Acne Vulgaris

Overview

Epidemiology

• The most common skin disease in the United States
• Affects approximately 80% of people at some point in life:
  • Frequently occurs in preadolescence, but can develop in adulthood
  • Often resolves by the 4th decade, but can persist in some patients
  • 20% of patients will develop severe acne and scarring.
• Demographics:
  • Boys are more commonly affected in adolescence.
  • Women are more likely to be affected as adults.
  • People of Asian and African descent more frequently suffer from severe acne.
  • Caucasians more often have mild acne.

Etiology

• Genetic predisposition (heritability: 50%–90%)
• Cutibacterium acnes (formerly known as Propionibacterium acnes)
• Aggravating factors:
  • Hormonal variation:
    • During puberty or menstrual cycle
    • Pregnancy
    • Congenital adrenal hyperplasia
    • Polycystic ovarian syndrome
  • Mechanical occlusion:
    • Underwire bras
    • Headbands
    • Shoulder pads
  • Cosmetics
  • Stress
  • Medications:
    • Lithium
    • Steroids
    • Anticonvulsants
  • Diet:
    • Dairy (due to hormonal components in milk)
    • High glycemic index foods

Pathophysiology

Acne vulgaris is a disorder of the pilosebaceous unit (which includes the hair follicle and sebaceous gland) and is characterized by 4 pathogenic factors:

• Follicular hyperkeratinization: corneocyte cohesiveness → hyperkeratotic plugging in the upper follicle, causing retention of sebum and leading to a microcomedo
• Excessive sebum production:
  • Androgens ↑ sebum production
  • Sebum accumulates with keratin → comedo formation
• Colonization of follicles by C. acnes:
  • Sebum acts as a nutrient and growth medium for C. acnes.
  • C. acnes produce enzymes that degrade keratin and stimulate inflammation.
• Inflammation:
  • C. acnes trigger an innate immune response → proinflammatory cytokine release → activation of neutrophils → mild perifollicular inflammation → inflammatory papule or pustule development
  • Neutrophils and C. acnes release enzymes → follicular rupture into the dermis → a more marked and deeper inflammatory response → inflammatory nodule (also called a cyst) development

Clinical Presentation

Classification and presentation of acne lesions

Noninflammatory acne (comedones):

• Hyperkeratotic plug composed of corneocytes in the lower portion of the follicular infundibulum
• Open comedones:
  • Commonly called “blackheads”
  • Dilation and plugging at the follicular orifice on the skin surface
  • Contains brown or black keratotic material (due to oxidization of fatty acids)
  • < 5 mm
• Closed comedones:
  • Frequently called “whiteheads”
  • Plugging occurs at the follicular orifice below the skin surface.
  • Skin-colored, white, or gray papules
  • Smooth
  • < 5 mm
  • Precursor lesion to inflammatory acne

Inflammatory acne:

• Papulopustular acne:
  • < 5 mm
  • Superficial papules or pustules
  • Inflamed
• Nodular acne:
  • Tender
  • Inflamed
  • Much deeper

Common locations

• Face
• Neck
• Upper chest
• Back
• Shoulders

Sequelae

• Postinflammatory hyperpigmentation:
  • Results at the site of an active or resolving lesion
  • Increased risk in those with darker skin pigmentation
  • Can persist for months
  • Resolves spontaneously
• Scarring:
  • More likely to occur with inflammatory acne
  • Types:
    • Atrophic (“ice pick” or “boxcar” scars)
    • Hypertrophic
    • Keloids

Severe variants

The following variants are rare forms of acne that more often affect adolescent boys and men.

• Acne fulminans:
  • Large, inflammatory, painful nodules
  • Friable plaques with:
    • Erosions
    • Ulcers
    • Hemorrhagic crusts
  • Commonly occurs on the trunk
  • Can be associated with systemic signs and symptoms:
    • Fever
    • Malaise
    • Arthralgias
    • Splenomegaly
    • Erythema nodosum
• Acne conglobata:
  • Aggregates of blackheads may be seen.
  • Nodules coalesce to form sinus tracts (large, fluctuant, linear lesions).
  • May drain foul-smelling discharge
  • Tender
  • Large, irregular scars form.
  • Increases in severity over time
  • Common locations:
    • Back
    • Chest
    • Buttocks

Diagnosis and Management

Diagnosis

The diagnosis is clinical and based on the physical examination. No laboratory or skin biopsy is required.

Patient counseling

• Skin care:
  • Use gentle skin cleansers.
  • Use non-comedogenic cosmetics and skin care products.
  • Avoid picking at lesions or aggressively scrubbing skin.
• Patient education:
  • Acne vulgaris is a long-term condition.
  • Improvement is often slow and requires consistency with the treatment regimen.
  • Response to treatment regimens vary.

