Acne Vulgaris

Acne vulgaris is a common disease that usually begins in adolescence. It also affects a large proportion of young adults.

Acne vulgaris can be quite a disfiguring condition and is usually obvious to anyone that has a face-to-face interaction with the individual.

Definition

Acne vulgaris, also known as 'pimples,' is a chronic inflammatory disease of the pilosebaceous units and usually occurs on the skin of the face, neck, chest, and upper back.

It is characterized by seborrhea, the formation of open and closed comedones (non-inflammatory lesions), erythematous papules and pustules (inflammatory lesions), and in more severe cases with nodules, deep pustules, and cysts.

In many cases, there is some degree of scarring.

Definition of Terms

• Pilosebaceous unit: Composed of hair follicle, hair shaft, and sebaceous gland.

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• Seborrhea: Excessive production of sebum, the predominant lipid on the skin surface.
• Papules: Elevated, solid lesion above the skin surface, 0.5 cm in diameter.
• Pustule: Papule that contains purulent material.
• Nodule: Elevated, solid lesion, 0.5 cm in diameter; a larger, deeper papule.
• Cyst: Nodule that contains fluid or semisolid material.
• Comedones:
• Closed comedones (whiteheads): 1mm skin-colored papules with no follicular opening.
• Open comedones (blackheads): Papules with dilated follicular outlets.

• Acne vulgaris is a universal condition in younger people and typically appears for the first time during early adolescence.
• Although acne vulgaris usually begins in adolescence and frequently resolves by mid-twenties, clinical acne persists into the 20s and 30s in around 64% and 43% of individuals, respectively.
• Community-based studies of acne prevalence range between 35% to 90.7% in Nigeria.
• Similar, and even higher prevalence, up to 100% in a US study, has been found in western societies.

Acne is a multifactorial disease, arising as a result of the interplay of four pathogenic mechanisms:

1. Excessive sebum production
2. Follicular hyperkeratinization
3. Microbial colonization of the pilosebaceous unit by Propionibacterium acnes (P. acnes)
4. Release of inflammatory mediators into the follicle and surrounding dermis

Sebaceous lipid composition, androgens, local cytokine production, and bacteria have been implicated in the abnormalities of the proliferation and differentiation of ductal keratinocytes.

There is retention of hyperproliferating ductal keratinocytes/corneocytes in the pilosebaceous duct. Keratinocytes are the major cells in the epidermis producing keratin, the structural protein in the skin.

The epithelium of the upper hair follicle, the infundibulum, becomes hyperkeratotic with increased cohesiveness of the keratinocytes.

The excess cells result in a plug in the follicular ostium with subsequent accumulation of keratin, sebum, and bacteria in the follicle. These packed concretions cause dilation of the upper hair follicle, producing a microcomedo.

The microcomedone may then evolve into visible open comedones or closed comedones.

Subsequently, inflammatory papules, pustules, and nodules may develop. Scarring and post-inflammatory hyperpigmentation may also occur.

• Genetic factors have been implicated as a risk factor for acne vulgaris, and the heritability of acne is almost 80% in first-degree relatives.
• Acne occurs earlier and is more severe in those with a positive family history.
• Other predisposing factors include:
• Premenstrual state
• Cigarette smoking
• High glycemic diet
• Drugs
• Sweating
• Ultraviolet radiation

Aggravating Factors

• Change in sebaceous activity and hormonal levels (e.g., before or during the premenstrual cycle)
• High humidity conditions
• Local irritation or friction
• Rough or occlusive clothing
• Cosmetics (having a greasy base)
• Diet; chocolate, nuts, fats, colas, or carbohydrates
• Oils, greases, or dyes in hair products

• Clinical features vary as acne is a polymorphic, inflammatory disease of the skin which occurs most commonly on the face (99% of cases) and to a lesser extent on the back (60%) and chest (15%).
• Seborrhea is a frequent and distressing feature.
• The clinical picture can vary from very mild comedonal acne, with or without sparse inflammatory lesions, to aggressive fulminant disease with associated systemic involvement.

• Classical acne (acne vulgaris)
• Neonatal acne: Seen in 20% of healthy newborns
• Infantile acne: After 3-6 months of age and resolves around 2 years. However, may persist into adulthood.
• Acne conglobata: Severe nodulocystic acne usually with severe scarring.
• Acne fulminans: Severe cystic acne with systemic features, including fever, arthralgia, myalgia, hepatosplenomegaly, severe prostration, and osteolytic bone lesions.
• Drug-induced acne: Lithium, isoniazid, phenytoin, iodides, corticosteroids, testosterone, etc.

• ACTH
• Azathioprine
• Barbiturates
• Isoniazid
• Lithium
• Phenytoin
• Disulfiram
• Halogens
• Iodides
• Steroids
• Cyclosporine
• Vitamins B2, B6, B12

Patients with hyperandrogenism may develop severe acne, which is usually difficult to treat. Other manifestations of an increased androgen state include:

• Hirsutism
• Irregular menses
• Clitoromegaly
• Androgenetic alopecia
• Increased libido

• Hyperpigmentation
• Scarring
• Keloids
• Pyogenic granulomas
• Psychological sequelae:
• Low self-esteem
• Depression
• Social withdrawal
• Anxiety
• Anger
• Reduced quality of life

DIAGNOSIS

• Usually clinical.
• Hormonal testing indicated if suspected endocrine abnormalities.

Grading of acne severity

• Acne is usually graded as mild, moderate, or severe based on the typical lesions seen on examination.
• Some of the grading systems count the lesions in terms of number and morphology. Some, however, use photographic standards for comparison.

Treatment Modalities

Aim

• Alleviate symptoms.
• Clear existing lesions.
• Prevent new lesions from forming.
• Treat associated complications.

Successful management of acne is dependent on detailed patient discussion and education. It includes a comprehensive assessment, including:

• Personal and family history.
• A record of present and previous therapies and response to these treatments.
• Careful physical examination.
• Psychosocial review.

Non-Drug Measures

• Basic twice daily washing.
• Use of non-comedogenic moisturizer.
• Avoid aggressive cleaning to avoid irritation or exacerbation of existing lesions.
• Avoid excessive rubbing or squeezing of acne lesions, as it causes further inflammation and scarring.

Drug Measures

Mild Acne: Topical agents are the primary treatment, either in monotherapy or combination. These include:

• Benzoyl peroxide.
• Retinoids.
• Azelaic acid.
• Topical antibiotics like erythromycin and tetracycline.

Moderate Acne: Combination of oral and topical agents may be used.

Severe Acne: Oral agents are the primary treatment. Options include:

• Oral retinoids, with Isotretinoin as the first-line agent for severe acne. It targets the major pathogenic components of acne formation.
• Other oral agents like systemic antibiotics (e.g., doxycycline, tetracycline, erythromycin) and combined oral contraceptives (e.g., cyproterone acetate, spironolactone, and flutamide) that decrease androgen-mediated effects on the sebaceous follicle.

Several factors can affect the severity and prognosis of acne, including:

• Family history.
• Course of inflammation.
• Persistent or late-onset disease.
• Hyperseborrhea (excessive sebum production).
• Truncal acne (acne affecting the trunk or back).
• Psychological sequelae (impact on mental well-being and self-esteem).

Preventing acne involves:

• Health education: Educating individuals about proper skincare and hygiene can help prevent acne.
• Early presentation to dermatologists: Seeking professional dermatological care at the earliest signs of acne can prevent complications.