Postadolescent acne in women

INTRODUCTION — Acne vulgaris is a skin disorder characterized by the presence of comedones and inflammatory lesions on the face, neck, shoulders, or trunk (picture 1A-B). Although the high prevalence of acne in the adolescent population has contributed to a perception that acne is a disorder of youth, acne remains a significant problem for many adults.

The unique features of postadolescent acne in women will be discussed here. General information on the pathogenesis, clinical features, diagnosis, and management of acne is reviewed separately. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris" and "Acne vulgaris: Overview of management" and "Oral isotretinoin therapy for acne vulgaris" and "Light-based, adjunctive, and other therapies for acne vulgaris" and "Acne vulgaris: Management of moderate to severe acne in adolescents and adults".)

EPIDEMIOLOGY — Postadolescent acne is a common disorder that is often defined as acne that occurs in individuals aged 25 years or older. The disorder appears to occur more frequently in women than men [1-8]. As an example, in a population-based study of more than 17,000 individuals in China, acne was more common in men prior to the age of 30 but was more prevalent in women thereafter [2]. Similarly, in a community-based study of 749 adults aged 25 years or older in the United Kingdom, clinically significant acne (defined as Leeds acne grade ≥1) was detected in 12 percent of women but only 3 percent of men [7,9].

In addition, women may be more likely to visit health care providers for the evaluation and treatment of postadolescent acne [4,10]. In a retrospective study performed in the United Kingdom, 152 out of 200 patients (75 percent) over the age of 25 who were referred to a dermatology department for acne were female [4].

The prevalence of acne in women steadily decreases with age. This was evident in a prospective study of 2895 women (aged 10 to 70 years) performed in the United States, England, Italy, and Japan [11]. Although acne was most prevalent at age 16 (present in almost 70 percent of subjects) and proceeded to decline after the age of 18, approximately one-half of women in their 20s, one-quarter of women in their 30s, and more than 10 percent of women in their 40s still had clinically significant acne (defined as more than four inflammatory lesions or comedones present on one side of the face). Acne occurred less frequently in postmenopausal women; among women aged 51 years and older, clinically significant acne was detected in less than 5 percent.

PATHOGENESIS — Similar to acne in other populations, multiple factors contribute to the development of acne lesions in women. The four local events in the skin that are linked to the formation of acne lesions are the following:

●Abnormal keratinization of the pilosebaceous follicles

●Excess sebum production

●Cutibacterium (formerly Propionibacterium) acnes colonization

●Inflammation

Excess sebum production and abnormal follicular keratinization contribute to the formation of comedones, which are considered the primary lesions of acne. Rupture of the comedones and inflammatory reactions to C. acnes, an organism that feeds on sebum, are associated with the development of inflammatory lesions. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Pathogenesis'.)

Endogenous or exogenous androgens, the menstrual cycle, smoking, and cosmetic use may contribute to comedone formation in women and may play a role in the development of acne:

●Androgens – Androgens are capable of stimulating the growth of sebaceous glands in the skin and can augment sebum production, characteristics that may contribute to lesion formation [12]. A role for androgens in the development of acne in women is supported by the observation that endogenously or exogenously derived increases in serum androgen levels have been linked to the development of acne [12-15]. In addition, acne in women often improves during treatment with antiandrogenic therapies [16,17]. (See "Acne vulgaris: Management of moderate to severe acne in adolescents and adults", section on 'Oral hormonal therapies'.)

The most common cause of endogenous hyperandrogenemia in women is polycystic ovarian syndrome; less common causes include late-onset adrenal hyperplasia, ovarian hyperthecosis, and virilizing ovarian or adrenal tumors [17,18]. Hyperandrogenemic states may also result from the administration of anabolic steroids or testosterone supplementation. In addition, progestin-only contraceptives that contain proandrogenic progestins and lack antiandrogenic estrogens may contribute to the development of acne [19,20]. (See "Clinical manifestations of polycystic ovary syndrome in adults" and "Genetics and clinical presentation of nonclassic (late-onset) congenital adrenal hyperplasia due to 21-hydroxylase deficiency" and "Ovarian hyperthecosis" and "Sex cord-stromal tumors of the ovary: Epidemiology, clinical features, and diagnosis in adults" and "Adrenal hyperandrogenism".)

However, most adult women with acne have normal androgen levels and do not receive exogenous androgens [18,21]. The relationship between circulating androgen levels and acne in these women is uncertain [17,22]. Proposed mechanisms through which androgens may contribute to acne in these patients include the effects of increased conversion of androgen precursors to androgens within the sebaceous glands and elevated sensitivity of sebaceous glands to androgens [17,23].

