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Acne vulgaris: Overview of management

Acne vulgaris: Overview of management
Literature review current through: Jan 2024.
This topic last updated: Feb 23, 2023.

INTRODUCTION — Acne vulgaris is a common cutaneous disorder that can have a profound psychologic impact, contributing to low self-esteem, depression, and anxiety (picture 1A-E) [1-3]. As a result, there is a significant demand for effective acne therapies.

There are numerous treatments for acne vulgaris, including topical, oral, and procedural therapies (table 1). The clinical presentation and patient preferences strongly influence the selection of therapy (algorithm 1A-B).

General concepts related to the management of acne vulgaris and the approach to the treatment of mild acne vulgaris in adolescents and adults are discussed here. The approach to the treatment of moderate to severe acne vulgaris; the diagnosis and management of acne in infants, young children, and preadolescents; and other concepts related to the diagnosis and management of acne vulgaris and acne scarring are reviewed in detail separately.

(See "Acne vulgaris: Management of moderate to severe acne in adolescents and adults".)

(See "Acne in infants, young children, and preadolescents".)

(See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris".)

(See "Oral isotretinoin therapy for acne vulgaris".)

(See "Postadolescent acne in women".)

(See "Light-based, adjunctive, and other therapies for acne vulgaris".)

(See "Management of acne scars".)

TREATMENT PRINCIPLES — Interventions for acne vulgaris consist of a wide variety of topical, oral, and procedural therapies aimed at combatting key aspects of the pathogenic mechanisms of acne lesion formation (figure 1). (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Pathogenesis'.)

Examples of therapeutic targets and associated common therapies include [4]:

Follicular hyperproliferation and abnormal desquamation:

Topical retinoids

Oral isotretinoin

Azelaic acid

Salicylic acid

Increased sebum production:

Oral isotretinoin

Oral contraceptives

Spironolactone

Clascoterone

Cutibacterium (formerly Propionibacterium) acnes proliferation:

Benzoyl peroxide

Topical and oral antibiotics

Azelaic acid

Inflammation:

Oral isotretinoin

Oral tetracyclines

Topical retinoids

Azelaic acid

Topical dapsone

In addition, the procedural therapies used as adjunctive therapies for acne vulgaris target one or more contributory factors. The mechanisms of these interventions are reviewed separately. (See "Light-based, adjunctive, and other therapies for acne vulgaris".)

PRETREATMENT ASSESSMENT — A careful pretreatment assessment is essential for selecting an appropriate treatment plan. In particular, the assessment should include evaluation for:

Acne lesion types – Comedones and/or inflammatory papules, pustules, or nodules (picture 1A-E)

Acne severity – Distribution and degree of skin involvement (table 2)

Presence of complications – Postinflammatory hyperpigmentation, postinflammatory erythema, scarring, psychologic distress (picture 2A-C)

Potential contributing factors – Comedogenic skin care products, acne-inducing medications, signs or symptoms of endocrinologic disorders associated with acne vulgaris (see 'Skin care' below and "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Associated diseases')

The assessment of the types of acne lesions present assists with treatment selection (algorithm 1A). For example, treatment with a topical retinoid alone may be sufficient for mild comedonal acne vulgaris. Patients with inflammatory papulopustular acne vulgaris may benefit from the addition of antimicrobial and anti-inflammatory therapies [5]. (See 'Approach to treatment' below.)

An assessment of the severity and complications of acne vulgaris helps to guide the aggressiveness of treatment. In patients with mild acne vulgaris, a more aggressive approach that incorporates systemic therapy is typically reserved for acne that is refractory to topical therapy; associated with scarring, disfiguring postinflammatory hyperpigmentation, or erythema; or causing significant psychologic distress (algorithm 1A). In contrast, systemic therapy is commonly prescribed for the initial treatment of moderate to severe acne vulgaris. (See 'Scarring, postinflammatory hyperpigmentation, or postinflammatory erythema' below and "Acne vulgaris: Management of moderate to severe acne in adolescents and adults".)

Assessing the severity of acne vulgaris can be challenging. There is no universally accepted grading system [5]. We consider the following a reasonable approach for classifying severity:

Mild acne vulgaris (picture 1B-C):

Scattered, small (<5 mm), comedonal or inflamed papules or pustules without associated scarring

Limited skin involvement (involvement of one body area or relatively few lesions in more than one body area)

Absence of nodules

Absence of near confluent skin involvement

Moderate to severe acne vulgaris (picture 1D-F, 2C):

Visually prominent acne consisting of many comedonal or inflamed papules or pustules

Presence of nodules

Involvement of multiple body areas with more than a few, scattered lesions

Associated scarring

The recognition of associated scarring and postinflammatory hyperpigmentation is helpful for electing acne treatments. For example, topical retinoids may inhibit both active acne and some types of scars [6,7]. Azelaic acid can also be beneficial for acne and postinflammatory hyperpigmentation. (See 'Management of complications' below and "Postinflammatory hyperpigmentation", section on 'Second-line therapy'.)

PATIENT COUNSELING — Counseling of patients seeking treatment for acne vulgaris should include a discussion of treatment expectations and skin care. In addition, patients often ask about the impact of dietary changes. (See 'Expectations' below and 'Skin care' below and 'Diet' below.)

Expectations — A discussion of treatment expectations may be helpful for maximizing adherence to treatment.

We aim to discuss the following concepts with all patients:

Improvement is often delayed – Improvement in acne is dependent upon both the resolution of existing lesions and the prevention of new lesion formation. In general, at least two to three months of consistent adherence to a regimen is necessary to assess treatment efficacy, and the initial response may consist of a noticeable reduction (rather than complete clearance) of active acne lesions. Failure to discuss this with patients may contribute to premature discontinuation of treatment due to perceived inefficacy.

Adjustments to the regimen may be needed to identify the most effective regimen – Responses to specific treatments vary. Changes to the treatment regimen to optimize tolerability and efficacy are often needed.

Long-term maintenance treatment is often necessary – Most acne therapies are suppressive and not curative. A long-term maintenance regimen (eg, topical retinoid use) is often necessary to maintain improvement. (See 'Maintenance of response' below.)

Skin care — Providing patients with guidance regarding gentle skin care practices may help promote tolerance of topical acne medications and avoidance of acne-promoting (comedogenic) products. We encourage patients to:

Utilize gentle skin cleansers rather than soaps or scrubs – Gentle skin cleansers (ie, synthetic detergent [syndet] cleansers) possess a pH of 5.5 to 7, which is close to normal skin pH, while soap has a pH of 9 to 10 [8]. The lower pH of syndets minimizes skin irritation and dryness [9-11].

Avoid aggressive scrubbing of the skin – Gentle massage with the fingertips is sufficient for cleansing. Repetitive mechanical trauma may aggravate inflammatory acne and promote the development of new acne lesions [8].

Select noncomedogenic skin care and cosmetic products – Selection of products with labeling that indicates "noncomedogenic" properties or a lower tendency to "block pores" may be helpful, although such labeling is not regulated and may not always be accurate [12].

Avoid picking of acne lesions – Additional skin trauma resulting from picking acne lesions may exacerbate scarring.

Diet — The role of dietary changes in the treatment of acne vulgaris remains uncertain. Associations between acne vulgaris and increased milk consumption and high glycemic load diets have been reported. However, given the absence of randomized trials that confirm a beneficial effect of specific dietary changes, we refrain from recommending specific dietary changes routinely [5]. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Diet'.)

If patients are highly motivated to make dietary changes, we discuss a trial of reducing milk intake. However, nutritional consequences of dietary restrictions (eg, reduced dietary calcium intake) should be considered, and nutritional counseling may be appropriate for patients engaging in long-term dietary restrictions. (See "Bone health and calcium requirements in adolescents".)

SPECIAL POPULATIONS — Certain populations with acne vulgaris require an adjusted approach to treatment. Examples include children, pregnant individuals, and patients with acne scaring, skin of color, severe variants (acne fulminans or acne conglobata), or associated disease.

Scarring, postinflammatory hyperpigmentation, or postinflammatory erythema — Acne scarring can cause permanent disfigurement. Therefore, achieving rapid control of active acne vulgaris is desired for patients with evidence of scarring. We typically manage these patients similarly to patients with more severe acne vulgaris, including consideration of early initiation of systemic therapy. (See "Acne vulgaris: Management of moderate to severe acne in adolescents and adults".)

Although the postinflammatory hyperpigmentation and postinflammatory erythema are not permanent, these features can be disfiguring and can persist for months to years. Similar to patients with scarring, patients with prominent or extensive, postinflammatory hyperpigmentation or postinflammatory erythema may also benefit from early consideration of systemic therapy. (See 'Postinflammatory hyperpigmentation' below and 'Postinflammatory erythema' below.)

Children — Preadolescent acne vulgaris, which results from normal adrenarche and ovarian or testicular maturation in children between the ages of 7 and 11 years, is common and can be treated with various therapies [13]. Acne in younger children (ages one to seven years) should prompt an evaluation for hyperandrogenism. The management of these presentations and infantile acne are reviewed in greater detail separately. (See "Acne in infants, young children, and preadolescents", section on 'Treatment'.)

Preadolescent children (age 7 to 12 years) – The approach to the treatment of acne vulgaris in preadolescent children is similar to the management of adolescents and adults. Exceptions include the need to avoid oral tetracyclines in children up to the age of eight years due to detrimental effects on tooth development and precautions related to the use of systemic hormonal therapy [13]. (See "Acne in infants, young children, and preadolescents", section on 'Preadolescents (children 7 to 12 years)'.)

