamoxifen, cyproterone acetate, systemic steroids and
cyclosporine.
Diagnosis is made clinically
Differential diagnosis include:
Seborrheic dermatitis
Steroid folliculitis/Perioral Dermatitis
Acne vulgaris
Erythromelanosis faciei and keratosis pilaris rubra
Lupus erythematosus
Lupus miliaris disseminatus faciei
Treatment
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Sunscreens
Avoidance of aggravating factors.
Topical medications include:
Metronidazole
Sodium sulfacetamide and sulfur
Azelaic acid
Benzoyl peroxide
Tretinoin
Erythromycin and Clindamycin
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Oral medications include:
Tetracyclines:
Tetracyclines are the most commonly prescribed oral
medications for the treatment of rosacea.
They act by their anti-inflammatory effects
Erythromycin (for children with granulomatous perioral
dermatitis)
Isotretinoin
Laser and light therapy
Laser and Intense Pulsed light IPL is useful in treating
persistent erythema and telangiectasias
 Pulsed dye laser (585 or 595 nm)
 Potassium-titanyl phosphate laser KTP 532nm, for
superficial small telangiectasias.
• Deep facial vessels require longer wavelengths :
Diode laser (810)
• The long pulsed alexandrite laser (755nm)
• Long pulse ND:YAG (1064nm)
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Treatment of Phymatous Rosacea
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Early to moderate Phymatous changes could be treated
with Isotretinoin.
Advanced phyma is treated with surgery or surgery
followed by isotretinoin.
Scalpel tangential excision
Electrosurgery
Laser CO2 ablation.
Fig 1, 2 www.scf-online.com/.../keratinization38_e.htm keratinization of the duct of the hair follicle.
www.nlm.nih.gov/.../ency/imagepages/2087.htm open (Blackheads) comedones, Medical Encyclopedia
Fig.3
Fig 4. Malassezia furfur www.doctorfungus.org/thefungi/Malassezia.htm Closed comedones Skin and
.allergy centre
Fig 5
Fig 6 www.ohiohealth.com/bodymayo.cfm?id=6&action=t... Mayo Foundation for Medical and research.
Fig 7
Fig 8 bacterial colonization www.healthcaresouth.com/pages/acnewhatis.htm
Fig 9 Breakage of follicular wall www.healthyskinbydesign.com/acne.cfm papule
Fig 10 open comedones www.healthcaresouth.com/pages/acnewhatis.htm
Fig 11
Fig 12 closed comedones www.healthcaresouth.com/pages/acnewhatis.htmfig
www.dermalogix.net/acne/acne.html open and closed comedones schematic pictures
www.dermalogix.net/acne/acne.html proriobionacterium acne in pilosabaceous unit
www.healthyskinbydesign.com/acne.cfm. follicular hyperkeratosis in acne
Fig 13
Fig 14
Fig 15
Fig 16 www.healthyskinbydesign.com/acne.cfm pustule
Fig 17. Courtesy of Skin and allergy centre
Fig 18 www.healthyskinbydesign.com/acne.cfm nodule
Fig 19 nodule www.acnekil.com/What's_Acne/photo_gallery2.htm
Fig 20
Fig 21 Courtesy of Skin and allergy centre
Fig 22 Courtesy of Skin and allergy centre
Fig 23 www.adhb.govt.nz/.../BenignLesions.htm at neonatal dermatology benign lesions Auckland
district health board.
Fig 24 Courtesy of Polonia, second edition
Fig 25
Fig 26 Courtesy of Skin and allergy centre
Fig 27 Acne conglobata www.consultantlive.com/showArticle.jhtml?arti...
Fig 28 acne Agminata Granulomatous rosacea in infants. Report of three cases and discussion of the
differential diagnosis João Borges da Costa, Sousa Coutinho V, L Soares de Almeida, M Marques
Gomes PhDDermatology Online Journal 14 (2): 22
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Fig 29, courtesy of Rook 2010
Fig 30, courtesy of Fitzpatrick 2008
Fig 31, courtesy of Polonia 2008
text:
Moulin G, Thomas L, Vigneau M, Fiere A.[A case of unilateral Elastosis with cyst and Comedones of Favre-Racuchet syndrome]. Amn. Dermatol
Venereol 1994, 121(10), 721-3
Sanchez-Yus E, DejRb E, Simon P, Requenal A, Vazquez H.[ The histopathology of close and open Comedones of Favre-Racuchet disease]. Arch
dermatol 1997 Dec. 133 (12) 1592.
Zugerman C. [ Chloracne, clinical manifestation and etiology]. Dermatol clin. 1990 jan. 8 (1) 209-13.
Birian B. [ Peri orbital Comedones ]. J Am Acad Dermatol 2000. 42. 622-7.
Khorsow Mehrany, Josedh M, Kist Roger H, Weenig, Patricia M, Witman. [ Acne Fulminana]. Inter. J. Dermatol 2005. 44 132.
Charles N, Ellis, Kent J, Krach. [ Uses and complications of isotretinoin therapy]. J Am Acad. Dermatol. 2001. 45: S1. 150-7.
