Professional Documents
Culture Documents
Contents
Abstract. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
1. Diagnostic Criteria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234
2. Causative Agents. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234
2.1 Hormones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234
2.1.1 Corticosteroids and Corticotropin (ACTH) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234
2.1.2 Androgens and Anabolic Steroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235
2.1.3 Hormonal Contraceptives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 235
2.1.4 Other Hormones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 236
2.2 Neuropsychotherapeutic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 236
2.2.1 Tricyclic Antidepressants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 236
2.2.2 Lithium . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
2.2.3 Antiepileptic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
2.2.4 Aripiprazole . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
2.2.5 Selective Serotonin Reuptake Inhibitors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
2.3 Vitamins B1, B6, and B12 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
2.4 Cytostatic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
2.4.1 Dactinomycin (Actinomycin D) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
2.4.2 Other Cytostatic Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
2.5 Immunomodulating Molecules . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
2.5.1 Cyclosporine (Ciclosporin) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
2.5.2 Sirolimus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
2.5.3 Other Immunosuppressants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
2.6 Antituberculosis Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
2.6.1 Isoniazid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
2.6.2 Rifampin (Rifampicin). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
2.6.3 Ethionamide . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
2.7 Halogens. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 238
2.7.1 Iodine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
2.7.2 Bromine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
2.7.3 Chlorine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 239
2.7.4 Other Agents. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240
2.8 Miscellaneous Drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240
2.9 Targeted Therapies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241
3. Conclusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 242
Abstract Drug-induced acne is a specific subset of acne that usually has some specific features, namely a mono-
morphic pattern, an unusual location of the lesions beyond the seborrheic areas, an unusual age of onset,
a resistance to conventional acne therapy and, of course, the notion of a recent drug introduction. Many
drugs can be responsible for such a clinical pattern. Corticosteroids, neuropsychotherapeutic drugs,
234 Du-Thanh et al.
antituberculosis drugs, and immunomodulating molecules are the more classical drugs associated with
induced acne. Recently, new drugs, mainly targeted therapy in the field of oncology, such as epidermal
growth factor receptor inhibitors, have been associated with an increased frequency of this adverse effect.
Disruption of the culprit drug is rarely mandatory in cases of drug-induced acne. Close cooperation between
the dermatologist and medical staff in charge of the patient is an important challenge to achieve optimal
management of the initial disease.
Acne is defined as a chronic disease of the pilosebaceous Table I. ‘Old’ and ‘new’ drugs involved in acneiform eruptions
follicle and is a frequent motive for referral in dermatology. Hormones
Whereas hormone-dependent juvenile acne is the more frequent Local and systemic corticosteroids
subset, some cases are related to a specific etiology especially
Corticotropin (ACTH)
during adulthood, including mechanical and drug-induced acne,
Androgens and anabolic steroids
with the latter being defined by the occurrence of an acne-like
Hormonal contraceptives
eruption arising after medication intake. Numerous drugs have
Other hormones (thyroid-stimulating hormone, danazol)
been classically involved or at least associated with this subset
Neuropsychotherapeutic drugs
of acne. The development of new molecules, especially among
Tricyclic antidepressants (amineptine, maprotiline, imipramine)
the so-called targeted therapies in the field of oncology, has also
been associated with an increased observation of such adverse Lithium
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Drug-Induced Acneiform Eruption 235
Table I. Contd treated group. Some boys developed severe papulopustular and
Targeted therapies nodulocystic acne, including four cases of acne fulminans. Acne
EGF inhibitors appeared on the face and the trunk from 1 week to 2 months
cetuximab, panitumumab after initiation of androgen injections.[11]
Multitargeted tyrosine kinase inhibitors Acne in young men should prompt the clinician to look for
gefitinib, erlotinib, lapatinib any anabolic androgenic steroid (AAS) intake in the context of
sorafenib, sunitinib fitness/body building practice (‘body building acne’) or any
imatinib another sport (‘doping acne’).[12-14] Indeed, approximately 50%
VEGF inhibitor: bevacizumab
of AAS abusers present with acne. Clinical presentation ranges
Proteasome inhibitor: bortezomib
from exacerbation of seborrhea to papulopustules, acne con-
globata, or acne fulminans.[13] Acne may have appeared de novo
TNFa inhibitors
or pre-existing acne may be found while taking the medical
lenalidomide
history. Furthermore, acne may be more difficult to treat if
infliximab
AASs are being taken. Concomitant vitamin abuse (vitamin B6
Histone deacetylase inhibitor: vorinostat
and B12) should also be considered as it may also potentially
EGF = epidermal growth factor; TNFa = tumor necrosis factor-a;
trigger acne (see section 2.3). Other symptoms that suggest AAS
VEGF = vascular endothelial growth factor.