Although hormonal therapy is a common and effective treatment for acne vulgaris in adolescent and adult females, avoiding treatment of acne vulgaris with oral contraceptives until one year after the onset of menstruation is advised in the absence of other indications for oral contraceptive therapy due to concerns about growth and bone density [13]. We do not use spironolactone for preadolescent acne given that the efficacy and safety of spironolactone for the treatment in this population is unclear.

As in adults, weight-based dosing of oral isotretinoin is an option for preadolescent children with severe, refractory, scarring acne vulgaris. (See "Acne in infants, young children, and preadolescents", section on 'Severe acne' and "Oral isotretinoin therapy for acne vulgaris".)

An additional important consideration for acne therapy in preadolescents and adolescents is the implementation of measures to optimize adherence to therapy. Careful efforts should be made to recognize when the complexity of the regimen, the child or adolescent's dislike of the vehicle prescribed (eg, cream, lotion, gel), or drug side effects inhibit consistent use of acne medication [13].

Discussing adherence to the treatment regimen and obstacles to adherence at each visit allows for therapeutic adjustments that may lead to more consistent treatment and a better clinical response. In addition, thorough, age-appropriate discussions of realistic expectations for treatment may help to prevent premature discontinuation of therapy by a child or adolescent who is discouraged by the lack of an immediate and complete disappearance of acne lesions. (See 'Patient counseling' above.)

Younger children (under seven years) – Acne occurring in young children between the ages of one and seven years (midchildhood acne) may indicate hyperandrogenism. The initial management of these children should include an evaluation for an underlying cause. This should include a complete physical examination looking for signs of precocious puberty. Additional tests may include radiographic assessment of bone age and laboratory testing for endocrinologic abnormalities. (See "Acne in infants, young children, and preadolescents", section on 'Diagnosis' and "Acne in infants, young children, and preadolescents", section on 'Infants and children <7 years'.)

The management of infantile acne is reviewed separately. Neonatal cephalic pustulosis, a condition formerly referred to as neonatal acne, is distinct from acne vulgaris. (See "Vesicular, pustular, and bullous lesions in the newborn and infant", section on 'Infantile acne' and "Vesicular, pustular, and bullous lesions in the newborn and infant", section on 'Neonatal cephalic pustulosis'.)

Skin of color — Patients with moderately to highly pigmented skin (skin phototypes IV through VI) are more likely to develop postinflammatory hyperpigmentation than patients with lower levels of skin pigmentation. Postinflammatory hyperpigmentation may result from both active acne vulgaris and skin irritation related to topical acne treatments. (See "Postinflammatory hyperpigmentation".)

Because of the risk for treatment-induced, postinflammatory hyperpigmentation, treatment selection for patients with skin of color should incorporate consideration of the potential for inducing skin irritation. In regards to topical retinoid therapy, slow titration of the frequency of application at the start of treatment may be helpful in addition to starting with a lower concentration of the selected retinoid [14]. (See 'Topical retinoids' below.)

In our experience, other measures that may be helpful include opting for short-contact therapy, such as selection of a benzoyl peroxide wash rather than gel, and selection of lotion, cream, or other drug formulations designed to minimize skin irritation, when feasible.

Special consideration for patients with acne-induced, postinflammatory hyperpigmentation is reviewed separately. (See 'Postinflammatory hyperpigmentation' below.)

Pregnant individuals — Treatment selection for pregnant individuals with acne vulgaris involves consideration of risk for detrimental effects of therapy on the fetus. Common acne therapies contraindicated for pregnant individuals or individuals attempting to become pregnant include oral isotretinoin and topical tazarotene. In addition, use of other topical retinoids is not recommended during pregnancy [15]. (See 'Topical retinoids' below.)

The decision to treat acne vulgaris in pregnant individuals warrants consideration of the severity of acne, the patient's risk tolerance, and guidance from the patient's obstetrical provider. If acne therapy is desired, reasonable options include oral or topical erythromycin, topical clindamycin, and topical azelaic acid [16,17]. Some experts consider use of benzoyl peroxide on limited skin areas during pregnancy to be safe [15].

Similar to oral tetracyclines, use of topical minocycline is not advised during pregnancy. There are insufficient data for conclusions on the safety of topical clascoterone and topical dapsone during pregnancy; therefore, we typically avoid use of these therapies.

Severe variants — Acne fulminans and acne conglobata are severe clinical presentations of acne vulgaris that may benefit from a distinct approach to therapy. Patients with these variants present with extensive, nodular acne lesions in conjunction with other features. Oral isotretinoin is often the central component of therapy. (See "Acne vulgaris: Management of moderate to severe acne in adolescents and adults", section on 'Approach to severe variants' and "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Acne fulminans' and "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Acne conglobata'.)

Patients with associated diseases — Hyperandrogenism occurring in association with disorders such as polycystic ovarian syndrome, late-onset adrenal hyperplasia, or adrenal or ovarian tumors may contribute to acne vulgaris. Treatment of the underlying disorder may contribute to improvement in acne. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Associated diseases'.)

Rare syndromes associated with acne vulgaris, such as SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome and PAPA (pyogenic sterile arthritis, pyoderma gangrenosum, acne) syndrome, may also require a different approach to therapy. (See "SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome", section on 'Treatment' and "The autoinflammatory diseases: An overview".)

MILD ACNE VULGARIS — Mild acne vulgaris may be considered acne presenting with scattered comedones or small (<5 mm), inflammatory papules without associated scarring (picture 1B-C). Additional qualifying features may include limited skin involvement (involvement of one body area or relatively few lesions in more than one body area), an absence of inflammatory nodules, and an absence of near confluent skin involvement (table 2). (See 'Pretreatment assessment' above.)

Approach to treatment — Topical therapy is the primary mode of treatment for mild acne vulgaris (algorithm 1A). Topical retinoids, benzoyl peroxide (an antimicrobial agent), and topical antibiotics are often utilized for treatment.

Principles — Topical retinoids (eg, tretinoin, adapalene, tazarotene, trifarotene) are beneficial for both comedones (picture 1A, 1C) and inflammatory papules and pustules (picture 3) and should be included in the initial management of most patients (algorithm 1A) [5].

Topical retinoid monotherapy can be sufficient for some patients with exclusively comedonal acne. Patients with inflammatory papulopustular acne may benefit from antimicrobial therapies (eg, benzoyl peroxide or topical antibiotics). Antimicrobial agents reduce the number of proinflammatory C. acnes colonizing the skin. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Cutibacterium acnes and inflammation'.)

A typical initial approach can be summarized as follows:

Mild comedonal acne (picture 4A-B):

Topical retinoid (alternatives include azelaic acid and salicylic acid)

Mild papulopustular and mixed (comedonal and papulopustular) acne (picture 1C, 1G):

Topical retinoid and topical antimicrobial(s) (eg, benzoyl peroxide alone or benzoyl peroxide +/- topical clindamycin)

Or

Benzoyl peroxide and topical antibiotic (for patients who cannot tolerate a retinoid or who require a simplified treatment regimen)

Of note, antibiotics may promote the appearance of antibiotic-resistant strains of C. acnes when used alone. Combining antibiotic therapy with the use of benzoyl peroxide decreases the development of antibiotic resistance and improves treatment efficacy [18-23]. Some experts prefer to initiate topical antimicrobial treatment with benzoyl peroxide alone rather than to routinely incorporate a topical antibiotic because of the potential to promote antibiotic resistance. If used, topical antibiotics should be used in conjunction with topical benzoyl peroxide whenever feasible.

Conscientious selection of the vehicle (eg, gel, cream, lotion, foam, solution, etc) for topical acne medications may help to improve the likelihood of adherence to treatment. The choice depends upon the patient's skin type (dry versus oily) and preference. Some gels have a drying effect and may be preferred by patients with oily skin. Creams and lotions tend to be moisturizing. Solutions are drying but cover large areas, such as the trunk, more easily than other preparations, and foams are easy to apply to hair-bearing areas. Pledgets are single-use absorbent pads impregnated with medication. They are convenient to use and facilitate the spreading of medication over large areas.

Although the treatment of both mild facial and mild truncal acne can be approached similarly, application of topical treatments to the back can be challenging. Often, for mild truncal papulopustular acne vulgaris, we find a benzoyl peroxide wash with or without a topical antibiotic a practical initial approach, provided the patient can apply the medication to the affected area relatively easily (eg, shoulders, chest, upper back). Pharmacy-provided medication applicators designed to aid with application of medications or emollients to the back are sometimes helpful for topical treatment.

Given that topical treatment of truncal acne vulgaris is sometimes challenging, we have a lower threshold for incorporating oral therapies into the treatment regimen.

Sample regimen — A sample regimen for a patient with mild papulopustular facial acne who is using a topical retinoid and benzoyl peroxide is as follows:

Morning – Wash the face with a benzoyl peroxide cleanser. Alternatively, wash the face with a gentle facial cleanser and then apply a thin layer of benzoyl peroxide gel to the entire face.

Night – Wash face with a gentle facial cleanser. Apply a thin layer of the topical retinoid to the entire face.

Some patients prefer the use of fixed-dose combination products to simplify treatment (table 3).

Initial treatment — Topical retinoids and topical antimicrobial agents (benzoyl peroxide, antibiotics) are the mainstays for initial treatment of mild acne vulgaris (algorithm 1A).

Topical retinoids — Topical retinoids (tretinoin, adapalene, tazarotene, trifarotene) are effective in the treatment of comedonal acne due to their ability to normalize follicular hyperkeratosis and prevent formation of the microcomedo, the primary lesion of acne [8]. The efficacy of topical retinoids for inflammatory papulopustular acne may be due to a combination of intrinsic anti-inflammatory properties and prevention of the formation of microcomedones [24,25]:

SelectionTopical tretinoin, adapalene, tazarotene, and trifarotene are all effective for acne vulgaris and are available in a variety of vehicles and concentrations (table 1). Combination gels containing a retinoid and an antimicrobial are also available (table 3).

