Supported by Promius Pharma, LLC
Dermatology
Therapeutic Update
An informational newsletter for pediatricians
Editor’s Message
n this edition of “Dermatology Therapeutic Update: Current Perspectives
I An Informational Newsletter for Pediatricians,” I
have chosen to cover seborrheic dermatitis and acne
vulgaris—two common conditions you are likely faced on the Diagnosis
with on a regular basis. As a practicing dermatologist
who is also very involved in clinical research, I am keen-
ly aware of the different types of therapies available for
these two prevalent dermatological conditions, including
and Management of
evolving and emerging therapies. My main objective for
this newsletter is to bring you up-to-date, clinical infor-
mation that will help you provide the best care possible
Seborrheic Dermatitis
to your patients with common dermatological disorders. by James Q. Del Rosso, DO, FAOCD, and Grace K. Kim, DO
Seborrheic dermatitis (SD) is a common, chronic,
recurrent, inflammatory skin disorder that may start in
childhood or adulthood. There are a number of factors,
eborrheic dermatitis (SD) is a common, chronic, recurrent, inflammatory
such as immune function, overproduction of Malassezia
yeast, and sebum production that can contribute to the
pathophysiology of infantile SD. In this article, I discuss
pathophysiology, epidemiology, the role of Malassezia
S skin disorder that may start in childhood or adulthood. In infants, SD pres-
ents as a patchy pink eruption often with fine scaling, which may be local-
ized (often to the head and neck region) or diffuse. Infantile SD usually presents
species in SD, clinical manifestations of SD, and treat- as “cradle cap,” typified clinically by diffuse, greasy, fine scaling with pink ery-
ment, such as therapeutic shampoos, topical corticos- thema on the head.1 Sometimes the eruption may be more diffuse with extension
teroids, topical calcineurin inhibitors, and a new nons- to the face, neck, and trunk. Although the pathophysiology of SD is not fully
teroidal cream formulation that contains several ingre-
understood, a pathogenic role has been correlated with proliferation of lipophilic
dients, including an antifungal complex and gly-
yeast species (Malassezia spp).1 Some researchers believe that precipitating
cyrrhetinic acid.
There are many treatment options for SD, and topical agents of SD include an overgrowth of or abnormal immunological response to
medication alone can be sufficient without the need for Malassezia spp, overproduction of sebum, or in infants, a response to maternal
oral medication. hormone.2 In some cases, the presence of severe and treatment-resistant SD can
The second topic covered in this edition of the be an indication of immunodeficiency, which may warrant further evaluation.3 It
newsletter is acne vulgaris. As the most common skin is not clear whether or not the infantile form of SD predisposes patients to the
disease, acne affects tens of millions of teenagers and development of SD in adulthood.
adults. More specifically, 85 percent of individuals
between 12 and 24 years of age have some form of acne, Epidemiology
which causes significant physical and emotional discom- SD is bimodal in incidence, exhibiting one peak in infancy and the other
fort. With more choices and newer formulations of exist-
between the fourth and sixth decades of life.3 The prevalence of SD ranges from
ing compounds, everyone has an opportunity to success-
1 to 3 percent in the immunocompetent population, with an increase in preva-
fully treat this skin disease.
Because acne is a common disorder that frequently lence in the immunocompromised population, especially in patients with
begins in preadolescence or adolescence, it is common acquired immunodeficiency syndrome (AIDS).4 Infantile SD occurs between the
for pediatric patients and their parents to ask pediatri- second and tenth week of life and peaks at three months of age, with some cases
cians about the appropriate management of acne. In this lasting for up to one year.4 Infantile SD differs from adult SD in that the infan-
newsletter, I cover epidemiology, pathophysiology, hor- tile form is confined primarily within the first 3 to 12 months of life, while adult
mones, clinical presentation, and treatment options SD is chronic and relapsing over several years.5 SD also occurs in all ethnicities
including topical therapy, combination therapy, oral and races with a reported predominance in males, possibly due to androgen stim-
antibiotics, and oral contraceptives. ulation of sebum production.1 SD can also occur in association with other skin
I hope this newsletter is informative and enlightens diseases, such as atopic dermatitis in children and rosacea in adults, which can
you in the areas of seborrheic dermatitis and acne vul-
create diagnostic confusion.6,7 One study showed that 49 percent of 2- to 12-
garis and their treatment options.