abuse include gynecomastia, striae, edema, increased body
mass index, and a decrease in testicular volume. Treatment is
intake,[6] and even after inhaled administration.[7,8] Acne has the immediate withdrawal of AAS followed by conventional
also been reported after treatment with corticotropin.[3,9] The management of acne.[13]
eruption begins after a variable delay, from shortly after the
introduction of topical or oral therapy (usually 2–4 weeks) to 2.1.3 Hormonal Contraceptives
several months. Dosage, duration of administration, and in- Hormonal contraceptives can worsen pre-existing acne
dividual susceptibility play a role in the clinical presentation. or induce it. The molecules responsible for such effects are
The clinical pattern is classically a monomorphic eruption of
small, flesh-colored or pink-to-red, dome-shaped inflamma-
Table II. Characteristics supporting a relationship between drug introduction
tory papules and pustules of the seborrheic areas (face, trunk),
and acneiform eruption
and a potential extension to the upper extremities (figure 1 and
Anamnesis
figure 2). After this initial phase, the inflammatory papules
1. Unusual age of onset: before or after teenage and early adulthood
resolve, while closed and open comedones or small keratin cysts
(aged >30 years)
appear on the same areas several months later. If corticosteroid
2. Abrupt onset of acne in the absence of past history of acne vulgaris
dosage is low, the eruption may consist only of comedones.
or
Inhaled and topically applied corticosteroids may be respon-
sible for perioral dermatitis, which often occurs in patients re- Unusual severity of an acne flare in a patient with a past history of ‘classic’
mild acne vulgaris
ceiving excessive doses or very protracted treatment (2–18 years’
or
duration).[7,8,10]
Aggravation of pre-existing acne
Clinical presentation of acne
2.1.2 Androgens and Anabolic Steroids
1. Monomorphic, inflammatory clinical pattern of the lesions
The effect of androgens on sebaceous glands is responsible
2. Lack of comedones and cysts or their late appearance secondary to
for the development of adolescent acne. Therefore, any androgens
inflammatory lesions
or anabolic steroids with androgenic activity will inevitably
3. Unusual localization of acne: extension beyond the seborrheic area,
affect sebaceous glands because of their structural analogy with
such as the arms, trunk, lower back, and genitalia
endogenous androgens. Fyrand et al.[11] performed a com-
Resistance to conventional acne therapy
parative, retrospective study in 176 Norwegian boys (mean age
Time relationship
14 years), 90 of them having being treated with an injectable
1. Delay of onset after recent drug implementation
testosterone blend for premature closure of epiphysial growth
2. Improvement after drug withdrawal
zones, and a prospective study in 23 boys over a 24-month
3. Recurrence after drug reintroduction
period. They observed a clear increase in acne incidence in the
ª 2011 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2011; 12 (4)
236 Du-Thanh et al.
Amineptine
In 1988, Thioly-Bensoussan et al.[22] published striking ob-
servations of a new subset of drug-induced acne after amineptine
intake. Rapidly, a large number of similar cases were reported
in 1988 during the French Congress of Dermatology.[22-26]
Since then, over 30 cases have been reported.[27-34] Amineptine
is a non-halogenated tricyclic antidepressant that was widely
used before its withdrawal in January 1999 because of the
high level of severe adverse events in France. Patients with
amineptine-induced acne presented with some characteristic Fig. 2. Corticosteroid acne: widespread inflammatory papules on the back.
ª 2011 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2011; 12 (4)
Drug-Induced Acneiform Eruption 237
surgical removal of macrocysts, and treatment with isotretinoin and antagonist at the 5-HT2A receptors. An Indian patient
(0.5–1 mg/kg/day). developed a papulopustular eruption on the forehead and nasal
bridge 10 days after initiation of aripiprazole. Drug withdrawal
Maprotiline and local treatment allowed complete resolution of skin
Maprotiline is also a tricyclic antidepressant. Only one case symptoms within 10 days.[50]
of induced acne has been described with this molecule.[35]
ª 2011 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2011; 12 (4)
238 Du-Thanh et al.
ª 2011 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2011; 12 (4)
Drug-Induced Acneiform Eruption 239
2.7.2 Bromine
Bromoderma, defined as a skin eruption occurring in the
context of bromide intoxication, is infrequent nowadays.[98-101]
However, some drugs containing bromide are still available and
used for their sedative, antiepileptic, spasmolytic, and ex-
pectorant properties.[101] Moreover, some preparations are also
available as non-prescription compounds on the French mar-
ket.[100] The clinical cutaneous presentation is rather similar to
iododerma. Bromide intoxication is also responsible for hy-
perpigmentation, photosensitivity, and macular eruption.[98]
Fig. 3. Inflammatory papules and pustules on the nose during erlotinib Diagnosis is confirmed by an elevated bromide level in serum
treatment for metastatic non-small-cell lung carcinoma.
