Hot Topics in Pediatric Dermatology

Lian Sorhaindo; Anthony Rossi; Andrew Alexis; Nanette B Silverberg


Expert Rev Dermatol. 2010;5(3):259-267. 

In This Article

Acne Vulgaris: What's New?

The session 'Acne vulgaris: what's new?' was presented by Nanette B Silverberg from St Luke's Roosevelt and Beth Israel Medical Centers (NY, USA). Acne vulgaris is an inflammatory disorder initiated by blockage of the sebaceous hair follicle seen most commonly on the face, shoulders, chest and back. Its onset is typically preceded by increased androgen production beginning in adolescence, which promotes occlusion of the sebaceous hair follicle or pore blockage, increased sebum production, bacterial overgrowth and inflammation. The bacterium Proprionobacterium acnes flourishes in the setting of blocked or clogged pores. P. acnes digests and metabolizes sebum, turning triglycerides into free fatty acids. The free fatty acids and other products of P. acnes, in turn, produce inflammation. Prolonged or severe inflammation causes rupture of the hair follicle or cysts. There are a number of variants of acne vulgaris, including comedonal, papular, pustular and nodulo-cystic. The development of acne vulgaris may result in the following sequelae, including hyperpigmentation, scarring and loss of self-esteem. Patients with acne have been shown to have significantly lower self-image scores than those without acne. Rigopoulous reported that 64.4% of Greek acne teens report impairment in body image.[1] A number of teens were noted to have poor self-esteem in the absence of obesity and depression.[2]

The current literature explores new concepts in the pathogenesis of acne vulgaris, including the chronicity of the disease, the formation of the microcomedone or subclinical pore blockage, and the role of peroxisomal proliferator-activated receptors (PPARs). PPARs are ligand-activated transcription factors (PPARa, PPARb/d and PPARg). PPARb/d is expressed on keratinocytes, and form heterodimers with RXR receptors. PPARs have prodifferentiating effects.[3] In addition, the consumption of milk, a bioactive compound, may influence comedogenesis due to natural hormonal content and usage of recombinant bovine growth hormones.[4]

High carbohydrate load or high glycemic index diets may exacerbate acne via insulin production. Endocrine abnormalities (including polycystic ovarian syndrome, congenital adrenal hyperplasia, metabolic syndrome and insulin resistance) in obese teenage patients can be associated with acne in both sexes, especially in girls with irregular menses and hirsutism. Laboratory studies (midcycle for female patients) may include dehydroepiandrosterone sulfate (DHEAS), luteinizing hormone/follicle-stimulating hormone, electrolytes, free testosterone, thyroid function tests, prolactin and 17-OH ketosteroids. An abdominal ultrasound, as well as a fasting glucose and insulin level, should be considered in both male and female patients, since insulin resistance and high glycemic load may, as studies suggest, exacerbate acne.[5]

Currently, standard regimens include benzoyl peroxide, retinoids, combination agents (including synergistic formulations of benzoyl peroxide with erythromycin, clindamycin or adapalene, as well as clindamycin and tretinoin combinations), oral antibiotics for moderate-to-severe acne and isotretinoin for patients with acne scarring, cysts and oral antibiotic resistance.[6] Additional therapies include topical dapsone and hormonal interventions with oral contraceptives. Devices for acne vulgaris including light therapy (blue light 10 J, 410 nm) have been shown to kill P. acnes, and decrease cysts, scars and acne lesions.[7] Current therapeutic challenges include antimicrobial resistance of P. acnes and the difficulty of prescribing isotretinoin. Reducing antibiotic or antimicrobial resistance can be achieved through subantimicrobial dosing, use of combination products with benzoyl peroxide, avoiding usage of topical erythromycin or clindamycin with an adapalene/benzoyl peroxide combination or topical dapsone and, finally, once-daily slow-release minocycline, thereby reducing noncompliance of adolescence.


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