month-old infants with atopic dermatitis had a history of infantile SD in contrast
James Q. Del Rosso, DO, FAOCD to 17 percent of controls.4 It is also seen in patients with other skin diseases asso-
Dermatology Residency Director
ciated with Malassezia spp, such as pityriasis (tinea) versicolor and Malassezia
Valley Hospital Medical Center
Las Vegas, Nevada folliculitis.8,9
Clinical Associate Professor
(Dermatology)
Role of Malassezia Species in Seborrheic Dermatitis
Touro University College of At birth, neonatal skin is sterile; however, resident flora may be detected as
Osteopathic Medicine early as the first three hours of life.10 Factors associated with neonatal coloniza-
Henderson, Nevada, and
University of Nevada
School of Medicine
Las Vegas, Nevada
Las Vegas Skin & Cancer Clinics Fall 2009
Las Vegas and Henderson, Nevada
Dermatology Therapeutic Update
An informational newsletter for pediatricians
continued from page 1
Figure 1. In preadolescent and teenage SD, the Figure 2. This patient has perinasal dermatitis, Figure 3. This is an example of perioral dermatitis,
eruption is characterized by pink-to-red macular which is often misdiagnosed as SD. which characteristically exhibits perivermillion
erythema that is often associated with fine yellow or sparing.
white scaling.
tion includes length of stay in an intensive yeast proliferation, and response of SD to preteens or early teens is perinasal der-
care department, gestational age, birth antifungal medications, such as ketocona- matitis, a clinical variant of perioral der-
weight, use of parenteral nutrition, use of zole and ciclopirox.5 matitis. Perioral dermatitis is a common
antimicrobial medication, presence of a facial inflammatory eruption seen in
central venous catheter (CVC), surgery, Clinical Manifestation female patients primarily between the
and surgery with the presence of a CVC or Infantile SD. Infantile SD is usually ages of 25 and 45 years. A perinasal erup-
nasogastric tube.10 The prevalence of diagnosed on clinical grounds and often tion involving the lateral nasal alar
Malassezia spp has been reported to be as presents as described above. In the diaper crease region, presenting as confluent
high as 13 to 50 percent in the first week area, SD may manifest as thin, dry scales pink erythema, and sometimes in associa-
of life.11,12 Many have suggested that tran- or sharply defined, round or oval patches tion with a few papules and fine scaling,
sient flora from the maternal genital tract covered by thick, yellowish-brown, greasy is often misdiagnosed as SD in preteen
is an origin of newborn sterile skin colo- crusts.16 Infantile SD usually does not and teenage girls. This presentation is
nization.10 Breast feeding has also been involve the extensor surfaces as extensive- referred to as perinasal dermatitis
assumed to be correlated with microbial ly as atopic dermatitis. (Figure 2), is inflammatory in nature, and
colonization of the newborn.13 The fre- Preadolescent/teenage SD. SD affect- is of unknown etiology. It may coexist
quency of bathing, use of skin care prod- ing preadolescents and teenagers exhibits with a similar eruption in the perioral
ucts and lubricants, and use of any occlu- features characteristic of adult SD. The region (perioral dermatitis), which char-
sive agents have all been associated with distribution is generally symmetric and acteristically exhibits perivermillion
colonization of neonatal skin by tends to affect the scalp, glabella region, sparing (Figure 3). Importantly, perinasal
Malassezia spp.13 eyebrows, nasolabial folds, and/or periau- dermatitis is worsened over time by appli-
Malassezia spp are a group of yeasts ricular region, including the external cation of some medications that can be
inclusive of nine lipophilic species, with auditory canals.1 The midchest, axillae, used to treat SD, especially topical corti-
seven being identified as components of groin, and genital area may also be costeroids. Perinasal and perioral der-
the human commensal flora.1 Investigators involved. Pruritus is often present. matitis are highly responsive within 4 to
have found M. furfur, M. sympodialis, M. Clinically, the eruption is characterized by 8 weeks to low-dose doxycycline therapy,
obtuse, and M. slooffiae in SD lesions.14 M. pink-to-red macular erythema that is including subantimicrobial doses of 40mg
globosa and M. restricta are reported to be often associated with fine yellow or white daily (Oracea).