Bedlow A J. Otter M. Marsder R A. [ Axillary acne agminata ( lupus Miliaria Desseminatus Facies)]. Clin. Exp. Dermatolo 1998 May. 22 (3) 125-8
Ogunbiyi A, George A. [ Acne keloidalis in female: Case report and review of literature]. Nati. Med assoc. 2005 Aug. 97 (8) 1178
Alfred L, Knable Jr, C William Hanke, Rene Gonin. [ Prevalence of acne Keloidalis Nuchae in Football players ]. J Am Acad Dermatol 1997. 37. 570-4
Shenefelt PD. [ Using hypnosis to facilitate resolution of psychogenic excoriation in Acne Excoriee]. Am. J. Clin. Hypn. 2004 Jan. 46 (3) 239-45
Griffiths WA. [The red face-an overview and delineation of the MARSH syndrome]
Clin. Exp. Dermatol. 1999 Jan. 24(1):42-7
Thomas B Fitzpatreick, Richard Allen Johnson, Klaus Wolf, Dick Suurmond, [Disorders of Sebaceous and Apocrine glands]. Color Atlas of Synopsis of
Clinical Dermatology by McGraw-Hill. 2001 . Page 2-17
Diane Thiboutot, MD Hershey, Pennsylvania [Acne: 1991-2001] . J Am Acad Dermatol July 2002 • Volume 47 • Number 1 • p109 to p117
Carolyn I. Jacob, MD,* Jeffrey S. Dover, MD, FRCPC, and Michael S. Kaminer, MD [Acne scarring: A classification system and review of treatment
options] J Am Acad Dermatol 2001; 45:109-17
Susan C. Taylor, Fran Cook-Bolden, Zakia Rahman, and Dina Strachan. [Acne vulgaris in skin of color] J Am Acad Dermatol 2002; 46:S98-106
Jerry K. L. Tan, Kirsten Vasey, Karen Y. Fung, [Beliefs and perceptions of patients with acne] J Am Acad Dermatol 2001;44:439-45
Clement A. Adebamowo, Donna Spiegelman, William Danby,
Lindsay Frazier, Walter C. Willett, Michelle D. Holmes. [High school dietary dairy intake and teenage acne]. J Am Acad Dermatol 2005;
52:207-14
.A
Brian B. Adams, MD, Viziam B. Chetty, MD, and Diya F. Mutasim, MD Cincinnati. [Periorbital comedones and their relationship to pitch tar: A crosssectional analysis and a review of the literature] J Am Acad Dermatol 2000;42:624-7
V. Goulden, G. I. Stables,W. J. Cunliffe. [Prevalence of facial acne in adults] J Am Acad Dermatol 1999; 41:577-80
Lowell A. Goldsmith, Jean L. Bolognia, Jeffrey P. Callen, Suephy C. Chen, Steven R. Feldman Henry W. Lim, Anne W. Lucky, Barbara R. Reed
Elaine C. Siegfried, Diane M. Thiboutot, onald G. Wheeland.[American Academy of Dermatology Consensus Conference* on the Safe and
Optimal Use of Isotretinoin: Summary and recommendations ] J Am Acad Dermatol 2004 june. Volume 50 number 6
Marvi Iqbal, Michael S. Kolodney, [Acne fulminans with synovitis-acne-pustulosishyperostosis- osteitis (SAPHO) syndrome treated with infliximab] .
J Am Acad Dermatol 2005;52:S118-20.
Harold P. Lehmann, MD, PhD, Karen A. Robinson, MSc, John S. Andrews, MD,Victoria Holloway, MD, and Steven N. Goodman, MD, MHS, PhD.
[Acne therapy: A methodologic review]. J Am Acad Dermatol 2002;47:231-40
Harald Gollnick, MD, and William Cunliffe, Diane Berson, Brigitte Dreno, Andrew Finlay, James J. Leyden, Alan R. Shalita, Diane Thiboutot.
[Management of Acne A Report From a Global Alliance to Improve Outcomes in Acne]. J AM ACAD DERMATOL JULY 2003. VOLUME 49,
NUMBER 1
Gary M. White. [Recent findings in the epidemiologic evidence, classification, and subtypes of acne vulgaris]. J Am Acad Dermatol 1998;39:S34-7
John Y. M. Koo, Jennifer H. Do, Chai Sue Lee. [Psychodermatology]. J AM ACAD DERMATOL NOVEMBER 2000. VOLUME 43, NUMBER 5
Sharam S Yashar, Ali Moiin, .[ TREATMENT OF PSYCHODERMATOSES WITH SEROTONIN-NOREPINEPHRINE REUPTAKE INHIBITORS]. J AM ACAD
DERMATOL MARCH 2004. P 33
Wilkin J et al: Standard classification of rosacea: Report of the National Rosacea Societv Exoert Committee on the classification and staging of
rosacea J Am Acad Dermatol 46:584, 2002
Plewig C, Kligman A: Acne and Rosacea, 3rd ed. Berlin, Springer-Verlag, 2000, p 455
Wilkin J et al: Standard grading system for rosacea: Report of the National Rosacea Society Expert Commiittee on the classification and
staging of rosacea J An Acad Dermatol 5O:907,2004
Crawford C, Pelle M, James W: Rosacea: I. Etiology, pathogenesis, and subtype classification J Am Acad Dermatol 5L:327,2004
Pelle M, Crawford C, James W: Rosacea: II Therapy J Au Acad Dermatol 5l:499, 2004
Marks R, Harcourt-Webster J: Histopathology of rosacea Arch Dermatol 100:683, 1969
BogeEEPi et al: Surgical treatmen! of rhinophyma: A comparison of techniques Aesth Plast Surg 26:57, 2002