creation date: 2025-07-04 16:20
tags: Pathologies
Acne Vulgaris
Background
Definitions
Acne vulgaris refers to the cutaneous disorder characterized by chronic or recurrent development of papules, pustules, or nodules on the face, neck, trunk, or proximal upper extremities.
Acne most frequently affects adolescents and young adults but is not limited to these ages.
Etiology and Pathogenesis
The formation of acne vulgaris lesions start with a microcomedo. This is a small, hyper keratotic plug composed of corneocytes in the lower portion of the follicular infundibulum. This is the precursor to closed comedones, open comedones, and inflammatory papules, pustules, and nodules.
The pathogenic factors that develop microcomedones into acne lesions may include:
- Follicular hyperkeratinization
- Increased sebum production by sebaceous glands
- Cutibacterium acnes, an anaerobic diphtheroid that is part of normal skin flora
- Inflammation
The sequence from microcomedones to acne lesions is theorized to be:
- Accumulation of sebum and keratinous material converts a microcomedo into a closed comedo
- Follicular orifice is opened with continued distension forming an open comedo (packed keratinocytes, oxidized lipids, and melanin contribute to dark colour)
- Immune response to C. acnes contribute to development of inflammatory papules and pustules.
- Follicular rupture releases bacteria, proinflammatory lipids, and keratin causing exacerbation to surrounding dermis.
Other factors that contribute to development of acne include:
- Androgens stimulate growth and secretory function of sebaceous glands which leads to increased sebum production
- Increased sebum is also good growth medium for C. acnes as triglycerides used as nutrients
- C. acnes contribute to inflammation and virulence with strains associated with acne more likely to have antibiotic resistance genes.
- Genetics may play a role
Further modifiable contributory factors are discussed with risk factors.
Clinical Presentation
Signs & Symptoms
Typical distribution of acne correlates with areas of the body with large, hormonally responsive sebaceous glands.
- Face
- Neck
- Chest
- Upper back
- Upper arms
Active lesions that may be present include:
- Closed comedones - noninflammatory, <5 mm, dome-shaped, smooth, skin-coloured/white/gray papules
- Open comedones - noninflammatory, <5 mm, papule with central, dilated, follicular orifice containing grey, brown, or black, keratotic material
- Papulopustular acne - inflamed, relatively superficial papules and pustiles, typically <5 mm
- Nodular acne - deep-seated, inflamed, often tender, large papules (≥5 mm) or nodules (≥1 cm); note that nodular is often inaccurate described as cystic
Severity can vary significantly and extent of erythema may be masked by skin pigmentation.
Sequelae includes:
- Postinflammatory hyperpigmentation - risk of hyperpigmentation at site of active or resolving lesion increases with increased baseline skin pigmentation. This can resolve spontaneously or persist for longer.
- Scarring - atropic scars (ice pick, rolling, and boxcar scars), hypertrophic scars, and keloids. More likely with inflammatory acne.
- Postinflammatory erythema
Variants of acne include:
- Acne conglobata - severe form of nodular acne most commonly with young males. Involves the back, chest, and buttocks predominantly. Large, draining lesions, sinus tracts, and severe scarring may occur.
- Acne excoriée - relatively mild acne comedones or inflammatory papules that are chronically and obsessively picked and excoriated, leading to erosions and scarring.
- Infantile acne - begins between 3-6 months of age resulting from elevated androgens from immature glands. Androgen levels fall by age 1-2 and acne will improve.
History & Physical Exam
History should attempt to identify:
- Exposures that may exacerbate or cause acne
- Associated diseases that may require further evaluation (eg. hyperandrogenism, SAPHO (synovitis, acne, pustulosis, hyperostosis, osteitis) syndrome, acne fulminans)
- Age of onset
- Medication, medical, and family history
- Menstrual history in females and association with acne flare
- Prior treatment and response
- Joint, bone, or systemic symptoms in patients with severe acne
Physical exam should assess:
- Lesion types and distribution
- Lesion stages
- Signs of hyperandrogenism (eg. early onset body odour, early development of axillary or pubic hair, accelerated growth, advanced bone age, genital maturation)
- Presence of complications and/or sequelae
Risk factors
Some contributory factors include:
- Skin trauma - repetitive mechanical trauma such as scrubbing with soaps, detergents, astringents, or other agents can worsen acne by rupturing comedones
- Diet - increased milk consumption and high glycemic load diets may result in acne
- Stress - psychogenic stress may exacerbate acne
- Insulin resistance - stimulates androgen production and increased cerem IGF-1 which is linked to increased facial sebum excretion
- BMI - inconclusive findings with association of decreased and increased risk with higher BMI
Diagnosis
Criteria
Diagnosis is made using physical examination and findings of characteristic lesions in characteristic distributions.
Work-up
Workup is generally unnecessary in most patients. Additional testing may be needed if:
- Signs of hyperandrogenism - endocrinology referral
- Acne fulminans - assessment of systemic involvement with blood work and other laboratory tests
- Symptoms suggestive of SAPHO syndrome
Differential
Alternative diagnoses include other skin diseases and acneiform eruptions.
- Rosacea
- Periorificial dermatitis
- Demodex folliculitis
- Pseudofolliculitis barbae
- Gram-negative folliculitis
- Pityrosporum folliculitis
- Facial angiofibromas
Certain drugs and substances may cause acneform eruptions as well.
Red Flags / Complications
Potential complications include:
- Psychologic effects - embarrassment, anxiety, and lowered self-esteem due to appearance of affected skin or disfiguring scars
- Gram-negative folliculitis - long-term systemic antibiotic treatment of acne vulgaris can lead to gram-neg folliculitis due to colonization of lesions by organisms such as Enterobacter, Klebsiella, Pseudomonas, Proteus, or Escherichia species. Presents as initial response to oral antibiotics followed by apparent resistance and worsening of acne.
- Acne fulminans - acute eruption of large, inflammatory nodules and friable plaques with erosions, ulcers, and hemorrhagic crusts. Systemic symptoms may be associated. Pathogenesis is unclear but can be triggered by isotretinoin therapy or spontaneously.
- Solid facial edema - facial soft tissue edema and erythema that may wax/wane but requires treatment.
Management
Lifestyle / Social
Lifestyle modifications are recommended in conjunction with treatment.
- Use gentle skin cleansers (pH 5.5-7) rather than soaps or scrubs (pH 9-10)
- Avoid aggressive scrubbing
- Use noncomedogenic cosmetic products
- Avoid picking acne
Expectation management is also important as improvement can take time and adjustment may be necessary. Additionally, therapies are often suppressive and not curative and thus a long-term maintenance regimen may be necessary.
Pharmacological / Interventional
In cases of mild acne vulgaris (scattered comedomes) or small (<5 mm), inflammatory papules without scarring and limited skin involvement), the approach is as follows.
Mild comedonal acne:
- Topical retinoid (eg. topical tretinoin, adapalene, tazarotene, and trifarotene)
Mild papulopustular and mixed (comedonal and papulopustular acne):
- Topical retinoid and topical antimicrobial (eg. benzoyl peroxide with or without topical clindamycin)
- Benzoyl peroxide and topical antibiotics
Alternatively, salicylic acid or azelaic acid can be used for patients who cannot use topical retinoids.
In cases of moderate to severe acne vulgaris, consider systemic therapy such as hormonal agents, antibiotics, and oral isotretinoin.
The typical approach to maintenance therapy requires transitioning to topical retinoid monotherapy following stable improvement for at least 3-6 months.