the most common organisms associated scaling (Figure 1). On the scalp, the scal-
with the presence of SD, identified in loca- ing is commonly referred to by patients as Treatment of Seborrheic Dermatitis
tions such as the scalp of individuals with “dandruff,” which may be present with or Scalp involvement. Therapeutic
SD or dandruff.5,15 These commensal yeasts without visible signs of inflammation (ery- shampoos are often effective in scalp SD,
are not easily cultured in vitro, requiring thema). Periods of exacerbation and primarily due to ease of use. Ketoconazole
an exogenous source of lipid to grow.2 In remission are the hallmark of SD, though shampoo 2% (Nizoral) and ciclopirox
vivo, they tend to emerge on the skin at persistence is common in some patients, shampoo 1.5% (Loprox) are effective, and
puberty, associated with an increase in especially on the scalp. In some cases, are usually prescribed 2 to 3 times per
both androgens and sebum production.2 thicker scalp scales may form, suggestive week.17 A foam formulation of ketocona-
Although the pathophysiology of SD is not of the scales seen in psoriasis. This presen- zole foam 2% (Extina) applied twice daily
fully understood, there has been a link to tation has been termed “seborrhiasis.” may also be used, as may selenium sulfide
sebum overproduction and the commensal foam (Tersi Foam). Other potentially
Malassezia spp.2 It has been strongly sug- Perinasal/Perioral Dermatitis: effective options include shampoos con-
gested that Malassezia spp play a role in A Clinical Simulant of Seborrheic taining salicylic acid 6% (Salex) and over-
the pathogenesis of SD due to identifica- Dermatitis the-counter preparations containing zinc
tion of yeast isolates in affected skin A clinical simulant of SD that is rela- pyrithione.18
lesions, correlation of flares of SD with tively common in female patients in their Glabrous skin involvement. After
2
Dermatology Therapeutic Update
An informational newsletter for pediatricians
Figure 4. Twice-daily treatment of facial seborrheic dermatitis: Investigator Figure 5. Twice-daily treatment of facial seborrheic dermatitis: Erythema
global assessment. Promiseb study PSC0801 (N=65). score. Promiseb study PSC0801 (N=65).
Figure 6. Twice-daily treatment of facial seborrheic dermatitis: Scaling score. Figure 7. Twice-daily treatment of facial seborrheic dermatitis: Pruritus score.
Promiseb study PSC0801 (N=65). Promiseb study PSC0801 (N=65).
the scalp, the face is the most common area models.20 In a randomized, investigator- and natural course of infantile SD can
affected by SD. Commonly involved sites blinded study of subjects with mild-to- help alleviate anxiety and concerns and
include hairline, eyebrows, glabella region moderate SD (n=77), Promiseb cream increase medication adherence.
of the forehead, and paranasal folds and exhibited equivalent efficacy based on
inner cheeks. Low-potency topical corticos- investigator global assessment (Figure 4), References
teroids, such as hydrocortisone and des- and reductions in erythema (Figure 5), 1. Elewski BE. Safe and effective treatment of
onide (Desonate, Verdeso) are effective; scaling (Figure 6), and pruritus (Figure 7) seborrheic dermatitis. Cutis. 2009;83:333–338.
however, the duration of continuous use on after 14 days (Day 14) comparable to topi- 2. Aditya KG, Bluhm R, Cooper EA, et al.
the face should generally be limited to two cal desonide, with a markedly lower rate of Seborrheic dermatitis. Dermatol Clinics.
weeks or less for SD.18 Topical calcineurin relapse at 14 days after therapy was 2003;21:401–412.
inhibitors, such as pimecrolimus 1% cream stopped (Day 28).20 The tolerability profile 3. Poindexter GB, Burkhart CN, Morrell DS.
(Elidel) and tacrolimus 0.1% or 0.03% oint- of Promiseb cream was very favorable. Therapies for pediatric seborrheic dermatitis.
ment, are effective in some cases; however, Promiseb cream offers a therapeutic Pediatric Annals. 2009;38(6):333–338.
their use in the treatment of SD is not US option that is effective and safe without 4. Gupta AD, Batra R, Bluhm R, et al. Skin dis-
Food and Drug Administration approved.19 limitation on duration of therapy. ease associated with Malassezia species. J Am
Certain antifungal agents, such as keto- Acad Dermatol. 2004;51:785–798.
conazole 2% cream (Nizoral), foam Conclusion 5. Bolognia JL, Jorizzo JL, Rapini RP, et al.
(Extina), or gel (Xolegel), and ciclopirox The prognosis of infantile SD is excel- Dermatology. 2nd ed. Spain: Elsevier; 2008.
1.5% cream (Loprox), lotion (Loprox), or gel lent with most cases spontaneously 6. Gupta AK. A random survey concerning aspects of
(Loprox), are effective for SD; however, the responding by 8 to 12 months of age or acne and rosacea. J Cutan Med Surg. 2001;5:38.
onset of clinical effect is usually slower earlier. There are a number of factors, 7. McCulley JP, Dougherty JM. Blepharitis associ-
than with a topical corticosteroid.18 such as immune function, overproduction ated with acne, rosacea and seborrheic dermati-
A new nonsteroidal cream formulation of Malassezia yeast, and sebum produc- tis. Int Ophthalmol Clin. 1985;25:159–172.