and urine.[98,100] Withdrawal of the culprit drug and conven-
tional acne treatments resolve the cutaneous symptoms.
violaceous and inflammatory nodules,[80] or sometimes as veg-
etating or bullous lesions, occasionally mimicking pyoderma 2.7.3 Chlorine
gangrenosum or ecthyma. Lesions may sometimes present only Chloracne was first described in 1899 by Herxheimer.[102] It
as severe inflammatory acne of the face and trunk. However, is defined as an acneiform eruption secondary to a systemic
lesions may occur on any part of the body and are not specif- toxicity of exogenous exposure to polyhalogenated aromatic
ically located on sebaceous areas. hydrocarbons (dioxins, naphthalenes, biphenyls, dibenzofurans,
azobenzenes, and azoxybenzenes).[103] Exposure to chloracnegens
2.7.1 Iodine may be due to occupational exposure,[104] or to non-occupational
Iododerma refers to the wide range of skin eruptions that exposures to local environmental contamination[105] or environ-
occur as a consequence of oral, parenteral, or topical iodine mental hazards such as the Seveso accident.[103] Exposure may
administration. It has been reported extensively in the literature also be familial or even as a result of a poisoning attempt.
since 1854.[81-97] The lesions may present as papules, vesicles, The clinical presentation is rather different from acne vul-
and pustules but also as erythematous, urticarial, furuncular, garis and other halogenodermas. Patients present with come-
carbuncular, bullous, and sterile vegetating lesions that may dones on the face, the malar crescent especially, and the
ulcerate. Lesions appear on the seborrheic regions (face, neck, retroauricular folds but also on the forearms, back, chest, lower
and back), but they may be more widespread and involve the
whole body.[85] Iododermas occur mostly in patients with renal
insufficiency as iodine is cleared by the kidneys. They have been
reported after various situations including intravenous injection
of iodinated contrast medium,[89] cardiac catheterization,[93]
urography,[84] lymphography,[85] iodized salt consumption,[82]
potassium iodide intake for thyroid protection,[86] and amio-
darone intake.[92] Histology shows a dense inflammatory in-
filtrate composed of neutrophils and eosinophils in the dermis.
In long-standing lesions, pseudoepitheliomatous hyperplasia
develops with epidermal abscesses.[86,93] Iodine serum levels are
above the normal range. Discontinuation of iodine intake is
sufficient to improve the patient’s symptoms, but local or systemic
corticosteroids may be necessary. The pathogenesis of iododerma
remains unclear. Various hypotheses have been suggested as Fig. 4. Papulopustular lesions on the seborrheic areas of the face during
follows: cell-mediated immune reaction, inflammatory mech- gefitinib treatment.
ª 2011 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2011; 12 (4)
240 Du-Thanh et al.
ª 2011 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2011; 12 (4)
Drug-Induced Acneiform Eruption 241
Table III. National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events, version 4.03[122]
NCI grade Grade 1 Grade 2 Grade 3 Grade 4 Grade 5
Criteria for rash Papules and/or pustules Papules and/or pustules Papules and/or pustules Papules and/or pustules Death
acneiform covering <10% BSA, which covering 10-30% BSA, which covering >30% BSA, which covering any % BSA, which
may or may not be may or may not be associated may or may not be may or may not be
associated with symptoms with symptoms of pruritus or associated with symptoms associated with symptoms
of pruritus or tenderness tenderness; associated with of pruritus or tenderness; of pruritus or tenderness
psychosocial impact; limiting limiting self-care ADL; and are associated with
instrumental ADL associated with local extensive superinfection
superinfection with oral with IV antibacterials
antibacterials indicated indicated; life-threatening
consequences
Suggested Cosmetics Topical antibacterials: erythromycin, clindamycin, If treatment fails, decrease
management metronidazole, or benzoyl peroxide dosage or interrupt
Oral doxycyline 100 mg/d for 4 wk + topical corticosteroids for treatment of causative drug
5 d/wk
ADL = activities of daily living; BSA = body surface area; IV = intravenous.