Adapalene 0.1% gel is the only topical retinoid available without a prescription in the United States. Topical isotretinoin, another topical retinoid, is not available in the United States.

Selection of a topical retinoid is primarily based upon consideration of availability, cost, tolerability, and the patient's vehicle preference (ie, gel, cream, lotion, foam) (see 'Principles' above). Although randomized clinical trials have compared the efficacy and tolerability of topical retinoids, the trials do not definitively support the use of one topical retinoid type over another [26-34]. Interpretation of results is complicated by the availability of various drug concentrations and formulations.

Micronized tretinoin 0.05% gel should be used with caution in patients with a known allergy to fish [35]. The drug contains soluble fish proteins.

Administration – The topical retinoids are applied once daily and traditionally at night due to photolability reported with tretinoin [36]. However, other forms of tretinoin (eg, tretinoin gel microsphere and micronized tretinoin 0.05% in a hydrogel vehicle, tretinoin 0.05% lotion in polymeric emulsion), adapalene, and trifarotene are more light stable [37-41].

Patients should apply a thin layer of the topical retinoid to the entire affected area rather than as a spot treatment to individual lesions. A pea-sized amount of medication is usually sufficient to cover the entire face. Skin should be dry at the time of application.

Approaches to the frequency of application at the start of treatment vary. Treatment may be started slowly to minimize risk for skin irritation (eg, application every other night or every third night), with the goal of progressively increasing to daily use over the course of a few weeks as tolerance improves. Alternatively, patients may begin with daily application and transition to the slower initiation regimen if initial daily use is poorly tolerated. Patients with a history of sensitive skin or skin of color (secondary to increased risk for skin irritation-induced hyperpigmentation) may benefit from the slower initiation of therapy. (See 'Skin of color' above.)

Topical tretinoin should not be applied at the same time as benzoyl peroxide. If both agents are prescribed, benzoyl peroxide should be applied in the morning and tretinoin in the evening. Tretinoin is less stable when exposed to benzoyl peroxide due to oxidation, an effect magnified during light exposure [36,39]. Of note, some newer formulations of tretinoin (eg, tretinoin gel microsphere, micronized tretinoin gel, tretinoin 0.05% lotion in polymeric emulsion) are stable in the presence of benzoyl peroxide. Adapalene, tazarotene, and trifarotene also remain more stable than tretinoin in the presence of benzoyl peroxide [5,26,36-39].

Skin irritation is a common and expected side effect of topical retinoid therapy. Irritation may be minimized by starting with the lowest concentration of a topical retinoid product and then increasing the potency as tolerated (table 1).

A short-contact regimen with tazarotene is an alternative to daily use of tazarotene and can decrease irritation. Patients apply tazarotene for up to five minutes daily, then wash off the medication [42].

Patients should avoid the concomitant use of harsh soaps, toners, astringents, and alpha-hydroxy acid or salicylic acid products in conjunction with topical retinoids to minimize risk for irritation [43]. Clinical experience suggests that delaying application of the retinoid for at least 20 minutes after washing and drying the face may also be helpful for reducing risk for skin irritation. (See 'Skin care' above.)

Efficacy of retinoids alone – Topical retinoids are vitamin A derivatives that act by binding to two nuclear receptor families within keratinocytes: the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs) [44]. Tretinoin, adapalene, and tazarotene target both RAR-beta and RAR-gamma receptors; additionally, tretinoin targets the RAR-alpha receptor. Trifarotene is selective for the RAR-gamma receptor.

The retinoid-receptor complexes are transported into the nucleus, where they activate specific regulatory DNA sequences called retinoid hormone response elements, thereby stimulating the transcription of target genes. These events contribute to the normalization of follicular keratinization and decreased cohesiveness of keratinocytes, resulting in reduced follicular occlusion and microcomedone formation [45].

Multiple randomized trials support the efficacy of topical retinoids in the treatment of acne vulgaris [46-55]. Most high-quality trials have focused on the response of facial acne; efficacy for truncal acne has been demonstrated in trials evaluating trifarotene [56]:

Two 12-week trials (PERFECT 1 [n = 1208] and PERFECT 2 [n = 1212]) in which patients with moderate facial and truncal acne were randomly assigned to once-daily application of either trifarotene 0.005% cream or vehicle found trifarotene an effective treatment [56]. In PERFECT 1 and PERFECT 2, 29 and 42 percent of patients who applied trifarotene achieved treatment success for facial acne (Investigator's Global Assessment rating of clear or almost clear and at least a two-grade change from baseline), respectively, compared with 20 and 26 percent of patients in the vehicle groups. Trifarotene was also effective for truncal acne, demonstrating treatment success in 36 and 43 percent of patients in the PERFECT 1 and PERFECT 2 trifarotene groups, respectively, compared with 25 and 30 percent of patients in the vehicle groups. A 52-week, open-label study (n = 453) suggests efficacy of trifarotene may increase with long-term use [57].

Efficacy of retinoids in conjunction with antimicrobial therapy – Multiple studies comparing monotherapy versus combination therapy with topical retinoids and antimicrobials (erythromycin, clindamycin, or benzoyl peroxide) have demonstrated improved treatment efficacy with combination therapy [58-68]. Representative trials include:

A randomized, controlled trial of 249 patients with mild to moderate acne vulgaris evaluated treatment with adapalene 0.1% gel plus clindamycin 1% lotion versus clindamycin plus vehicle [61]. Significantly greater reductions in total lesions were seen in patients who received combination therapy (46.7 versus 25.5 percent). Improvement was seen in both inflammatory and noninflammatory lesions.

Two 12-week, randomized, controlled trials involving a total of 2219 patients with acne vulgaris compared treatment with a combination hydrogel containing 1% clindamycin and 0.025% tretinoin with one of three treatments: each agent as monotherapy or vehicle [59]. The efficacy of the combination hydrogel was superior to monotherapy and vehicle in the reduction of inflammatory, noninflammatory, and total lesions. The reductions in total lesion counts for the combination hydrogel, clindamycin gel, tretinoin gel, or vehicle were 48.7, 38.3, 40.3, and 23.2 percent, respectively.

A 12-week, randomized, controlled trial with 517 subjects compared treatment of acne vulgaris with an adapalene 0.1% and benzoyl peroxide 2.5% combination gel with monotherapy with each drug and with vehicle [60]. Treatment with the combination gel was more effective, with a significantly greater reduction in total lesion counts noted as early as one week after starting therapy. At the end of treatment, the combination gel, adapalene, benzoyl peroxide, and vehicle groups exhibited 51, 35.4, 35.6, and 31 percent reductions in total lesion counts, respectively.

Adverse effects – Topical retinoids cause irritation, dryness, and flaking of the skin, an effect most notable during the first month of therapy [44].

Fine skin flaking can be gently exfoliated with a washcloth [27]. A noncomedogenic facial moisturizer can be applied if needed.

Topical retinoids are not true photosensitizing drugs, but patients using topical retinoids have described symptoms of increased sun sensitivity. This is thought to be due to thinning of the stratum corneum, leading to a decreased barrier against ultraviolet light exposure, as well as an enhanced sensitivity due to the presence of cutaneous irritation [27]. The use of sun-protective clothing and/or sunscreen is advised, particularly when prolonged sun exposure is anticipated [27].

Topical retinoid therapy is not recommended in pregnancy. A systematic review and meta-analysis did not find significant increases in risk for major congenital abnormalities with first trimester topical retinoid exposure, providing information that may be reassuring for women who have inadvertent topical retinoid exposure during early pregnancy [69]. However, the study was insufficiently powered to conclude that topical retinoid use is safe in pregnancy. There are case reports documenting fetal malformations in infants of women exposed to topical retinoid therapy during pregnancy [70-74]. (See 'Pregnant individuals' above.)

Benzoyl peroxide — Benzoyl peroxide is a topical agent with antibacterial and comedolytic properties:

AdministrationBenzoyl peroxide is available in a variety of vehicles (eg, cleansers, gels, lotions, creams, pads, masks, washes) and concentrations, generally ranging from 2.5 to 10%. Benzoyl peroxide is usually applied once daily. Patients should also be advised that direct contact with benzoyl peroxide can cause bleaching of fabrics or hair.

We typically use lower concentrations (eg, 2.5%) because concentrations higher than 2.5% may not contribute to increased benefit and may be more likely to cause skin irritation [75,76]. In addition, the time required for onset of action for varying concentrations of benzoyl peroxide appears to be similar [76]. Visible improvement typically occurs within three weeks, with maximum results evident after 8 to 12 weeks [5].

There are rare reports of serious and potentially life-threatening hypersensitivity reactions to nonprescription topical acne products containing benzoyl peroxide or salicylic acid [77]. Thus, the US Food and Drug Administration (FDA) recommends limiting application of these products to one or two small, affected areas during the initial three days of use to test for hypersensitivity [77].

Tretinoin and benzoyl peroxide should not be applied simultaneously to the skin due to the oxidizing effect of benzoyl peroxide on tretinoin. If both agents are prescribed, benzoyl peroxide should be applied in the morning and tretinoin in the evening. Adapalene, the microsphere formulation of tretinoin, the polymeric emulsion formulation of tretinoin, tazarotene, and trifarotene are stable in the presence of benzoyl peroxide. (See 'Topical retinoids' above.)