(Promiseb), which contains several ingre- tion, that can contribute to the patho- 8. Faergemann J, Johansson S, Back O. An immuno-
dients, including an antifungal complex physiology of infantile SD. It is important logic and cultural study of Pityrosporum folliculi-
and glycyrrhetinic acid, has been shown to to counsel parents of babies with infantile tis. J Am Acad Dermatol. 1986;14:429–433.
be effective for SD, exhibiting therapeutic SD, explaining that the condition is not 9. Sunenshine PJ, Schwartz RA, Janniger CK.
efficacy similar to desonide 0.05% cream.20 contagious and that infants with SD may Tinea versicolor: an update. Cutis. 1998;61–72.
Glycyrrhetinic acid has been shown to not necessarily develop SD as adults.3 10. Ayhan M, Sancak B, Karaduman A, et al.
exhibit anti-inflammatory activity, and There are many treatments that exist for Colonization of neonate skin by Malassezia
piroctone olamine demonstrates antifun- SD, and topical medications alone are suf- species: relationship with neonatal cephalic
gal activity, with Promiseb cream reducing ficient without the need for oral medica- pustulosis. J Am Acad Dermatol. 2007;57(6):
M. furfur in both humans and in animal tion. Educating parents about the nature 1012–1018.
3
Dermatology Therapeutic Update
An informational newsletter for pediatricians
11. Ahtonen P, Lehtonen OP, Kero P, et al. with seborrheic dermatitis, atopic dermatitis, Clinical efficacies of shampoos containing
Malassezia furfur colonization of neonates in an pityriasis versicolor, and normal subjects. Med ciclopirox olamine 1.5% and ketoconazole 2%
intensive care unit. Mycoses. 1990;33:543–547. Mycol. 2000;38:337–341. in the treatment of seborrheic dermatitis. J
12. Shattuck KE, Cochran CK, Zabransky RJ, et 15. Dawson TL. Malassezia globosa and restricta: Dermatol Treat. 2007;18:88–96.
al. Colonization and infection associated with breakthrough understanding of the etiology 18. Gupta AK, Bluhm R, Cooper EA. Seborrheic
Malassezia and Candida species in a neonatal and treatment of dandruff and seborrheic der- dermatitis. Dermatol Clin. 2003;21:401–412.
unit. J Hosp Infect. 1996;34:123–129. matitis through whole-genome analysis. J 19. Cook BA, Warshaw EA. Role of topical cal-
13. Bernier V, Weill FX, Hirigoyen V, et al. Skin Investig Dermatol Symp Proc. 2007;12:15–19. cineurin inhibitors in the treatment of sebor-
colonization by Malassezia species in neonates: 16. Moises-Alfaro CB, Cacere-Rios HW, Rueda M, rheic dermatitis: a review of pathophysiology,
a prospective study and relationship with et al. Are infantile seborrheic and atopic der- safety, and efficacy. Am J Clin Dermatol.
neonatal cephalic pustulosis. Arch Dermatol. matitis clinical variants of the same disease? 2009;10:103–118.
2002;138:215–218. The International Society of Dermatol. 20. Promiseb Cream [product monograph].
14. Nakabayashi A, Sei Y, Guillot J. Identification 2002;41:349–351. Bridgewater, New Jersey: Promius Pharma
of Malassezia species isolated from patients 17. Ratnavel RC, Squire RA, Boorman GC. LLC; 2009.