●Menstrual cycle – Many women with acne note correlation of acne severity with their menstrual cycle. Up to 83 percent of women with acne note premenstrual flares [3,5,24-27]. In one series of 41 women between the ages of 18 and 44 with acne, 63 percent showed a premenstrual increase in the number of inflammatory lesions, and the number of inflammatory lesions present increased by 25 percent [24].

Accumulation of sebum within the sebaceous glands due to a reduction in the size of the pilosebaceous orifice during the premenstrual period has been proposed as a potential contributor to premenstrual flares [28,29]. However, the mechanism responsible for this phenomenon remains unknown.

●Smoking – Several studies have linked smoking to adult female acne, including one study that specifically linked smoking with the presence of noninflammatory acne lesions [30-32]. Effects of nicotine on sebum production or keratinization have been proposed as potential contributing factors [30,31]. Yet, other studies have found conflicting results, and the existence of a causative relationship remains uncertain [33-36].

●Cosmetic products – The terms "acne cosmetica" and "pomade acne" have been used to describe an association between the use of cosmetic skin or hair products and acne, a phenomenon that was attributed to follicular plugging induced by certain agents [37-39]. This phenomenon may contribute to the insidious, slow development of comedones and, eventually, inflammatory lesions. In addition, follicular irritation related to the application of cosmetics may result in the rapid appearance of an eruption characterized by small, inflammatory papules that closely resembles acne vulgaris (vellus hair folliculitis). (See 'Skin care' below and "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Pathogenesis'.)

The degree to which cosmetic use contributes to acne in the adult female population is unclear [5,22,23,27,40]. The methods used to test comedogenicity of products vary considerably across the cosmetic industry, and products that contain comedogenic ingredients are not necessarily comedogenic when applied to human skin [40,41]. In addition, individual responses to certain products may vary [40].

●Other factors – Other factors that may play a role in acne include stress, diet, and genetic factors [23,26,42]. Data on risk factors specifically for postadolescent acne in women are limited. A case-control study of 248 women with acne and 270 controls found associations between adult female acne and a history of adolescent acne, family history of acne, no prior pregnancies, hirsutism, office work, high level of reported psychologic stress, and low weekly consumption of fruits, vegetables, or fish [43]. Additional studies are required to confirm these findings. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Diet'.)

A more detailed discussion of the pathogenesis of acne is included elsewhere. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris".)

CLINICAL FEATURES

Onset — Acne in the adult woman may present as a continuation of adolescent acne (persistent acne), which represents the most common presentation, or as a newly developing disorder (late-onset acne) [4,5,7,21,44]. In a prospective study of patients over the age of 25 who presented to a dermatology department in the United Kingdom for acne, only 28 of 152 women (18 percent) had late-onset acne (onset after the age of 25 years) [4]. An international prospective study of 374 adult females (≥25 years of age) who presented to a dermatologist for the evaluation of acne found similar results; only 10 percent of women recalled the onset of acne after age 25 years [21].

Physical findings — As with acne in adolescents, acne in adult women commonly presents with both small, noninflammatory papules (comedones (picture 2A-B)) and inflammatory acne lesions (papules, pustules, or nodules (picture 1A)). Acne presenting as only noninflammatory or only inflammatory lesions is less common [21]. The face is a common site for involvement, but lesions on the neck and trunk may also occur frequently [4,27]. In the study evaluating acne in 374 adult females with acne, approximately 50 percent of women had truncal involvement [21].

Some authors have divided facial acne in adult females into two clinical presentations [5,30]. One clinical presentation is characterized by multiple comedones that may be accompanied by a few inflammatory lesions. In this variant, comedones may occur on multiple areas, including the upper face. The other presentation is an inflammatory form characterized by papules, pustules, or nodules that primarily occur on the lower face (eg, chin, perioral skin, and mandible) (picture 1A-B). The reason for this particular distribution is unknown.

Although lower facial acne has often been viewed as a characteristic presentation of adult female acne (picture 1B), the findings of the prospective study of 374 adult females with acne described above suggest that lesions limited to this area actually may occur in only a small subset of patients [21]. Only 11 percent of women in the study had lesions limited to the mandibular area.

The severity of acne in women is typically mild to moderate [3,5,21,30]. It is common for adult patients with inflammatory acne to have only several active lesions at the time of evaluation.

DIAGNOSIS — The diagnosis of acne is made based upon the physical examination. Supportive clinical features are comedones and/or inflammatory papules or pustules involving the face, neck, chest, back, and/or shoulders.

ADDITIONAL EVALUATION — The evaluation of women with acne should include an assessment for signs of underlying hyperandrogenism and exposure to medications that may cause acne or acneiform eruptions.