EfficacyC. acnes resistance to benzoyl peroxide has not been identified. In three nonrandomized studies involving a total of 153 patients with acne vulgaris, each comparing two interventions (vehicle versus 2.5% benzoyl peroxide gel, 2.5% versus 5% benzoyl peroxide gel, and 2.5% versus 10% benzoyl peroxide gel), 2.5% benzoyl peroxide was more effective than vehicle and as effective as 5% and 10% benzoyl peroxide in reducing the number of inflammatory acne lesions [75].

Adverse effectsBenzoyl peroxide can cause skin irritation, particularly at higher concentrations. Irritation may appear as erythema, scaling, xerosis, or stinging, tightening, or burning sensations [78]. Temporary orange skin discoloration may occur if applied simultaneously with topical dapsone. (See 'Topical dapsone' below.)

True allergic contact dermatitis to benzoyl peroxide is uncommon. Only 0.25 to 2.5 percent of patients develop a true allergic contact sensitivity [79,80]. Life-threatening hypersensitivity reactions are rare [77].

Topical clindamycin — Topical clindamycin is available in a variety of vehicles, such as a gel, solution, lotion, foam, or as pledgets (antibiotic impregnated wipes (table 1)). Combination gels containing clindamycin combined with benzoyl peroxide or a retinoid are also available (table 3):

Administration – Topical clindamycin is applied once or twice daily. Topical clindamycin should be used in conjunction with benzoyl peroxide. (See 'Benzoyl peroxide' above.)

Efficacy – Combining antibiotic therapy with benzoyl peroxide decreases the development of antibiotic resistance and improves treatment efficacy [18-23]. In an open-label study, the combination of benzoyl peroxide and clindamycin decreased the number of C. acnes found on healthy skin more effectively than clindamycin alone [81].

The clinical efficacy of combination benzoyl peroxide and clindamycin gel was assessed in a meta-analysis of randomized trials [82]. The meta-analysis found that gels containing benzoyl peroxide and clindamycin were modestly more effective than benzoyl peroxide alone for the treatment of inflammatory acne lesions (mean percent reduction in lesions 56 [95% CI 54-58] versus 44 percent [95% CI 41-46] after treatment for 10 to 12 weeks). In addition, treatment with gels containing benzoyl peroxide and clindamycin resulted in more rapid improvement of both inflammatory and noninflammatory lesions than clindamycin alone (mean percentage reductions in lesions were 41 [95% CI 37-44] versus 21 percent [95% CI 17-26] and 26 [95% CI 22-30] versus 10 percent [95% CI 5-15], respectively, after two to four weeks of treatment).

Adverse effects – Topical clindamycin is generally well tolerated. Skin irritation may occur.

Alternative agents — Patients who cannot tolerate topical retinoids may benefit from incorporation of other comedolytic therapies in the treatment regimen. Although topical retinoid therapy is preferred, salicylic acid or azelaic acid can be used in place of retinoids, when needed. Topical erythromycin is an alternative antibiotic agent.

Salicylic acid — Topical salicylic acid is an alternative comedolytic agent that is useful for patients who cannot tolerate or cannot obtain a topical retinoid. In the United States, salicylic acid is available without a prescription. Salicylic acid is discussed in greater detail separately. (See "Light-based, adjunctive, and other therapies for acne vulgaris", section on 'Salicylic acid'.)

Azelaic acid — Azelaic acid is a naturally occurring dicarboxylic acid with antimicrobial, comedolytic, and mild anti-inflammatory properties. Azelaic acid also has an inhibitory effect on tyrosinase and can improve acne-induced, postinflammatory hyperpigmentation.

Azelaic acid is applied twice daily. The product is available in a 15% gel and 20% cream.

Azelaic acid 20% cream is effective for the treatment of both inflammatory and noninflammatory acne and has demonstrated comparable efficacy with tretinoin 0.05% cream, benzoyl peroxide 5% gel, or topical 2% erythromycin for mild to moderate acne vulgaris in clinical studies [83]. The 15% gel is FDA approved only for the treatment of rosacea but is approved for the treatment of acne in many European countries. Two randomized, controlled trials revealed that azelaic acid 15% gel is well tolerated and as effective as 5% benzoyl peroxide gel or 1% clindamycin gel in the treatment of mild to moderate acne vulgaris [84].

Topical erythromycin — Topical erythromycin is an alternative to topical clindamycin; however, concern for higher rates of C. acnes resistance to erythromycin contributes to the preferred use of clindamycin [5,85]. Erythromycin is available as a 2% gel, pad, or solution and is applied once or twice daily.

Similar to clindamycin, erythromycin should be used in conjunction with benzoyl peroxide to minimize risk for the bacterial resistance. A combination gel containing benzoyl peroxide and erythromycin is available (table 3).

Assessing response — In general, improvement from topical acne treatments is expected within 12 weeks. Complete clearance of acne is not necessarily expected; a favorable initial response may consist of a noticeable reduction in active acne lesions.

Resistant disease — Failure of acne vulgaris to respond to first-line topical therapy may occur for a variety of reasons, including the need for different or more aggressive treatment. Additional factors to consider prior to concluding inefficacy of a specific regimen include:

Poor adherence to the treatment regimen

Incorrect diagnosis

Contributory underlying disease

Topical acne therapy requires long-term, consistent use of one or more medications, and the possibility of poor adherence to treatment should always be assessed prior to assuming that a change in the prescribed regimen is needed. We find open-ended questions particularly helpful for assessing adherence (eg, asking a patient to describe their regimen rather than asking if the patient has been using a specific treatment every day).

Misdiagnosis of other conditions as acne vulgaris (eg, Pityrosporum folliculitis, Demodex folliculitis) may lead to apparent inefficacy of treatment. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Differential diagnosis'.)

Underlying conditions, such as hyperandrogenism, may contribute to treatment-resistant acne vulgaris. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Associated diseases'.)

Approach to adjusting treatment — If a patient with an insufficient response to treatment reports close adherence to the treatment regimen, the clinician is confident of the diagnosis, and contributory underlying disease is not suspected, changes can be made to the treatment regimen (algorithm 1A).

Changes to the treatment regimen are made on an individual basis and are influenced by the clinical findings, patient tolerance of the current regimen, and patient preference.

One approach is as follows:

Exclusively comedonal acne – Change retinoid (increase concentration [eg, change tretinoin 0.025% to tretinoin 0.05%] or change agent [eg, change tretinoin to tazarotene or adapalene]).

Papulopustular acne or mixed comedonal and papulopustular acne – Continue or change retinoid. Add benzoyl peroxide +/- topical antibiotic (if not already using) or start topical dapsone. Alternative approaches include the addition of topical clascoterone or topical minocycline. (See 'Topical dapsone' below.)

When topical therapy for mild acne vulgaris is insufficiently effective or topical treatment proves poorly tolerated (eg, persistent skin irritation despite therapeutic adjustments) or proves impractical for the patient (eg, difficulty with application to the trunk), we often proceed to the systemic therapies primarily reserved for moderate to severe acne. (See "Acne vulgaris: Management of moderate to severe acne in adolescents and adults".)

Alternative topical therapies — Patients who fail to improve sufficiently with initial therapies (topical retinoids, benzoyl peroxide, and/or clindamycin) may benefit from the initiation of other topical therapies.

Topical dapsone — Topical dapsone is an effective treatment for acne vulgaris. Both inflammatory papulopustular and comedonal acne lesions improve with treatment, with the greatest improvement occurring in inflammatory papulopustular lesions [86,87].

We primarily use topical dapsone for patients with inflammatory papulopustular acne who fail to respond to initial treatments (see 'Initial treatment' above):

Administration – Topical dapsone is available as a 5% or 7.5% gel. The 5% formulation is applied twice daily, while the 7.5% formulation is applied once daily.

Dapsone should not be applied at the same time as benzoyl peroxide if patients are using both agents. Temporary yellow to orange discoloration of the skin and hair may occur when dapsone gel and benzoyl peroxide are applied concomitantly [88,89]. Discoloration may persist for several days to two months [88]. Applying the drugs at separate times of the day and washing skin between applications may reduce the risk of this side effect.

Topical dapsone is not contraindicated in sulfonamide ("sulfa") allergic patients [90]. Dapsone is a sulfone, not a sulfonamide.

Efficacy – Oral dapsone is known to have anti-inflammatory and antimicrobial properties, but the mechanism through which topical dapsone improves acne has not been confirmed. Randomized trials support the efficacy of topical dapsone:

In two phase 3, randomized trials of dapsone 5% gel with a total of 3010 patients, the percent reduction of inflammatory lesions after 12 weeks of twice-daily treatment was significantly greater in patients treated with topical dapsone than in those treated with vehicle (48 versus 42 percent) [86]. An open-label, long-term study of patients treated with the same regimen for up to 12 months (mean 253 days) found a reduction in inflammatory lesions of 58 percent [87]. Benefit of dapsone 5% gel may be slightly greater in females than in males [91].

A 12-week, randomized trial (n = 2102) found dapsone 7.5% gel superior to vehicle, with mean percent reductions in inflammatory lesions of 56 and 49 percent, respectively [92]. A second identical trial (n = 2238) found similar results, with mean percent reductions in inflammatory lesions for dapsone 7.5% gel and vehicle of 54 and 48 percent, respectively [93].

Adverse effects – Although oral dapsone therapy has been associated with increased risk for hemolytic anemia in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency, patients with G6PD deficiency and acne have tolerated topical dapsone gel [86,94]. Testing for G6PD deficiency is not considered necessary for use of the topical preparation of dapsone.

