Fig. 15.1
Primary lesions
Secondary Lesions
Comedones and cysts can arise secondary to inflammatory papules and pustules but are often not present. Pits and scars are evident in severe cases.
Distribution
The papules and pustules occur on the face, neck, chest, upper back, and also commonly extend beyond the seborrheic areas to affect the arms, trunk, lower back, and genitalia.
Course
The course can vary. Some may have an abrupt onset of an acneiform eruption in the absence of a history of acne vulgaris or an unusually severe acne flare in a patient with a past history of mild acne vulgaris or an aggravation of pre-existing acne. Depending on the medication inducing the acneiform eruption, papules and pustules may begin appearing within the first weeks of therapy or after several months or years. The acne often continues to appear until the inciting drug has been terminated or temporarily discontinued.
There is no seasonal preference as opposed to the idiopathic disease, and acne is not contagious.
Age Group
Acneiform eruptions can occur in teenage and early adulthood years, which coincide with the time period when hormone-dependent juvenile acne most frequently occurs. Also, they can affect children before teenage years as well as adults >30.
Differential Diagnosis
Idiopathic Acne Vulgaris
Any combination of comedones, pustules, cysts, and scarring of varying severity. Commonly affects adolescents and young adults beginning between 9 and 12 years. Onset can occur in later teenage years and into early adulthood and it lasts, with new outbreaks, for months or years. It subsides in most cases by the early 20s, but occasional flare-ups may occur for years. Occurs on the face and neck and, less commonly, on the back, chest, and arms. More rare locations are the scalp, buttocks, and upper legs.
Contact Dermatitis from Industrial Oils
Eczematous features; commonly located on distal extremities in atopic individuals and those with occupational exposure to many chemicals (Fig. 15.2).
Fig. 15.2
Contact dermatitis from industrial oils
Perioral Dermatitis
Characterized by red papules, small pustules, and some scaling on chin, upper lip, and nasolabial fold, and almost exclusively affects women. There is a perioral halo of clear skin. The cause is unknown.
Adenoma Sebaceum
Rare skin condition which is often found in patients with tuberous sclerosis and is often also associated with epilepsy, mental retardation, and angiofibromas (adenoma sebaceum is a misnomer). It is characterized by 2–4 mm papules (angiofibromas) over central face without comedones, pustules, or cysts.
Drug-Induced Perioral Dermatitis
Occurs in patients receiving excessive doses or very protracted treatment with inhaled and topically applied corticosteroids (Fig. 15.3).
Fig. 15.3
Drug-induced perioral dermatitis on a patient using topical steroids
Pyoderma Gangrenosum or Ecthyma
Can mimic iododerma and bromoderma.
Cause of Idiopathic Acne Vulgaris
Idiopathic acne vulgaris is a condition of the sebaceous follicles. The pathogenesis of acne is not yet fully understood, but factors which promote the development of acne are: increased sebum production (which is influenced by endogenous androgens), ductal hypercornification, abnormal follicular keratinization, colonization of the pilosebaceous ducts by P. acnes, inflammation, and genetic predisposition. Propionibacteria are gram-positive, anaerobic, non-motile, pleomorphic rod-shaped cells. P. acnes commonly reside on sebaceous gland-rich areas of skin in humans and can be found on skin from birth until death. A high association between P. acnes levels and sebum production has been shown.
Propionibacteria is thought to be pathogenic in acne due to its production of exocellular enzymes and other bioactive exocellular products, such as proinflammatory lipids, which may act as virulence determinants, as well as its interaction with the immune system. People suffering from severe acne have shown to have increased cellular and humoral immunity to P. acnes, illustrating the interaction of propionibacteria with the immune system. Acne lesions have an early infiltrate of predominantly lymphocytes (CD4+>CD8+), which later progresses to a general infiltrate of mixed cell types including HLA-DR+ Langerhans cells, HLA-DR+ basal keratinocytes, neutrophils, macrophages, and complement factors. It is believed propionibacteria activate lymphocytes via antigens and mitogens, resulting in cytokine release and the beginning of the inflammatory cascade with resulting increases in IL-1α, TNFα, HLA-DR, IL-8, and ICAM-1. The inflammatory cascade leads to disruption of the sebaceous follicle and possibly keratinocyte damage, worsening the acne.
Acneiform skin eruptions very similar to the presentation of idiopathic acne vulgaris has been reported to be caused by several drug categories including: corticosteroids, neuropsychotherapeutic drugs, antituberculosis drugs, immunomodulating drugs, and targeted therapy in the field of oncology. The mechanism by which each drug causes acneiform eruptions varies and is not always known. However, given each drug’s mechanism of action or target of action, many of the drugs can be hypothesized as to why they cause acne based on their effects on natural pathways involved in idiopathic acne vulgaris. The mechanisms will be described further on in the chapter.
Differentiating Factors
There are no specific criteria established to diagnose drug-induced acne or acneiform eruptions, however there are several differentiating characteristics that can aid in diagnosing drug-induced acne versus other more common skin conditions, like idiopathic acne vulgaris. Unlike idiopathic acne, which generally affects people during teenage and young adulthood years, drug-induced acne can have an unusual onset of age in early childhood or later in adulthood (>30 years of age). Drug-induced acne can occur de novo as an abrupt onset of an acneiform eruption in the absence of a history of acne vulgaris, as an unusually severe acne flare in a patient with a past history of mild acne vulgaris, or as an aggravation of pre-existing acne. Unlike idiopathic acne vulgaris, drug-induced acne is characterized by a monomorphic, inflammatory pattern of pustules and papules with either a lack of or late appearance of comedones and cysts occurring secondary to the inflammatory lesions. While idiopathic acne vulgaris commonly occurs on the face and neck and, less commonly, on the back, chest, and arms, drug-induced acne will extend beyond the seborrheic areas, often involving the arms, trunk, lower back, and genitalia. Drug-induced acne is more resistant to conventional acne therapy than idiopathic acne. With no defined criteria and a lack of any overwhelming distinguishing features, diagnosis can be difficult, but an exhaustive search for a causative agent must be completed in all suspected cases. A time relationship between medication ingestion and development of symptoms is crucial in establishing a diagnosis of drug-induced acne. Onset of acne after drug implementation, improvement after drug withdrawal, or recurrence after drug reintroduction can establish this relationship.
Helpful hints for clinicians to differentiate drug induced acneiform eruptions from idiopathic acne vulgaris can be found in Table 15.1.
Table 15.1
Differentiating drug-induced acneiform eruptions from idiopathic acne vulgaris
Drug-induced acneiform eruption | Idiopathic acne vulgaris |
|---|---|
Monomorphic, inflammatory pattern of papules and pustules | Polymorphic pattern of comedones, pustules, cysts, and scarring of varying severity |
Lack of comedones and cysts or their late appearance secondary to inflammatory lesions | Comedones and cysts are characteristic skin lesions |
Extension beyond seborrheic areas to include arms, trunk, lower back, and genitalia | Localized primarily on seborrheic areas such as the face and neck and, less commonly, on the upper back, chest, and arms |
Can affect young children and adults >30 years of age | Commonly affects adolescents and young adults |
Resistant to conventional acne therapy | Improves with conventional acne therapy
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