Acne Vulgaris
A Practical Primer on
Pathogenesis and Treatment
by James Q. Del Rosso, DO, FAOCD, and Grace K. Kim, DO
cne vulgaris is the most common of patients present between 12 and 24 tinization leading to follicular obstruction
A skin disease, affecting an estimated
17 million people in the United
States with 85 percent being adolescents
years of age.3 Persistence past teenage
years also occurs, with 12 percent of
women and three percent of men continu-
(comedo formation); and (4) the activation
of inflammatory mediators.3 Individual
acne lesions start within pilosebaceous
and young adults.1 In general, most mild- ing to have acne until the age of 44.4 units, which are concentrated mainly on
to-moderate cases of preadolescent and Studies have shown that Caucasian men the face, upper chest, and upper back.10
adolescent acne can be managed success- experience more severe nodulocystic dis- Microcomedones, which are not visible clin-
fully by pediatricians, usually with combi- ease than do their African-American coun- ically, are the first lesions formed in acne
nation topical therapy. In some cases, terparts.5 In addition, those having an vulgaris.5 It is theorized that in patients
understanding the pathophysiology of XYY chromosomal genotype or endocrine with acne, keratinization is significantly
acne can also help to diagnose hormonal disorders, such as hyperandrogenism, altered and the epithelial cells from the fol-
abnormalities, especially in treatment- polycystic ovarian syndrome, hypercorti- licular lining are not desquamated proper-
resistant cases. Successful acne treatment solism, and precocious puberty, are at ly (comedogenesis).10 This cascades into cell
is based on the type of lesions, overall increased risk for severe acne that is usu- and sebum impaction within the follicle, fol-
severity, and anatomical location, with 50 ally unresponsive to standard treatments.5 lowed subsequently by P. acnes prolifera-
percent of patients with facial acne vul- Psychological sequelae of acne include, tion, and, in some follicles, the triggering of
garis also demonstrating truncal involve- anxiety, depression, and social withdrawal an inflammatory cascade of events.11,12
ment. Recently, acne has been described by related to both acne lesions and acne Comedos are theorized to precede inflam-
the Global Alliance to Improve Outcomes scars.6–9 Additionally, hyperpigmentation matory lesions, but the mechanisms trig-
in Acne as a chronic condition character- and scarring are prolonged sequelae that gering acne lesion progression still remain
ized by flares with many physicians under require physical therapies that are costly unknown.
recognizing disease severity.2 Although and without consistent results.3
acne is often viewed by many caretakers Correlation of P. acnes with Acne
as a “natural part of growing up,” research Pathogenesis of Acne Vulgaris Pathogenesis
suggests that the quality of life of many Although all of the pieces of the “acne P. acnes is an anaerobic gram-positive
adolescents is adversely affected and suc- pathogenesis puzzle” are not known, there diphtheroid that is a normal inhabitant of
cessful treatment has been shown to are many reported mechanisms that con- the skin found deep within sebaceous folli-
improve psychological wellbeing.3 tribute to acne lesion formation.2,5,9,10 Acne is cles. Proliferation of P. acnes significantly
an inflammatory disorder of the piloseba- contributes to the production of acne
Epidemiology ceous unit comprising a follicle, sebaceous lesions.2,5,7 Inflammatory events have been
Acne is a chronic inflammatory disease gland, and rudimentary or vellus hair.10 found to precede hyperkeratinization,
that usually starts in preadolescence or There are four main pathogenic factors with P. acnes contributing to the inflam-
early adolescence and often exhibits a pro- leading to the formation of acne lesions: (1) matory response and possibly comedogen-
longed pattern of recurrence or relapse. increased sebum production; (2) follicular esis.3 Although higher numbers of P. acnes
Acne vulgaris has led to an estimated colonization with Propionibacterium acnes, have been reported in acne patients, the
annual cost of at least $2.5 billion a year which stimulates inflammation and possi- colony numbers do not directly correlate
in the United States. Eighty-five percent bly comedogenesis; (3) alterations in kera- with disease severity.13 Ultimately, it is the
4
Dermatology Therapeutic Update
An informational newsletter for pediatricians
exuberance of the host’s innate immune Associated with ris-
response, along with other mechanisms of ing DHEAS levels,
inflammation, that dictates the severity of enlargement of seba-
inflammatory acne in a given patient.5 P. ceous glands and ele-
acnes can trigger an inflammatory vated sebum produc-
response by producing chemoattractant tion occur.19,20 High
factors that can attract lymphocytes and DHEAS levels corre-
cause polymorphonuclear neutrophils late with a clinical
(PMNs) to enter the pilosebaceous follicles.10 presentation charac-
As PMNs ingest P. acnes, hydrolytic terized by multiple
enzymes are released, which in turn damage facial comedonal
the follicular wall, causing its contents to acne lesions, which
enter the dermis. Spillage of follicular con- become prominent in
tents into the dermis further promotes more prepuberty and are
severe inflammation, akin to a foreign body sometimes associat-
reaction. The end result is a mixed clinical ed with inflammato-
presentation of comedones, papules, pus- ry acne lesions
tules, and/or nodules, depending on the (Figure 1).19,21 When
degree of inflammation expressed within comparisons of ser-
individually affected pilosebaceous units.10 um hormones were
The type and depth of inflammation also made in girls be-
Figure 1. Facial acne vulgaris in an 11-year-old girl: Multiple closed comedos
plays a role in the formation of acne scars.5,14 tween groups with with scattered superficial inflammatory papules
and without acne,
Sebum Production and Acne there were no differences in estradiol, total A study of young premenarchal girls
The sebaceous gland is primarily con- or free testosterone, sex hormone binding revealed that the most common locations
trolled by hormonal stimulation, which is globulin (SHBG), progesterone, or the ratio for acne in this age group were mid-fore-
primarily androgenic. Sebaceous gland of testosterone to estradiol.9,19 However, head, nose, and chin, with such findings
stimulation is elevated in the first six there was a statistically significant eleva- also noted in boys.23 Other studies have
months of life, then decreases and remains tion of DHEAS in young girls who exhibit- shown that early adolescent boys exhibit-
stable throughout childhood until ed inflammatory or comedonal acne.9,19 ed initial acne lesions correlating with
adrenarche.5 The sebaceous gland acts as Some studies have also shown that DHEAS advancing maturation with predominance
an independent endocrine organ in and testosterone levels were above the 90th in the midfacial region.23
response to changes in androgens and hor- percentile in 29 and 28 percent, respective-
mones.3 P. acnes begins to colonize pilose- ly, of girls with severe comedonal acne, with Clinical Presentation
baceous follicles as a normal inhabitant 20 percent demonstrating low SHBG.10 It is essential to have in mind a method
following an increase in sebum production DHEAS levels were shown to correlate to categorize clinical presentations of acne
that accompanies adrenarche.10 Since the directly with the initiation of acne in young because effective treatment depends on
organism uses sebum as a nutrient for girls.21 In one study, 71.3 percent of prepu- the severity and location of acne lesions.