Methemoglobinemia, a known complication of systemic dapsone therapy, is a rare adverse effect of topical dapsone [95]. (See "Methemoglobinemia".)

Topical minocycline — Topical minocycline is an alternative topical antibiotic for acne vulgaris. Oral tetracyclines have a long history of use for the treatment of acne vulgaris. FDA approval for minocycline 4% foam is limited to moderate to severe acne vulgaris (see "Acne vulgaris: Management of moderate to severe acne in adolescents and adults", section on 'Tetracyclines'):

AdministrationMinocycline 4% foam is applied once daily.

Efficacy – Randomized trials support the efficacy of minocycline foam for moderate to severe acne vulgaris.

Two identical phase 3 trials in which a total of 961 patients (ages nine years and older) with moderate to severe acne vulgaris were randomly assigned in a 2:1 ratio to either minocycline 4% foam or vehicle applied once daily for 12 weeks found minocycline 4% foam effective for reducing inflammatory and noninflammatory lesion counts in both studies and for achieving treatment success (a score of 0 or 1 [clear or almost clear] on the six-point Investigator's Global Assessment scale with at least a two-grade improvement) in the second study [96]. Rates of treatment success for the minocycline and vehicle groups were 15 versus 8 percent (risk ratio [RR] 1.88, 95% CI 1.02-3.46) in the first study and 8 versus 5 percent (RR 1.72, 95% CI 0.73-4.05) in the second study, respectively.

In addition, a larger, 12-week, phase 3 trial found minocycline 4% foam effective for reducing inflammatory and noninflammatory lesion counts and achieving the same measure of treatment success. In the trial, 1488 patients (ages nine years and older) with moderate to severe acne vulgaris were randomly assigned (in a 1:1 ratio) to once-daily application of minocycline 4% foam or vehicle [97]. In the minocycline group, 31 percent achieved treatment success compared with 20 percent of the vehicle group (RR 1.58, 95% CI 1.32-1.88).

Adverse effectsMinocycline foam was generally well tolerated in the randomized trials. The most common treatment-emergent adverse effects included headache and increased creatinine phosphokinase levels [96,97].

Topical clascoterone — Clascoterone is a topical androgen receptor inhibitor that was approved by the FDA in 2020 for the treatment of acne vulgaris in individuals age 12 and older:

Administration – A thin layer of clascoterone 1% cream is applied to the affected areas twice daily.

Efficacy – Efficacy of clascoterone may involve competitive inhibition of binding of dihydrotestosterone to the androgen receptor. This may contribute to inhibition of transcription of androgen-responsive genes that promote sebum production and activation of inflammatory pathways.

Data from two phase 3, randomized trials (n = 708 and n = 732) support efficacy of clascoterone 1% cream, an investigational topical androgen receptor inhibitor, for acne vulgaris [98]. In the trials, female and male patients (ages nine years and older) with moderate to severe acne vulgaris were randomly assigned to twice-daily application of either clascoterone 1% cream or vehicle cream to the entire face for 12 weeks. At week 12, 18 percent (point estimate 2.3, 95% CI 1.4-3.8) and 20 percent (point estimate 3.7, 95% CI 2.2-6.3) of patients in the clascoterone groups achieved treatment success compared with only 9 and 7 percent of patients in the vehicle groups. Treatment success was defined as at least a two-point reduction in the five-point Investigator's Global Assessment score and a score of 0 (clear) or 1 (almost clear).

Adverse effects – Skin irritation is a potential adverse effect [98]. Hypothalamic-pituitary-adrenal axis suppression has also been reported [99].

Others — Adjunctive therapies and therapies with less certain efficacy are reviewed separately. (See "Light-based, adjunctive, and other therapies for acne vulgaris", section on 'Other topical medications'.)

MODERATE TO SEVERE ACNE VULGARIS — The management of moderate to severe acne vulgaris involves consideration of systemic therapy, such as hormonal agents, antibiotics, and oral isotretinoin (table 2). The approach to moderate to severe acne vulgaris is reviewed in detail separately. (See "Acne vulgaris: Management of moderate to severe acne in adolescents and adults".)

MAINTENANCE OF RESPONSE — Topical therapies for acne vulgaris suppress, rather than cure, the condition. Thus, maintenance therapy is generally needed (algorithm 1A).

Topical retinoids are the preferred option for maintenance therapy for patients with acne vulgaris. In addition to their ability to combat active acne through comedolytic and anti-inflammatory properties, these drugs play a critical, preventive role through the inhibition of the formation of the microcomedone, the precursor lesion in acne vulgaris.

Several randomized, controlled trials support the use of retinoids as maintenance therapy following the cessation of antimicrobial agents [58,100-103]. Representative trials include:

A 12-week, randomized, controlled trial involving 241 patients with moderate to moderately severe acne evaluated the effect of maintenance therapy with adapalene 0.1% gel for patients who had at least moderate improvement after treatment with adapalene 0.1% gel and clindamycin 1% solution or clindamycin solution alone [58]. Patients who continued therapy with adapalene 0.1% gel had a 41.6 percent reduction in total lesion counts. Patients who stopped treatment exhibited a 92 percent increase in total lesion counts.

In a 16-week trial, 253 subjects with severe acne who had achieved at least moderate improvement after treatment with adapalene 0.1% gel and doxycycline 100 mg or doxycycline 100 mg and a vehicle gel in a preceding trial were randomly assigned to adapalene or vehicle gel for an additional 16 weeks [101]. The percentage of patients sustaining 50 percent improvement in lesion counts was 75 percent in the adapalene group versus 54 percent in the vehicle group.

Our typical approach to maintenance therapy for patients using topical retinoids in conjunction with other topical therapies consists of transitioning to topical retinoid monotherapy following the achievement of stable, satisfactory improvement for at least three to six months. For some patients, monotherapy with a topical retinoid may not be sufficient to sustain clinical improvement. In these cases, an antimicrobial agent containing benzoyl peroxide can be added to the treatment regimen [104,105]. Concern regarding antibiotic resistance provides an incentive to limit the use of antibiotics as long-term therapy.

MANAGEMENT OF COMPLICATIONS

Postinflammatory hyperpigmentation — Postinflammatory hyperpigmentation can be a significant problem for patients with acne vulgaris, particularly patients with skin of color (eg, skin phototypes IV to VI (table 4)). In many cases, patients are more distressed by the "dark spots," which take several months or more to resolve, than by active acne lesions, which resolve more quickly (picture 1B, 2A-B) [106]:

Photoprotection – Photoprotection is an essential component of the treatment of postinflammatory hyperpigmentation. Daily use of sunscreen and/or sun-protective clothing is indicated. (See "Postinflammatory hyperpigmentation", section on 'Photoprotection'.)

Topical retinoids and azelaic acid – We suggest the use of a topical retinoid as a component of acne treatment regimens for patients with acne-induced, postinflammatory hyperpigmentation [107]. Azelaic acid is an alternative to a topical retinoid in patients who cannot tolerate the latter. (See 'Topical retinoids' above and 'Azelaic acid' above.)

Both topical retinoids and azelaic acid accelerate the resolution of postinflammatory hyperpigmentation [6,108]. In one randomized trial, African American patients who applied tretinoin 0.1% cream exhibited significantly greater lightening of facial postinflammatory hyperpigmentation than those treated with vehicle [6].

Topical hydroquinone – Topical hydroquinone can be applied twice daily to individual hyperpigmented lesions for greater improvement. Topical hydroquinone is a depigmenting agent that inhibits melanin production and is considered the "gold standard" for treatment of hyperpigmentation [106,108,109]. (See "Postinflammatory hyperpigmentation", section on 'Topical hydroquinone'.)

Exogenous ochronosis, a condition in which grayish discoloration of the skin occurs in sites of application, is an uncommon consequence of topical hydroquinone usage [110]. Additional safety concerns were raised when oral hydroquinone was reported to be tumorigenic in rodents [111]. Carcinogenic effects have not been reported in humans [110].

Superficial chemical peels – Additionally, patients may benefit from superficial chemical peels with glycolic acid or salicylic acid, although care must be taken to avoid chemical peel-induced, postinflammatory hyperpigmentation. (See "Postinflammatory hyperpigmentation", section on 'Chemical peels' and "Chemical peels: Principles, peeling agents, and pretreatment assessment" and "Chemical peels: Procedures and complications".)

An overview of the management of postinflammatory hyperpigmentation is provided separately. (See "Postinflammatory hyperpigmentation", section on 'Treatment'.)

Postinflammatory erythema — Postinflammatory erythema, manifesting as residual, persistent, pink to red discoloration of the skin, may persist following the resolution of an active acne lesion. This finding is most often detected in patients with skin phototypes I to III (table 4). Data on the treatment of postinflammatory erythema are limited. Examples of treatments that have been associated with improvement in case reports include pulsed dye laser, fractional microneedling radiofrequency treatment, topical 5% tranexamic acid, and intense pulsed light [112-115].

Scarring — Early, effective treatment to prevent acne scarring is ideal (picture 2C). A variety of interventions may improve acne scars. Good control of active acne with topical or oral therapy is indicated prior to beginning treatment for scarring.

Options for patients who desire treatment of scars include minor surgical procedures, laser therapy, chemical peels, injectable soft tissue fillers, microneedling, and other interventions. The treatment of acne scars is discussed in detail separately. (See "Management of acne scars".)