Hyperandrogenism — Laboratory evaluation for a hyperandrogenic state is indicated in women who exhibit symptoms or signs suggestive of hyperandrogenism [45]. Examples of such features include [23]:

●Signs of virilization, such as hirsutism (male pattern hair growth), frontotemporal hair loss, or clitoromegaly

●Irregular/infrequent menses

●Infertility

●Polycystic ovaries

●Abrupt onset of severe acne

●Acne that is severe or resistant to therapy

●Cushingoid features

●Acanthosis nigricans

●Obesity

Of note, since hair removal may make signs of hirsutism undetectable, physical examination is not sufficient for ruling out a hirsute state. Patients should be specifically questioned about male pattern hair growth and hair removal practices. (See "Evaluation of premenopausal women with hirsutism".)

Oral contraceptive agents should be discontinued at least four to six weeks prior to laboratory testing for hyperandrogenism. The laboratory evaluation of patients with acne and suspected hyperandrogenism is reviewed separately. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Additional tests'.)

Medications — The medication history should be reviewed to identify any medications and supplements that may induce acne or acneiform eruptions (table 1). In particular, progestin-only contraceptive agents, including oral, injected, and implanted agents, have been associated with exacerbation of acne. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Acneiform eruptions' and "Acne vulgaris: Management of moderate to severe acne in adolescents and adults", section on 'Oral contraceptives'.)

DIFFERENTIAL DIAGNOSIS — Multiple disorders may present with clinical features that resemble acne vulgaris. In particular, in adult women, the following disorders should be considered:

●Rosacea – Rosacea is a common inflammatory disorder that may present with inflammatory papules, pustules, telangiectasias, or erythema involving the central face (picture 3). The absence of comedones and the centrofacial location of rosacea help to distinguish rosacea from acne. (See "Rosacea: Pathogenesis, clinical features, and diagnosis".)

●Perioral dermatitis – Perioral dermatitis (also known as periorificial dermatitis) is a disorder most commonly seen in young women that presents with clusters of small papules around the mouth (picture 4A-B). The skin immediately adjacent to the vermilion border of the lip is typically spared. This disorder may also occur in a periocular distribution. (See "Perioral (periorificial) dermatitis".)

●Pseudofolliculitis barbae – Pseudofolliculitis barbae is a condition most commonly seen in Black men that occurs as a result of re-entry of the free ends of short, cut beard hairs into the skin (picture 5A-C). Women with terminal hair growth on the face may also develop this condition. (See "Pseudofolliculitis barbae".)

●Pathologic skin picking – Pathologic skin picking is a behavioral disorder characterized by deliberate and repeated picking or scratching at skin. The term "acne excoriée" has been used to describe patients who repeatedly pick, scratch, or squeeze relatively minor acne lesions, resulting in visible tissue damage that often greatly exceeds the severity of acne (picture 6A-C). (See "Skin picking (excoriation) disorder and related disorders".)

●Drug-induced acne (acne medicamentosa) – Multiple drugs may precipitate acneiform eruptions, including topical or systemic corticosteroids, lithium, epidermal growth factor inhibitors, and other agents (table 1). (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Acneiform eruptions'.)

Other disorders to be considered in the differential diagnosis of postadolescent acne in women include bacterial folliculitis or furunculosis, eosinophilic folliculitis (picture 7), acne mechanica (development of inflammatory papules at sites of friction or pressure on the skin), and lupus miliaris disseminata faciei (picture 8). The differential diagnosis of acne vulgaris is discussed in greater detail separately. (See "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Differential diagnosis'.)

TREATMENT — Treatment of acne is not mandatory but is often beneficial for patients for whom acne causes distress, cosmetic concerns, or otherwise negatively impacts quality of life and patients who desire to minimize common sequelae, such as postinflammatory hyperpigmentation and scars (picture 1A, 1C). Even acne that appears mild to the clinician may have significant negative psychosocial effects on the patient [46,47].

Pretreatment assessment — As with all patients with acne, assessment of the type of acne lesions present (comedones versus inflammatory lesions), the severity of acne, and the presence of acne sequelae (eg, hyperpigmentation, scarring) is of value for the selection of an appropriate therapeutic regimen. In addition, treatable contributors to acne (eg, hyperandrogenemic states, acne-inducing medications) should be addressed. (See "Acne vulgaris: Overview of management", section on 'Pretreatment assessment'.)

Considerations that are particularly relevant for postadolescent acne in women include:

●Prior therapies – Postadolescent acne in women can be difficult to treat, and patient complaints regarding prior ineffective therapies are not uncommon [4]. A history of previous therapeutic interventions should be carefully obtained prior to treatment selection to determine whether specific treatments were truly ineffective. A failure to respond to therapy is sometimes due to a lack of adherence to the treatment regimen for an appropriate amount of time or early discontinuation of an agent due to adverse effects [48]. At least 8 to 12 weeks of consistent treatment is required to judge the effectiveness of many acne medications. (See "Acne vulgaris: Overview of management".)