growth, colonization tends to correlate bertal girls had acne and significantly high- There are noninflammatory acne lesions,
with the concentration of triglycerides in er serum levels of DHEAS.21 Despite the which are both open and closed come-
sebum.12,15 Sebum peaks during adoles- overall correlation of higher DHEAS levels dones. Closed comedones, or whiteheads,
cence and begins to decrease after the age with initiation and severity of acne, meas- are typically small, skin-colored papules
of 20.16–18 Acne severity typically correlates urement of DHEAS levels in an individual with no follicular opening and no associat-
with rates of sebum secretion.3,6,7 patient is not practical for predicting the ed erythema.5 Open comedones, or black-
Androgens also have an influence on follic- severity of acne in that patient. heads, are dilated follicular outlets con-
ular corneocytes.3 Hormonal effects on Measurement of serum androgen levels are taining black debris (due to oxidation of
sebum secretion are key to the production warranted only when there is suspicion of superficial follicular contents).5 Inflam-
of acne.5 Androgen receptors are found in an underlying hormonal disorder, such as matory lesions are believed to originate as
the cells of the basal layer of the sebaceous congenital adrenal hyperplasia, polycystic comedonal lesions that transform into
gland and are responsive to testosterone ovarian disease, or tumor.2,5,7,9 papules or pustules.5 With progression of
and dihydrotestosterone, the most potent inflammation, lesions become more
androgen.5 Adrenarche and Acne indurated and tender with nodules devel-
The prevalence and severity of acne can oping especially after spillage of contents
Hormonal Relationship To Acne be correlated with stages of sexual maturi- around some follicles.5 Acne lesions ulti-
Lesion Development ty.21–23 One of the predictors of severe facial mately resolve over time, leaving behind
Adrenarche is characterized by a rise of acne seems to be the presence of acne itself normal skin, dyspigmentation, or perma-
adrenal androgens and the appearance of in earlier years of life.9,19,20 In one study, the nent scarring.5
secondary sexual characteristics.2,5,7,9 De- mean lesion counts of acne were higher in
hydroepiandrostenedione sulfate (DHEAS) girls who would later have severe disease Treatment Options for Acne in
is the adrenal androgen that is among the at ages 9 to 10, and although the degree of Teenage Patients
earliest hormones to rise during puberty.9,19 acne was not always severe early on, it A full discussion on the treatment of
This stage usually occurs around the age of was a reasonably good predictor of future acne in all patient subtypes is beyond the
eight or nine before the appearance of sec- inflammatory lesions.19 The comedonal scope of this review. The following recom-
ondary sexual characteristics, with the type of acne can also be the first sign of mendations refer primarily to manage-
adrenal glands beginning to produce pubertal maturation in girls, even preced- ment of facial acne vulgaris in teenage
increasing amounts of DHEAS.9,19,20 ing pubic hair and areolar development.21 patients and are based on literature
5
Dermatology Therapeutic Update
An informational newsletter for pediatricians
review and the clinical such cases, topical combination therapy is
experience of the lead considered the standard of care as multi-
author (JDR).1,2,5,7,9–12 ple mechanisms of action are incorporated
Reasonable expecta- into the regimen (Figure 3).1,2,13 A benzoyl
tions. It is important to peroxide (BP)-clindamycin gel (Duac,
emphasize that there is no Acanya, Benzaclin) or BP gel or cream
available treatment that (NeoBenz Micro) in the morning, and a
cures acne. However, ration- topical retinoid, such as adapalene
ally selected therapy cou- (Differin), tretinoin (Retin-A Micro,
pled with strict adherence Atralin), or tazarotene (Tazorac), at night
to the regimen can achieve may be used.1,2,13 For acne vulgaris, topical
reasonable control of future clindamycin (Cleocin T, Evoclin,
outbreaks by reducing the Clindagel) has proven to be superior to
number and intensity of erythromycin based on evaluation of data
acne lesions. It is not rea- from several studies.26,27 In cases that also
sonable to expect complete present with truncal acne, a BP liquid
clearance of acne, although (Brevoxyl Creamy Wash, NeoBenz Micro
it sometimes occurs.1,2,5,7,11 Wash) or cloth cleanser (Triaz Foaming
With initiation of an acne Cloths) may be used on both the face and
treatment regimen, based trunk instead of the “leave-on” BP-con-
on available data, it is rea- taining gel or cream. Another alternative
sonable to expect a 50- to that may be used in combination with top-
Figure 2. Facial acne vulgaris in a 15-year-old girl: Multiple superficial
60-percent reduction in ical retinoid therapy is dapsone 5% gel
inflammatory papules, pustules, and comedos.