PROCEDURAL THERAPY — Treatment of acne vulgaris with lasers, visible light, chemical peels, and other procedures is discussed separately. (See "Light-based, adjunctive, and other therapies for acne vulgaris", section on 'Light/laser therapies' and "Light-based, adjunctive, and other therapies for acne vulgaris", section on 'Adjunctive therapies'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Acne vulgaris".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Acne (The Basics)")

Beyond the Basics topics (see "Patient education: Acne (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

Overview – Acne vulgaris is a common cutaneous disorder than can lead to disfigurement or psychologic distress (picture 1A-E). Treatments for acne vulgaris include topical, oral, and procedural interventions that target one or more of the pathogenic mechanisms for acne vulgaris. Key targets include follicular hyperproliferation and abnormal desquamation, increased sebum production, Cutibacterium (formerly Propionibacterium) acnes proliferation, and inflammation. (See 'Treatment principles' above.)

Pretreatment assessment – A careful pretreatment assessment is helpful for selecting an approach to treatment (algorithm 1A-B). This should include assessment of the types of acne lesions present, the severity of acne, the presence of complications (eg, postinflammatory hyperpigmentation or scarring (picture 2A-C and table 2)), and potential contributing factors. (See 'Pretreatment assessment' above.)

Patient counseling – Long-term adherence to therapy is essential for the successful treatment of acne vulgaris. Examples of interventions that may support adherence include discussions with patients regarding expected outcomes, product and regimen preferences, and skin care measures that support tolerance of acne therapies. (See 'Patient counseling' above.)

Special considerations – Certain populations may require adjustments to the approach to management of acne vulgaris. Examples include patients with scarring, children, pregnant individuals, and patients with severe variants, such as acne conglobata and acne fulminans. (See 'Special populations' above and "Acne in infants, young children, and preadolescents", section on 'Treatment'.)

Management of specific presentations:

Exclusively comedonal acne vulgaris – For patients with mild and exclusively comedonal acne vulgaris (picture 4A-B), we suggest treatment with a topical retinoid, rather than other topical therapies (algorithm 1A) (Grade 2C). Examples of effective topical retinoids include tretinoin, adapalene, tazarotene, and trifarotene. Alternatives for patients who cannot tolerate a topical retinoid include salicylic acid and azelaic acid. (See 'Approach to treatment' above and 'Initial treatment' above.)

Mild acne vulgaris – For patients with mild inflammatory papulopustular acne vulgaris or mild mixed comedonal and papulopustular acne vulgaris (picture 1C, 1G), we suggest treatment with a topical retinoid and topical antimicrobial agent, rather than a retinoid or antimicrobial agent alone (algorithm 1A) (Grade 2A). Preferred initial options for topical antimicrobials include benzoyl peroxide and topical clindamycin. Benzoyl peroxide may be used as a solitary antimicrobial agent. In contrast, topical clindamycin should be used in conjunction with benzoyl peroxide to reduce risk for the development of antibiotic resistance. (See 'Approach to treatment' above and 'Initial treatment' above.)

Moderate to severe acne vulgaris – The approach to moderate to severe acne vulgaris is reviewed separately. (See "Acne vulgaris: Management of moderate to severe acne in adolescents and adults".)

Management of complications – Postinflammatory hyperpigmentation, postinflammatory erythema, and scarring are potential complications of acne vulgaris. Photoprotection, topical retinoids, hydroquinone, azelaic acid, or chemical peels can be beneficial for postinflammatory hyperpigmentation. Data on treatments for postinflammatory erythema are more limited. (See 'Postinflammatory hyperpigmentation' above and 'Postinflammatory erythema' above.)

The approach to the treatment of scarring secondary to acne vulgaris is reviewed in detail separately. (See "Management of acne scars".)