Medical therapy for mild disease

These treatments are indicated for all patients with inflammatory disease in order to prevent sequelae and complications.

• Topical retinoids:
  • Normalizes follicular hyperproliferation and minimizes inflammation
  • Also helps with postinflammatory hyperpigmentation
  • Options:
    • Tretinoin
    • Adapalene
    • Tazarotene
• Topical benzoyl peroxide:
  • Has antibacterial properties
  • Should not be used simultaneously with topical retinoids
• Topical antibiotics:
  • Not used as monotherapy due to antibiotic resistance
  • Options:
    • Clindamycin
    • Minocycline
    • Erythromycin
• Salicylic acid:
  • May be used as an alternative to topical retinoids
  • Targets follicular hyperproliferation and abnormal desquamation
• Azelaic acid:
  • May also be used as an alternative to topical retinoids
  • Comedolytic and anti-inflammatory, and has antibacterial properties
  • Also helps with postinflammatory hyperpigmentation

Medical therapy for moderate and severe disease

In addition to the above measures, the following may be added:

• Oral contraceptives and/or spironolactone:
  • Used in women
  • Reduces androgen effects in order to minimize sebum production
• Oral antibiotics:
  • Used if a patient is not a candidate for other systemic therapies
  • Options:
    • Tetracyclines (preferred)
    • Cephalosporins
    • Macrolides
    • Penicillins
    • Trimethoprim-sulfamethizole (TMP-SMX)
• Isotretinoin:
  • Targets all 4 pathogenic factors
  • Indicated for severe or resistant acne (including acne fulminans and acne conglobata)
  • Requires close monitoring due to the risk of: 
    • Hyperlipidemia
    • Transaminitis
    • Vision changes
    • Teratogenic effects
  • Patients must use 2 forms of contraception while on therapy and for 1 month post-therapy.

Complications and Prognosis

Complications

• Psychosocial impacts due to the appearance of the affected skin:
  • Low self-esteem
  • Anxiety and depression
• Folliculitis: 
  • May develop with prolonged use of topical antibiotics
  • Often results from gram-negative organisms
• Morbihan disease: 
  • Rare
  • Soft tissue edema and erythema of the face
• Acne fulminans can occur from isotretinoin use (despite also being a treatment for the condition).

Prognosis

• Acne vulgaris is a long-term condition.
• Most cases will eventually clear spontaneously.
• In some patients, acne may persist throughout adulthood.
• Overall, the prognosis is good with treatment.

Differential Diagnosis

• Rosacea: a chronic inflammatory disease of the skin associated with capillary hyperreactivity, usually seen in middle-aged women. Patients present with facial erythema, telangiectases, papules, pustules, and phymatous changes. The absence of comedones distinguishes rosacea from acne vulgaris. The diagnosis is clinical, and management involves avoiding triggers, gentle skin care, topical and/or oral antibiotics, and laser or surgical therapies.
• Folliculitis: a common skin condition characterized by inflammation of hair follicles due to an infectious agent (most commonly Staphylococcus aureus). Patients present with pruritis, follicular pustules, and erythematous papules. There are no comedones. The diagnosis is clinical. Management is generally supportive, but may involve topical or oral antibiotics for severe cases.
• Hidradenitis suppurativa: a chronic inflammatory condition of the hair follicle and associated structures. The condtion leads to follicular occlusion and rupture which, in turn, causes abscesses, sinus tracts, and scarring, which commonly occur in axillary, groin, and inframammary regions. The diagnosis is clinical. Management is based on the severity, and can include topical or oral antibiotics, intralesional corticosteroids, oral retinoids, debridement or surgical excision, and immunosuppressive medications.
• Keratosis pilaris: a common condition that causes small, pointed, follicular papules on the extensor surfaces of the upper arms or thighs secondary to keratinization. Erythema may be present. The diagnosis is clinical. Management is unnecessary, but salicylic acid and retinoids may be used.
• Periorificial dermatitis: a condition that causes an erythematous, papulopustular eruption that starts at the nasolabial folds and spreads periorally. Comedones are not present. The diagnosis is clinical. Management involves avoiding causative agents (such as steroids or fluoride) and topical or oral antibiotics.
• Sebaceous hyperplasia: a common condition caused by enlargement of sebaceous glands. Patients with a history of “oily skin” may develop umbilicated, skin-colored, or yellowish papules, frequently involving the forehead, nose, and cheeks. The diagnosis is clinical, although biopsy may be performed to rule out basal cell carcinoma (due to its similar appearance). Management is not necessary, but dermabrasion, laser therapy, isotretinoin, or surgical removal may be done for cosmetic reasons.