●Childbearing status – Avoidance of many acne therapies is preferable in pregnancy. Women who are candidates for these therapies should be asked about the possibility of existing pregnancy and plans for childbearing in the near future. The results guide appropriate patient counseling and selection of therapy. (See "Oral isotretinoin therapy for acne vulgaris", section on 'Teratogenicity' and "Acne vulgaris: Overview of management", section on 'Pregnant individuals'.)

Active acne — The therapeutic approach to postadolescent acne in women is similar to the approach to acne in other adults and adolescents. In addition to the standard acne therapies available to the general population of acne patients (eg, topical retinoids, azelaic acid, salicylic acid, antimicrobial agents, and oral isotretinoin), hormonal therapy is an option for women with acne that can yield clinical improvement even in the absence of hyperandrogenism [16,17]. Oral contraceptives with or without antiandrogenic progestins and spironolactone are the most common hormonal therapies prescribed. A more detailed discussion of hormonal therapy in the management of acne is presented separately. (See "Oral isotretinoin therapy for acne vulgaris" and "Acne vulgaris: Management of moderate to severe acne in adolescents and adults" and "Acne vulgaris: Overview of management".)

Acne sequelae — Features such as postinflammatory hyperpigmentation and scarring may persist long beyond the successful suppression of active lesions and can be highly distressing for patients (picture 1C-D). Thus, interventions that improve these features can be of value and are reviewed in detail separately. (See "Postinflammatory hyperpigmentation" and "Management of acne scars" and "Acne vulgaris: Overview of management", section on 'Postinflammatory hyperpigmentation'.)

SKIN CARE — Many women also desire advice on skin care regimens. Picking or squeezing lesions, which can increase the risk for scar formation, should be discouraged, and gentle skin cleansing practices are recommended [49]. Many topical acne medications can be particularly irritating in adult skin, and the daily application of moisturizers can limit transepithelial water loss and decrease skin inflammation [49]. Daily sunscreen use is also recommended. (See "Acne vulgaris: Overview of management", section on 'Skin care'.)

Although the methods for determining comedogenicity in skin care and cosmetic products vary and the importance of cosmetic products as contributors to acne is uncertain [40,41], most dermatologists, including ourselves, continue to favor the use of skin care products (eg, moisturizers, cleansers, cosmetics, etc) labeled as "noncomedogenic" and "nonacnegenic" for patients with acne and suggest the avoidance of occlusive agents. In addition, we advise patients who desire to use foundation as part of their makeup routine to select "oil-free" liquid silicone (dimethicone or cyclomethicone) matte foundations over oil-containing products, as the silicone-based products may be less likely to cause follicular occlusion.

PROGNOSIS — Although the progressive decrease in the prevalence of acne with increasing age indicates that spontaneous resolution is likely to occur [11], women may suffer from acne for many years. In one survey study of adult women with acne, the mean age of disease onset was 16 years, and patients reported an average duration of acne of 20 years [26].

The effect of pregnancy on acne vulgaris is variable. Acne may improve, remain unchanged, or worsen during pregnancy [26].

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".)

SUMMARY AND RECOMMENDATIONS

●Acne is a common disorder that affects both adolescents and adults. Although the prevalence of acne vulgaris decreases with age, acne is a significant concern for many adult women. (See 'Epidemiology' above.)

●The factors that contribute to acne in adult women and other populations are similar. Sebum production, keratinization abnormalities, Cutibacterium (formerly Propionibacterium) acnes colonization, and inflammation involving the pilosebaceous follicle contribute to the development of acne vulgaris. (See 'Pathogenesis' above and "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Pathogenesis'.)

●Although hyperandrogenemia promotes the occurrence of acne vulgaris, many women with acne have normal serum androgen levels. Local production of androgens within the pilosebaceous follicles or an increased sensitivity of sebaceous glands to tissue androgens may contribute to acne in these women. (See 'Pathogenesis' above.)

●Many women with postadolescent acne experience premenstrual flares. The reason for this observation is unknown. (See 'Pathogenesis' above.)

●Postadolescent acne most commonly occurs as a consequence of the persistence of adolescent acne. Women often present with both inflammatory and noninflammatory acne lesions. A subset of women with acne may present with lesions primarily distributed on the lower face (picture 1B). (See 'Clinical features' above.)

●The possibility of a hyperandrogenemic state should be considered in women who present with acne. If signs or symptoms of hyperandrogenism are present, laboratory evaluation is indicated. (See 'Hyperandrogenism' above and "Pathogenesis, clinical manifestations, and diagnosis of acne vulgaris", section on 'Acneiform eruptions'.)

●The treatment of adult women with acne involves a review of prior therapies, assessment of lesion types, and the evaluation for conditions that may influence the selection of therapy. Topical retinoids, antimicrobial agents, and hormonal drugs are often used for the management of acne. Gentle skin care practices are also recommended. (See 'Treatment' above and "Acne vulgaris: Overview of management".)