  1. Klassen AF, Newton JN, Mallon E. Measuring quality of life in people referred for specialist care of acne: comparing generic and disease-specific measures. J Am Acad Dermatol 2000; 43:229.
  2. Dalgard F, Gieler U, Holm JØ, et al. Self-esteem and body satisfaction among late adolescents with acne: results from a population survey. J Am Acad Dermatol 2008; 59:746.
  3. Yazici K, Baz K, Yazici AE, et al. Disease-specific quality of life is associated with anxiety and depression in patients with acne. J Eur Acad Dermatol Venereol 2004; 18:435.
  4. Williams HC, Dellavalle RP, Garner S. Acne vulgaris. Lancet 2012; 379:361.
  5. Zaenglein AL, Pathy AL, Schlosser BJ, et al. Guidelines of care for the management of acne vulgaris. J Am Acad Dermatol 2016; 74:945.
  6. Bulengo-Ransby SM, Griffiths CE, Kimbrough-Green CK, et al. Topical tretinoin (retinoic acid) therapy for hyperpigmented lesions caused by inflammation of the skin in black patients. N Engl J Med 1993; 328:1438.
  7. Tan J, Tanghetti E, Baldwin H, et al. The Role of Topical Retinoids in Prevention and Treatment of Atrophic Acne Scarring: Understanding the Importance of Early Effective Treatment. J Drugs Dermatol 2019; 18:255.
  8. Gollnick H, Cunliffe W, Berson D, et al. Management of acne: a report from a Global Alliance to Improve Outcomes in Acne. J Am Acad Dermatol 2003; 49:S1.
  9. Draelos ZD. Cosmetics and cosmeceuticals. In: Dermatology, 2nd ed, Bolognia JL, Jorizzo JL, Rapini RP, et al (Eds), Elsevier, 2008. p.2301.
  10. Draelos ZD. Cosmetic therapy. In: Comprehensive Dermatologic Drug Therapy, 2nd ed, Wolverton SE (Ed), Elsevier Inc, 2007. p.761.
  11. Subramanyan K, Johnson AW. Role of mild cleansing in the management of sensitive skin. Poster presented at the American Academy of Dermatology 61st Annual Meeting, San Francisco, CA, March 21 to 26, 2004.
  12. Boozalis E, Patel S. Clinical utility of marketing terms used for over-the-counter dermatologic products. J Dermatolog Treat 2018; 29:841.
  13. Eichenfield LF, Krakowski AC, Piggott C, et al. Evidence-based recommendations for the diagnosis and treatment of pediatric acne. Pediatrics 2013; 131 Suppl 3:S163.
  14. Alexis AF, Harper JC, Stein Gold LF, Tan JKL. Treating Acne in Patients With Skin of Color. Semin Cutan Med Surg 2018; 37:S71.
  15. Murase JE, Heller MM, Butler DC. Safety of dermatologic medications in pregnancy and lactation: Part I. Pregnancy. J Am Acad Dermatol 2014; 70:401.e1.
  16. Worret WI, Fluhr JW. [Acne therapy with topical benzoyl peroxide, antibiotics and azelaic acid]. J Dtsch Dermatol Ges 2006; 4:293.
  17. Leachman SA, Reed BR. The use of dermatologic drugs in pregnancy and lactation. Dermatol Clin 2006; 24:167.
  18. Leyden JJ, Del Rosso JQ, Webster GF. Clinical considerations in the treatment of acne vulgaris and other inflammatory skin disorders: a status report. Dermatol Clin 2009; 27:1.
  19. Webster GF, Graber EM. Antibiotic treatment for acne vulgaris. Semin Cutan Med Surg 2008; 27:183.
  20. Cunliffe WJ, Holland KT, Bojar R, Levy SF. A randomized, double-blind comparison of a clindamycin phosphate/benzoyl peroxide gel formulation and a matching clindamycin gel with respect to microbiologic activity and clinical efficacy in the topical treatment of acne vulgaris. Clin Ther 2002; 24:1117.
  21. Eady EA, Farmery MR, Ross JI, et al. Effects of benzoyl peroxide and erythromycin alone and in combination against antibiotic-sensitive and -resistant skin bacteria from acne patients. Br J Dermatol 1994; 131:331.
  22. Thiboutot D, Zaenglein A, Weiss J, et al. An aqueous gel fixed combination of clindamycin phosphate 1.2% and benzoyl peroxide 2.5% for the once-daily treatment of moderate to severe acne vulgaris: assessment of efficacy and safety in 2813 patients. J Am Acad Dermatol 2008; 59:792.
  23. Lookingbill DP, Chalker DK, Lindholm JS, et al. Treatment of acne with a combination clindamycin/benzoyl peroxide gel compared with clindamycin gel, benzoyl peroxide gel and vehicle gel: combined results of two double-blind investigations. J Am Acad Dermatol 1997; 37:590.
  24. Thielitz A, Gollnick H. Topical retinoids in acne vulgaris: update on efficacy and safety. Am J Clin Dermatol 2008; 9:369.
  25. Leyden JJ, Shalita A, Thiboutot D, et al. Topical retinoids in inflammatory acne: a retrospective, investigator-blinded, vehicle-controlled, photographic assessment. Clin Ther 2005; 27:216.
  26. Torok HM, Pillai R. Safety and efficacy of micronized tretinoin gel (0.05%) in treating adolescent acne. J Drugs Dermatol 2011; 10:647.
  27. Zaenglein AL. Topical retinoids in the treatment of acne vulgaris. Semin Cutan Med Surg 2008; 27:177.
  28. Galvin SA, Gilbert R, Baker M, et al. Comparative tolerance of adapalene 0.1% gel and six different tretinoin formulations. Br J Dermatol 1998; 139 Suppl 52:34.
  29. Lucky AW, Cullen SI, Jarratt MT, Quigley JW. Comparative efficacy and safety of two 0.025% tretinoin gels: results from a multicenter double-blind, parallel study. J Am Acad Dermatol 1998; 38:S17.
  30. Lucky AW, Sugarman J. Comparison of micronized tretinoin gel 0.05% and tretinoin gel microsphere 0.1% in young adolescents with acne: a post hoc analysis of efficacy and tolerability data. Cutis 2011; 87:305.
  31. Voelker R. Tretinoin in New Lotion Formula. JAMA 2018; 320:1309.
  32. Altreno (tretinoin) lotion, for topical use. US FDA approved product information; Bridgewater, NJ: Valeant Pharmaceuticals; August 2018. www.accessdata.fda.gov/drugsatfda_docs/label/2018/209353s000lbl.pdf (Accessed on October 05, 2018).
  33. Cunliffe WJ, Poncet M, Loesche C, Verschoore M. A comparison of the efficacy and tolerability of adapalene 0.1% gel versus tretinoin 0.025% gel in patients with acne vulgaris: a meta-analysis of five randomized trials. Br J Dermatol 1998; 139 Suppl 52:48.
  34. Brand B, Gilbert R, Baker MD, et al. Cumulative irritancy comparison of adapalene gel 0.1% versus other retinoid products when applied in combination with topical antimicrobial agents. J Am Acad Dermatol 2003; 49:S227.
  35. Atralin (tretinoin) gel, 0.05%. US FDA approved product information; Fort Worth, TX: Coria Laboratories; July 2007. http://www.accessdata.fda.gov/drugsatfda_docs/label/2007/022070lbl.pdf (Accessed on August 12, 2013).
  36. Nyirady J, Lucas C, Yusuf M, et al. The stability of tretinoin in tretinoin gel microsphere 0.1%. Cutis 2002; 70:295.
  37. Martin B, Meunier C, Montels D, Watts O. Chemical stability of adapalene and tretinoin when combined with benzoyl peroxide in presence and in absence of visible light and ultraviolet radiation. Br J Dermatol 1998; 139 Suppl 52:8.
  38. Stockton E, December 10, 2019, personal communication.
  39. Nighland M, Yusuf M, Wisniewski S, et al. The effect of simulated solar UV irradiation on tretinoin in tretinoin gel microsphere 0.1% and tretinoin gel 0.025%. Cutis 2006; 77:313.
  40. Del Rosso JQ, Harper J, Pillai R, Moore R. Tretinoin photostability: comparison of micronized tretinoin (0.05%) gel and tretinoin (0.025%) gel following exposure to ultraviolet a light. J Clin Aesthet Dermatol 2012; 5:27.
  41. Rosso JD, Harper J, Pillai R, Moore R. Tretinoin photostability: comparison of micronized tretinoin gel 0.05% and tretinoin gel 0.025% following exposure to fluorescent and solar light. J Clin Aesthet Dermatol 2013; 6:25.
  42. Bershad S, Kranjac Singer G, Parente JE, et al. Successful treatment of acne vulgaris using a new method: results of a randomized vehicle-controlled trial of short-contact therapy with 0.1% tazarotene gel. Arch Dermatol 2002; 138:481.
  43. Sami N, Harper JC. Topical retinoids. In: Comprehensive Dermatologic Drug Therapy, 2nd ed, Wolverton SE (Ed), Elsevier Inc, 2007. p.625.
  44. Kang S, Voorhees JJ. Topical retinoids. In: Fitzpatrick's Dermatology in General Medicine, 7th ed, Wolff K, Goldsmith LA, Katz SI, et al (Eds), McGraw Hill, 2008. p.2106.
  45. Fernandez [Graber] EM, Zaenglein A, Thiboutot D. Acne treatment methodologies. In: Cosmetic Formulation of Skin Care Products, Taylor and Francis Group, 2006. p.273.
  46. Krishnan G. Comparison of two concentrations of tretinoin solution in the topical treatment of acne vulgaris. Practitioner 1976; 216:106.
  47. Webster GF. Safety and efficacy of Tretin-X compared with Retin-A in patients with mild-to-severe acne vulgaris. Skinmed 2006; 5:114.
  48. Webster G, Cargill DI, Quiring J, et al. A combined analysis of 2 randomized clinical studies of tretinoin gel 0.05% for the treatment of acne. Cutis 2009; 83:146.
  49. Berger R, Barba A, Fleischer A, et al. A double-blinded, randomized, vehicle-controlled, multicenter, parallel-group study to assess the safety and efficacy of tretinoin gel microsphere 0.04% in the treatment of acne vulgaris in adults. Cutis 2007; 80:152.
  50. Thiboutot D, Pariser DM, Egan N, et al. Adapalene gel 0.3% for the treatment of acne vulgaris: a multicenter, randomized, double-blind, controlled, phase III trial. J Am Acad Dermatol 2006; 54:242.
  51. Lucky A, Jorizzo JL, Rodriguez D, et al. Efficacy and tolerance of adapalene cream 0.1% compared with its cream vehicle for the treatment of acne vulgaris. Cutis 2001; 68:34.
  52. Pariser DM, Thiboutot DM, Clark SD, et al. The efficacy and safety of adapalene gel 0.3% in the treatment of acne vulgaris: A randomized, multicenter, investigator-blinded, controlled comparison study versus adapalene gel 0.1% and vehicle. Cutis 2005; 76:145.
  53. Shalita AR, Berson DS, Thiboutot DM, et al. Effects of tazarotene 0.1 % cream in the treatment of facial acne vulgaris: pooled results from two multicenter, double-blind, randomized, vehicle-controlled, parallel-group trials. Clin Ther 2004; 26:1865.
  54. Kawashima M, Harada S, Loesche C, Miyachi Y. Adapalene gel 0.1% is effective and safe for Japanese patients with acne vulgaris: a randomized, multicenter, investigator-blinded, controlled study. J Dermatol Sci 2008; 49:241.
  55. Eichenfield LF, Jarratt M, Schlessinger J, et al. Adapalene 0.1% lotion in the treatment of acne vulgaris: results from two placebo-controlled, multicenter, randomized double-blind, clinical studies. J Drugs Dermatol 2010; 9:639.
  56. Tan J, Thiboutot D, Popp G, et al. Randomized phase 3 evaluation of trifarotene 50 μg/g cream treatment of moderate facial and truncal acne. J Am Acad Dermatol 2019; 80:1691.
  57. Blume-Peytavi U, Fowler J, Kemény L, et al. Long-term safety and efficacy of trifarotene 50 μg/g cream, a first-in-class RAR-γ selective topical retinoid, in patients with moderate facial and truncal acne. J Eur Acad Dermatol Venereol 2020; 34:166.
  58. Zhang JZ, Li LF, Tu YT, Zheng J. A successful maintenance approach in inflammatory acne with adapalene gel 0.1% after an initial treatment in combination with clindamycin topical solution 1% or after monotherapy with clindamycin topical solution 1%. J Dermatolog Treat 2004; 15:372.