acne lesions over a dura- (Aczone) twice daily. If after an adequate
tion of 12 weeks of thera- 8- to 12-week trial of topical combination
py.24 Additionally, postin- therapy there is persistent development
flammatory hyperpigmen- of new active acne lesions, an adjustment
tation or postinflammatory in therapy may be needed. If a significant
erythema are common number of inflammatory acne lesions is
sequelae after resolution of observed, the addition of an oral antibiot-
acne lesions in individuals ic (e.g., doxycycline [Doryx, Adoxa],
with dark skin and light extended-release minocycline [Solodyn])
skin, respectively. These may be warranted.28
dys-chromic changes may Presence of deep inflammatory acne
take months to resolve and lesions. In the presence of multiple, deeper,
do not reflect active acne. inflammatory lesions, including larger/deep-
Adjunctive skin care. er papules, pustules, and/or nodules, the
It is important that severity is then considered to be moderate-
patients treated for acne to-severe to severe acne (Figure 4). In such
Figure 3. Combination topical therapy. Multiple mechanisms of action
incorporated into the treatment regimen. consistently use adjunctive cases, topical therapy alone is not likely to be
gentle skin care, including a effective. Use of topical combination therapy
gentle cleanser and mois- and an oral antibiotic agent is a reasonable
turizer. Such skin care prac- starting point, with 8 to 12 weeks represent-
tices reduce signs and ing an adequate therapeutic trial.2,28 In
symptoms of cutaneous irri- refractory cases, or in cases characterized up
tation often associated with front as severe, deep, inflammatory acne
use of many topical acne with scarring, referral for oral isotretinoin is
medications, including ben- a rational consideration.
zoyl peroxide and topical Oral contraceptive therapy. Oral
ret-inoids (e.g., tretinoin, contraceptives (OCs) may be helpful
adapalene, tazarotene).25 adjunctively in the management of acne;
Superficial acne however, their efficacy is variable in the
lesions. Many preadoles- teenage population.2 In fact, clinicians tend
cent or early teenage to encounter those acne cases that have not
patients present with pre- adequately responded to OC monotherapy.
dominantly comedonal acne Teenage girls with acne responsive to OC
involving the midface. In use do not seek treatment for acne as they
such cases, a topical have responded adequately. The use of OCs
retinoid once daily may be for acne treatment may be combined with
used as monotherapy. other conventional topical and systemic
However, most patients in approaches to acne therapy.
their early teens present
with a combination of Conclusion
Figure 4. Facial acne vulgaris in a 16-year-old girl: Multiple deep and
superficial inflammatory papules, pustules, and comedos. comedos and superficial Acne is a common disorder that fre-
inflammatory papules and/ quently begins in preadolescence or ado-
or pustules (Figure 2). In lescence. Therefore, it is common for pedi-
6
Dermatology Therapeutic Update
An informational newsletter for pediatricians
atricians to be asked about the appropri- 11. Leyden JJ. Therapy for acne vulgaris. N Engl
ate management of acne. As most cases of J Med. 1997;336:1156.
acne present as mild or moderate in sever- 12. Webster GF. Acne. Curr Probl Dermatol.
ity, combination topical therapy is effec- 1996;8:237. MATRIX MEDICAL COMMUNICATIONS
tive in many cases. A reasonable therapeu- 13. Leyden JJ, McGinley KJ, Mills OH, et al.
