| Table 3-1 Acne Variants |
| Type | | Clinical Features |
| | Acne fulminans | | – Severe form of nodulocystic acne in young males (13–16 years old)
– Presents with sudden-onset suppurative nodular acne with ulceration, eschars and systemic symptoms (may include myalgias, arthralgias, fever, ↑ ESR, ↑ WBCs, ± sterile osteolytic bone lesions typically over clavicle or sternum)
– Treat with low-dose accutane and prednisone or prednisone alone initially, followed by isotretinoin (to prevent flare and formation of granulation tissue) |
| | Acne conglobata
(Figures 3.1A, 3.2A) | | – Acute-onset nodulocystic acne without systemic manifestations
– Part of the follicular occlusion triad (dissecting cellulitis of scalp, pilonidal cyst and hidradenitis suppurativa) |
| | Acne excoriée
(Figure 3.1B) | | – Mainly seen in young women with emotional or psychological disorders (such as obsessivecompulsive disorder) who repeatedly pick at lesions
– Presents as mild acne with several excoriations, crusted erosions and sometimes ulcerations with subsequent scarring
– Antidepressants may be warranted |
| | Acne with underlying
endocrinologic abnormality
(Figure 3.1C) | | – If acne with accompanying hirsutism ± irregular menses, check lab work for hormonal abnormality (check LH, FSH, DHEA-S, free and total testosterone) – Source of androgens Ovarian androgens: testosterone
Adrenal androgens: DHEA-S, 17-hydroxyprogesterone Polycystic ovarian syndrome (PCOS): – Seen in 5–10% of women of reproductive age – Androgen excess causing hirsutism, irregular menses, ± polycystic ovaries, obesity, insulin resistance, ↑ LH/FSH ratio, ↓ fertility, ↑ testosterone – Acne lesions typically nodular and involve lower ½ of face (especially jawline) – Treatment: oral contraceptive pill (resulting in ↑ SHBG, ↓ free testosterone), spironolactone (off-label, blocks androgen receptor) Late congenital adrenal hyperplasia: – ↑ DHEA-S or 17-hydroxyprogesterone due to partial deficiency of adrenal enzymes (commonly 21-hydroxylase or 11-hydroxylase) |
| | Industrial acne | | – Due to exposure to insoluble cutting oils or chlorinated aromatic hydrocarbons (such as chlorinated dioxins and dibenzofurans)
– Chloracne (form of industrial acne): presents with comedones, pustules and cysts over malar cheeks, retroauricular region, and scrotum |
| | Acne mechanica | | – Due to repeated obstruction of the pilosebaceous unit through friction/pressure |
| | Neonatal acne (Cephalic
neonatal pustulosis) | | – Begins around 2 weeks of age and often resolves by third month of age
– Presents with erythematous small papules on cheeks |
| | Infantile acne | | – Typically begins around 3–6 months of age, resolves within 1–2 years |
| | Drug-induced acne
(Acneiform eruption) | | – Due to corticosteroid, phenytoin, lithium, isoniazid, iodides, epidermal growth factor receptor inhibitors (EGFRI: cetuximab, erlotinib, gefitinib), anabolic steroids
– Presents with abrupt-onset monomorphic-appearing papules and pustules; comedones typically not seen |
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