  59. Leyden JJ, Krochmal L, Yaroshinsky A. Two randomized, double-blind, controlled trials of 2219 subjects to compare the combination clindamycin/tretinoin hydrogel with each agent alone and vehicle for the treatment of acne vulgaris. J Am Acad Dermatol 2006; 54:73.
  60. Thiboutot DM, Weiss J, Bucko A, et al. Adapalene-benzoyl peroxide, a fixed-dose combination for the treatment of acne vulgaris: results of a multicenter, randomized double-blind, controlled study. J Am Acad Dermatol 2007; 57:791.
  61. Wolf JE Jr, Kaplan D, Kraus SJ, et al. Efficacy and tolerability of combined topical treatment of acne vulgaris with adapalene and clindamycin: a multicenter, randomized, investigator-blinded study. J Am Acad Dermatol 2003; 49:S211.
  62. Zouboulis CC, Derumeaux L, Decroix J, et al. A multicentre, single-blind, randomized comparison of a fixed clindamycin phosphate/tretinoin gel formulation (Velac) applied once daily and a clindamycin lotion formulation (Dalacin T) applied twice daily in the topical treatment of acne vulgaris. Br J Dermatol 2000; 143:498.
  63. Richter JR, Förström LR, Kiistala UO, Jung EG. Efficacy of the fixed 1.2% clindamycin phosphate, 0.025% tretinoin gel formulation (Velac) and a proprietary 0.025% tretinoin gel formulation (Aberela) in the topical control of facial acne. J Eur Acad Dermatol Venereol 1998; 11:227.
  64. Rietschel RL, Duncan SH. Clindamycin phosphate used in combination with tretinoin in the treatment of acne. Int J Dermatol 1983; 22:41.
  65. Shalita AR, Rafal ES, Anderson DN, et al. Compared efficacy and safety of tretinoin 0.1% microsphere gel alone and in combination with benzoyl peroxide 6% cleanser for the treatment of acne vulgaris. Cutis 2003; 72:167.
  66. Del Rosso JQ. Study results of benzoyl peroxide 5%/clindamycin 1% topical gel, adapalene 0.1% gel, and use in combination for acne vulgaris. J Drugs Dermatol 2007; 6:616.
  67. Draelos ZD, Tanghetti EA, Tazarotene Combination Leads to Efficacious Acne Results (CLEAR) Trial Study Group. Optimizing the use of tazarotene for the treatment of facial acne vulgaris through combination therapy. Cutis 2002; 69:20.
  68. Tanghetti E, Abramovits W, Solomon B, et al. Tazarotene versus tazarotene plus clindamycin/benzoyl peroxide in the treatment of acne vulgaris: a multicenter, double-blind, randomized parallel-group trial. J Drugs Dermatol 2006; 5:256.
  69. Kaplan YC, Ozsarfati J, Etwel F, et al. Pregnancy outcomes following first-trimester exposure to topical retinoids: a systematic review and meta-analysis. Br J Dermatol 2015; 173:1132.
  70. Camera G, Pregliasco P. Ear malformation in baby born to mother using tretinoin cream. Lancet 1992; 339:687.
  71. Lipson AH, Collins F, Webster WS. Multiple congenital defects associated with maternal use of topical tretinoin. Lancet 1993; 341:1352.
  72. Autret E, Berjot M, Jonville-Béra AP, et al. Anophthalmia and agenesis of optic chiasma associated with adapalene gel in early pregnancy. Lancet 1997; 350:339.
  73. Navarre-Belhassen C, Blanchet P, Hillaire-Buys D, et al. Multiple congenital malformations associated with topical tretinoin. Ann Pharmacother 1998; 32:505.
  74. Selcen D, Seidman S, Nigro MA. Otocerebral anomalies associated with topical tretinoin use. Brain Dev 2000; 22:218.
  75. Mills OH Jr, Kligman AM, Pochi P, Comite H. Comparing 2.5%, 5%, and 10% benzoyl peroxide on inflammatory acne vulgaris. Int J Dermatol 1986; 25:664.
  76. Jacobs A, Starke G, Rosumeck S, Nast A. Systematic review on the rapidity of the onset of action of topical treatments in the therapy of mild-to-moderate acne vulgaris. Br J Dermatol 2014; 170:557.
  77. www.fda.gov/Safety/MedWatch/SafetyInformation/SafetyAlertsforHumanMedicalProducts/ucm402722.htm?source=govdelivery&utm_medium=email&utm_source=govdelivery (Accessed on June 26, 2014).
  78. Bowe WP, Shalita AR. Effective over-the-counter acne treatments. Semin Cutan Med Surg 2008; 27:170.
  79. Morelli R, Lanzarini M, Vincenzi C, Reggiani M. Contact dermatitis due to benzoyl peroxide. Contact Dermatitis 1989; 20:238.
  80. Gollnick H, Schramm M. Topical drug treatment in acne. Dermatology 1998; 196:119.
  81. Leyden J, Kaidbey K, Levy SF. The combination formulation of clindamycin 1% plus benzoyl peroxide 5% versus 3 different formulations of topical clindamycin alone in the reduction of Propionibacterium acnes. An in vivo comparative study. Am J Clin Dermatol 2001; 2:263.
  82. Seidler EM, Kimball AB. Meta-analysis comparing efficacy of benzoyl peroxide, clindamycin, benzoyl peroxide with salicylic acid, and combination benzoyl peroxide/clindamycin in acne. J Am Acad Dermatol 2010; 63:52.
  83. Graupe K, Cunliffe WJ, Gollnick HP, Zaumseil RP. Efficacy and safety of topical azelaic acid (20 percent cream): an overview of results from European clinical trials and experimental reports. Cutis 1996; 57:20.
  84. Gollnick HP, Graupe K, Zaumseil RP. [Azelaic acid 15% gel in the treatment of acne vulgaris. Combined results of two double-blind clinical comparative studies]. J Dtsch Dermatol Ges 2004; 2:841.
  85. Eady EA, Cove JH, Holland KT, Cunliffe WJ. Erythromycin resistant propionibacteria in antibiotic treated acne patients: association with therapeutic failure. Br J Dermatol 1989; 121:51.
  86. Draelos ZD, Carter E, Maloney JM, et al. Two randomized studies demonstrate the efficacy and safety of dapsone gel, 5% for the treatment of acne vulgaris. J Am Acad Dermatol 2007; 56:439.e1.
  87. Lucky AW, Maloney JM, Roberts J, et al. Dapsone gel 5% for the treatment of acne vulgaris: safety and efficacy of long-term (1 year) treatment. J Drugs Dermatol 2007; 6:981.
  88. Fleischer AB, Draelos ZD, Abramovits W, Pariser DM. Dapsone gel 5% in combination with adapalene gel 1%, benzoyl peroxide gel 4%, or vehicle gel for the treatment of acne vulgaris: a randomized, double-blind study. J Am Acad Dermatol 2007; 56:AB16.
  89. Dubina MI, Fleischer AB Jr. Interaction of topical sulfacetamide and topical dapsone with benzoyl peroxide. Arch Dermatol 2009; 145:1027.
  90. Webster GF. Is topical dapsone safe in glucose-6-phosphate dehydrogenase-deficient and sulfonamide-allergic patients? J Drugs Dermatol 2010; 9:532.
  91. Tanghetti E, Harper JC, Oefelein MG. The efficacy and tolerability of dapsone 5% gel in female vs male patients with facial acne vulgaris: gender as a clinically relevant outcome variable. J Drugs Dermatol 2012; 11:1417.
  92. Stein Gold LF, Jarratt MT, Bucko AD, et al. Efficacy and Safety of Once-Daily Dapsone Gel, 7.5% for Treatment of Adolescents and Adults With Acne Vulgaris: First of Two Identically Designed, Large, Multicenter, Randomized, Vehicle-controlled Trials. J Drugs Dermatol 2016; 15:553.
  93. Aczone (dapsone) gel, 7.5%, for topical use. US FDA approved product information; Irvine, CA: Allergan; February 2016. http://www.accessdata.fda.gov/drugsatfda_docs/label/2016/207154s000lbl.pdf (Accessed on June 09, 2016).
  94. Piette WW, Taylor S, Pariser D, et al. Hematologic safety of dapsone gel, 5%, for topical treatment of acne vulgaris. Arch Dermatol 2008; 144:1564.
  95. Swartzentruber GS, Yanta JH, Pizon AF. Methemoglobinemia as a complication of topical dapsone. N Engl J Med 2015; 372:491.
  96. Gold LS, Dhawan S, Weiss J, et al. A novel topical minocycline foam for the treatment of moderate-to-severe acne vulgaris: Results of 2 randomized, double-blind, phase 3 studies. J Am Acad Dermatol 2019; 80:168.
  97. Raoof TJ, Hooper D, Moore A, et al. Efficacy and safety of a novel topical minocycline foam for the treatment of moderate to severe acne vulgaris: A phase 3 study. J Am Acad Dermatol 2020; 82:832.
  98. Hebert A, Thiboutot D, Stein Gold L, et al. Efficacy and Safety of Topical Clascoterone Cream, 1%, for Treatment in Patients With Facial Acne: Two Phase 3 Randomized Clinical Trials. JAMA Dermatol 2020; 156:621.
  99. Mazzetti A, Moro L, Gerloni M, Cartwright M. Pharmacokinetic Profile, Safety, and Tolerability of Clascoterone (Cortexolone 17-alpha propionate, CB-03-01) Topical Cream, 1% in Subjects With Acne Vulgaris: An Open-Label Phase 2a Study. J Drugs Dermatol 2019; 18:563.
  100. Leyden J, Thiboutot DM, Shalita AR, et al. Comparison of tazarotene and minocycline maintenance therapies in acne vulgaris: a multicenter, double-blind, randomized, parallel-group study. Arch Dermatol 2006; 142:605.
  101. Thiboutot DM, Shalita AR, Yamauchi PS, et al. Adapalene gel, 0.1%, as maintenance therapy for acne vulgaris: a randomized, controlled, investigator-blind follow-up of a recent combination study. Arch Dermatol 2006; 142:597.
  102. Alirezai M, George SA, Coutts I, et al. Daily treatment with adapalene gel 0.1% maintains initial improvement of acne vulgaris previously treated with oral lymecycline. Eur J Dermatol 2007; 17:45.
  103. Thielitz A, Sidou F, Gollnick H. Control of microcomedone formation throughout a maintenance treatment with adapalene gel, 0.1%. J Eur Acad Dermatol Venereol 2007; 21:747.
  104. Thiboutot D, Gollnick H, Bettoli V, et al. New insights into the management of acne: an update from the Global Alliance to Improve Outcomes in Acne group. J Am Acad Dermatol 2009; 60:S1.
  105. Poulin Y, Sanchez NP, Bucko A, et al. A 6-month maintenance therapy with adapalene-benzoyl peroxide gel prevents relapse and continuously improves efficacy among patients with severe acne vulgaris: results of a randomized controlled trial. Br J Dermatol 2011; 164:1376.
  106. Taylor SC, Cook-Bolden F, Rahman Z, Strachan D. Acne vulgaris in skin of color. J Am Acad Dermatol 2002; 46:S98.
  107. Callender VD. Considerations for treating acne in ethnic skin. Cutis 2005; 76:19.
  108. Draelos ZD. Skin lightening preparations and the hydroquinone controversy. Dermatol Ther 2007; 20:308.
  109. Palumbo A, d'Ischia M, Misuraca G, Prota G. Mechanism of inhibition of melanogenesis by hydroquinone. Biochim Biophys Acta 1991; 1073:85.
  110. Levitt J. The safety of hydroquinone: a dermatologist's response to the 2006 Federal Register. J Am Acad Dermatol 2007; 57:854.
  111. Department of Health and Human Services. Food and Drug Administration. Skin Bleaching Drug Products For Over-the-Counter Human Use; Proposed Rule. 71 Federal Register 51146-5115521 (2006) (codified at 21 CFR Part 310).
  112. Bae-Harboe YS, Graber EM. Easy as PIE (Postinflammatory Erythema). J Clin Aesthet Dermatol 2013; 6:46.
  113. Min S, Park SY, Yoon JY, et al. Fractional Microneedling Radiofrequency Treatment for Acne-related Post-inflammatory Erythema. Acta Derm Venereol 2016; 96:87.
  114. Jakhar D, Kaur I. Topical 5% tranexamic acid for acne-related postinflammatory erythema. J Am Acad Dermatol 2020; 82:e187.
  115. Mathew ML, Karthik R, Mallikarjun M, et al. Intense Pulsed Light Therapy for Acne-induced Post-inflammatory Erythema. Indian Dermatol Online J 2018; 9:159.
Topic 42 Version 58.0

References

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