ª 2011 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2011; 12 (4)
242 Du-Thanh et al.
figure 6). Histologically, the lesions display a poorly specific munobiologic drug adverse effects proposed by Pichler.[125]
neutrophilic folliculitis along with perifolliculitis (figure 7),[117,118] There are EGFRs on keratinocytes that could become involved
while no bacterial infection is detected on skin swabs. with apoptosis, forming vesicles and then pustules.[126]
The National Cancer Institute established Common Terminol- Acne has also been reported in association with other newer
ogy Criteria for Adverse Events (CTCAE) version 4.03, which targeted therapies, although the incidence and severity seem less
includes criteria for grading acneiform rash (table III).[122] Both important so far than with the EGFRIs (table IV). Interestingly,
incidence and severity of rash seem dose dependent. Treatment not all drugs from this family appear to be responsible for acnei-
depends on the severity grading and guidelines have been es- form eruption. For instance, among the tumor necrosis factor-a
tablished. Tetracyclines are used to control severe lesions in antagonists, only infliximab has been reported to cause acne thus
association with topical corticosteroids, but their efficiency is far. Lenalidomide, derived from thalidomide, has major anti-
sometimes limited. In a randomized, double-blind trial, oral tumor necrosis factor-a activity and has been described to be
minocycline appears useful in an attempt to decrease the severity responsible for an acneiform rash by Michot et al.[133]
of the eruption during the first month of treatment, whereas
tazarotene is not recommended.[123] The CYTAR study showed 3. Conclusions
that preventive treatment with oral doxycyline 100 mg/day
during erlotinib treatment for non-small-cell bronchopulmon- Drug-induced acne is a frequent adverse effect. The increased
ary cancer did not decrease the incidence of acneiform rash but use of new targeted therapies in oncologic patients has been
reduced its severity grade and did not influence the efficacy of associated with an increased incidence of acneiform eruption.
erlotinib.[124] Medical history data may provide clues as to the potential role
The underlying pathophysiologic mechanisms remain un- of a newly introduced drug in the development of these erup-
clear, but the major tropism of EGFRIs for the skin and skin tions, as do unusual clinical features, i.e. high age at onset,
appendages is obvious. This rash is a d-type adverse effect atypical location, resistance to conventional therapy, and a
(cross reaction) according to the classification of the im- monomorphic clinical pattern. Moreover, some drug-related
ª 2011 Adis Data Information BV. All rights reserved. Am J Clin Dermatol 2011; 12 (4)
Drug-Induced Acneiform Eruption 243
eruptions are erroneously called induced ‘acne’; however, the 20. Ilse JR, Greenberg HL, Bennett DD. Levonorgestrel-releasing intrauterine
system and new-onset acne [letter]. Cutis 2008; 82: 158
lack of comedones does not favor such a designation. There-
21. Greenberg RD. Acne vulgaris associated with antigonadotropic (Danazol)
fore, the terms ‘acneiform eruption’ or ‘induced folliculitis’
therapy. Cutis 1979; 24: 431-3
should probably be considered instead. 22. Thioly-Bensoussan D, Charpentier A, Triller R, et al. Iatrogenic acne caused
Preventing drug-induced acne is often challenging. The main by amineptin (Survector): apropos of 8 cases. Ann Dermatol Venereol 1988;
issue in management remains whether the culprit drug should 115: 1177-80
23. Grupper C. New iatrogenic acne: acne caused by amineptin (Survector). Ann
be withdrawn. Direct discussion with the medical staff in charge
Dermatol Venereol 1988; 115: 1174-6
of the patient is mandatory in making this decision. 24. Vexiau P, Gourmel B, Husson C, et al. Severe lesions of acne type induced by
chronic amineptin poisoning: apropos of 6 cases. Ann Dermatol Venereol
1988; 115: 1180-2
Acknowledgments
25. Teillac D, Weber MJ, Lowenstein W, et al. Acne caused by Survector [in
French]. Ann Dermatol Venereol 1988; 115: 1183-4
No funding sources or financial disclosures/conflicts of interest to report.
Aurélie Du-Thanh and Nicolas Kluger contributed equally to this work. 26. Lévigne V, Faisant M, Mourier CG, et al. Monstrous acne in the adult: inducer
role of Survector? Ann Dermatol Venereol 1988; 115: 1184-5
27. Vexiau P, Gourmel B, Julien R, et al. Severe acne-like lesions caused by
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