publisher of
tic trial is 8 to 12 weeks, assuming ade- Propionibacterium acnes levels in patients
quate adherence. In some cases of greater with and without acne vulgaris. J Invest
severity, or when acne is persistent or Dermatol. 1975;65:382–384.
refractory despite an adequate trial of 14. Holland DB, Jeremy AH, Roberts SG, et al.
treatment, consultation with a dermatolo- Inflammation in acne scarring: a comparison PRESIDENT
gist may be indicated. Studies of young of the responses in lesions from patients prone Robert L. Dougherty
girls with acne lesions showed that serum and not prone to scar. Br J Dermatol.
rdougherty@matrixmedcom.com
levels of DHEAS are important in the ini- 2004;150:72–81.
tiation of acne lesions in preteens and 15. McGinley KJ, Webster GF, Ruggieri MR, et al. PARTNER
early teens. Early initiation of therapy for Regional variations in density of cutaneous Patrick D. Scullin
acne helps to prevent the sequelae of dys- Propionibacteria: correlation of Propioni- pscullin@matrixmedcom.com
pigmentation and scarring that is often bacterium acnes populations with sebaceous VICE PRESIDENT, PUBLISHER
irreversible and costly to treat later in life. secretion. J Clin Microbiol. 1980;12:672. Joseph J. Morris
If the presence of early comedonal lesions 16. Pochi PE, Strauss JS. Endocrinologic control of
jmorris@matrixmedcom.com
is a reasonably reliable best predictor of the development and activity of the human seba-
future acne severity, then awareness and ceous gland. J Invest Dermatol. 1974;62:191. VICE PRESIDENT, EDITORIAL DIRECTOR
intervention in preadolescent children 17. Pochi PE, Strauss JS. Sebaceous gland Elizabeth A. Klumpp
may ultimately alter the course of inflam- response in man to the administration of testos- eklumpp@matrixmedcom.com
matory acne throughout the teenage terone, Delta-androstenedione and dehy- EXECUTIVE EDITOR
years. In such cases, treatment can be ini- droisoandrosterone. J Invest Dermatol. Kimberly B. Chesky
tiated early and adjusted appropriately 1969;52:32.
kchesky@matrixmedcom.com
over time as acne severity progresses. 18. Rothman KF, Lucky AW. Acne vulgaris. Adv
Simply stated, it is easier to keep the Dermatol. 1993;8:347. ASSISTANT EDITOR
horse inside the fences of the corral, than 19. Lucky AW, Biro FM, Simbartl LA, et al. Angela M. Hayes
to try and catch the horse once he escapes Predictors of severity of acne vulgaris in ahayes@matrixmedcom.com
and runs free! young adolescent girls: results of a five year CLASSIFIED SALES MANAGER
longitudinal study. J of Pediatrics. 1997;130:1. Melanie A. Wolfrom
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mwolfrom@matrixmedcom.com
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1998;196:108–115. 1991:127;210. 1595 Paoli Pike, Suite 103
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Toll-free: (866) 325-9907
Prevalence of facial acne in adults. J Am Acad impact of vehicle technology using a patented Fax: (484) 266-0726
Dermatol. 1999;41:577–580. formulation of benzoyl peroxide 5%/clin-
5. Bolognia JL, Jorizzo JL, Rapini RP, et al. damycin 1% gel: comparative assessments of
Copyright © 2009 Matrix Medical
Dermatology. 2nd ed. Spain: Elsevier; 2008. skin tolerability and evaluation of combina- Communications. All rights reserved.
6. Goulden V, McGeown CH, Cunliffe WJ. The tion use with a retinoid. J Drugs Dermatol. Opinions expressed by authors,
contributors, and advertisers are their
familial risk of adult acne: a comparison 2006;5:160–164. own and not necessarily those of Matrix
between first-degree relatives of affected and 25. Subramanyan K. Role of mild cleansing in the Medical Communications, the editorial
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printed herein. The appearance of
Med. 2005;352:1463–1472. with topical antibiotics: lessons learned from advertisements in this journal is not a
8. Kellet SC, Gawkrodger DJ. The psychological clinical studies. Br J Dermatol. warranty, endorsement, or approval of the
products or services advertised or of their
and emotional impact of acne and the effect of 2005;153:395–403. effectiveness, quality, or safety. Matrix
treatment with isotretinoin. Br J Dermatol. 27. Del Rosso JQ, Kim GK. Topical antibiotics: Medical Communications disclaims
1999;140:273–282. therapeutic value or ecologic mischief? responsibility for any injury to persons or
property resulting from any ideas or
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