5 Things to Know About Pediatric Acne

Barry S. Goldberg, MD

Disclosures

April 01, 2019

1. Acne Can Affect Quality of Life as Much as a Chronic Disease

The effects of acne on the quality of a child's life are comparable to those caused by such chronic diseases as asthma, seizures, and diabetes.

The most common skin disease in teens, acne affects more than 80% of adolescents by age 17 years. Although it typically begins in puberty, acne tends to have an earlier onset in girls (often by age 8 or 9 years), yet tends to be more severe in boys.

This skin condition carries risk for significant long-term physical and emotional sequelae. Postacne scarring is common (Figure 1). In one recent study,[1] 43% of nearly 2000 patients had acne scarring. Furthermore, although scarring was more frequent in those with severe acne, more than two thirds of the patients had only mild or moderate acne. Scarring correlated significantly with a delay in effective acne treatment.

Figure 1. Postacne scarring. (A) Scarring from infantile acne. (B) "Ice-pick" scarring. (C) Atrophic scarring with discoloration. (D) Hypertrophic scarring. Image courtesy of DermNet NZ

Acne also is associated with developmental disturbances involving body image and sexuality.[2] Teens with acne or postacne scarring can experience a loss of confidence and avoid social interactions with peers at a critical time in their social development. Depression and anxiety can follow, and suicidal ideation is not uncommon.[3]

2. Inflammation Is a Key Event in the Development of Acne

Acne is a disorder of the pilosebaceous unit, found on the face, neck, chest, shoulders, and back. During adrenarche in mid childhood, the zona reticularis of the adrenal gland matures, inducing an increase in circulating adrenal androgens dehydroepiandrosterone (DHEA) and DHEA sulfate. Insulin-like growth factor 1 has a pivotal role in inducing androgen synthesis. These androgens bind to receptors in the sebaceous gland and outer root sheath keratinocytes of the hair follicle. Sebum production rises, and Cutibacterium acnes proliferate to break sebum down into free fatty acids. In turn, this activates proinflammatory mediators, resulting in inflammatory acne.

Pubarche (age 9-11 years) is characterized by a further increase in androgens: adrenal androstenedione and gonadal testosterone. Enlarging microcomedones are apparent at this time (Figure 2).

Figure 2. (A) Open comedones ("blackheads"). Image courtesy of DermNet NZ (B) Closed comedones. Image from Getty Images

Even with normal circulating androgen levels, the sebaceous glands have increased sensitivity. Local 5-alpha reductase levels increase in the sebaceous glands and hair follicles, catalyzing the conversion of testosterone to dihydrotestosterone, a much more potent androgen.

C acnes is an anaerobic, aerotolerant, lipophilic, gram-positive diphtheroid that colonizes the skin after comedogenesis. C acnes thrives with the qualitative and quantitative changes in sebum during puberty, stimulating an inflammatory reaction through innate immunity (Figure 3). Keratinocytes express protease activated receptors, tumor necrosis factor alpha, Toll-like receptors, interferon-gamma, interleukins (IL-8, IL-12, IL-1), and matrix metalloproteinases. Another recently identified factor is the role of biofilms. These microorganisms adhere to each other, and become enmeshed in an extracellular matrix of polysaccharides, proteins, and nucleic acids. Resistant to penetration by antibiotics, biofilms perpetuate acne by upregulating lipase, which converts the sebaceous gland triglycerides into free fatty acids.

Figure 3. Inflammation associated with acne. Image courtesy of DermNet NZ

3: Myth Versus Reality: Beliefs About Causes of Acne

Diet. Many patients believe that their acne is worsened by eating certain foods, but what is the evidence? Indeed, a few foods have been linked with acne; these include high-glycemic foods,[4] whole and skim milk,[5] and saturated fats.[6]

Emotional stress. Although it is widely accepted that acne can lead to emotional or psychological stress, little research has been conducted to show that psychological distress could be the cause, rather than the result, of acne.[7] In one study,[8] acne exacerbations among university students were associated with exam-related stress.

Drugs. The known causes of drug-induced acne, for which the evidence is considered strong, include the following[9]:

  • Halogens (bromides, iodines)

  • Anabolic steroids

  • Testosterone

  • Corticotropin; corticosteroids

  • Lithium

  • Epidermal growth factor receptor inhibitors

  • Isoniazid

Acne ranging in severity is associated with the use of masculinizing doses of testosterone in female-to-male transgender patients.[10]

Friction and manipulation. Acne can be associated with the use of occlusive products or close-fitting athletic equipment, such as a face mask or cap.

4. Neonatal Acne Is a Different Animal Altogether

Figure 4. Acne in a 2-week-old newborn. Image from Alamy

A typical pattern of pustules (without comedones) occurs in up to 20% of neonates (Figure 4).[11] The condition is self-limited, however, and does not predict acne of puberty. The differential diagnosis for these pustules includes the following:

  • Neonatal cephalic pustulosis (Figure 5), caused by the yeast-like Pityrosporum (Malassezia) species overgrowth on the face, scalp, or upper trunk. The condition is self-limited or can be treated with 2% ketoconazole cream.

Figure 5. Neonatal cephalic pustulosis. Image courtesy of DermNet NZ

  • Transient neonatal pustular melanosis (Figure 6), characterized by pustules on the chin, neck or trunk that rupture spontaneously in 24 hours. Residual hyperpigmentation can be seen.

Figure 6. Transient neonatal pustular melanosis. Image courtesy of DermNet NZ

5. Some Childhood Acne Presentations Warrant Endocrine Referral

A sudden onset of acne or treatment-resistant acne can be a red flag for an underlying endocrine disorder—hyperandrogenism of congenital adrenal hyperplasia or polycystic ovary disease.

Infantile acne. Infantile acne (Figure 7) begins at about 6 weeks of age (differentiating it from earlier, neonatal acne) and can last 6-12 months. Features of infantile acne include comedones and inflammatory lesions. Unresolving or severe infantile acne can suggest hyperandrogenism.

Figure 7. Infantile acne. Image courtesy of DermNet NZ

Mid-childhood acne. Acne in children aged 1-7 years (Figure 8) is quite rare, owing to low androgen levels.

Figure 8. Mid-childhood acne. Image courtesy of DermNet NZ

Preadolescent acne. At age 7-12 years, acne could be the first sign of puberty (Figure 9). Typical features are comedones of the central face (the "T-zone") and ears. An endocrine workup is indicated if the acne is severe or accompanied by other signs of androgen excess.

Figure 9. Preteen acne. Image from Alamy

These children should be assessed for signs of virilization, sexual precocity, and growth abnormalities. The endocrine evaluation should include bone age and levels of follicle-stimulating hormone, luteinizing hormone, testosterone, and DHEA sulfate. A referral to pediatric endocrinology may be indicated.

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