Pustules

Definition

Acne vulgaris (common acne) is a disorder affecting pilosebaceous units in the skin ( Fig. 12.1 ). The cause is multifactorial. Clinical lesions range from noninflamed comedones to inflammatory papules , pustules , and nodules .

Incidence

Acne is the most common disease seen by a dermatologist. It begins at a surprisingly young age; comedones can be found on examination in 50% of boys aged 9 to 11 years. Acne is a physically and psychologically devastating condition and must be treated aggressively. The incidence and severity of the disease increase during the teenage years and early adulthood, affecting approximately 85% of young people between the ages of 12 and 24 years. Contrary to popular belief, acne is not confined to teenagers. It may continue into the third and fourth decades of life, especially in women; in some patients, it does not begin until then.

History

The patient usually makes the diagnosis and often has attempted therapy with over-the-counter medication. A history of hirsutism, hair thinning usually localized to top of the scalp, or irregular menses in a woman with acne should lead to the consideration of possible androgen excess. Adult women often complain of acne along the jawline that worsens around the time of their period ( Fig. 12.2 ). For any ethnicity with darker skin, acne can lead to marks of postinflammatory hyperpigmentation, which can take many months to resolve. Topical or systemic corticosteroids can also cause an acneiform eruption.

Physical Examination

The noninflamed lesions in acne are called comedones and are of two types: (1) the open comedone or “blackhead,” which appears as a dilated pore filled with black keratinous material (not dirt); and (2) the closed comedone or “whitehead,” which is a small, flesh-colored, dome-shaped papule that often is difficult to see ( Fig. 12.3 ). Inflammatory acne lesions are seen more easily by both patient and physician. They appear as papules, pustules, or nodules, depending on the magnitude of the inflammatory response ( Fig. 12.4 ) . Acne is found in areas with numerous sebaceous glands, usually the face and upper trunk. The lower trunk is less often involved, and the distal extremities are always spared.

Differential Diagnosis

The diagnosis of acne is rarely difficult, particularly in teenagers. Occasionally, acne comedones may be confused with flat warts , which are small, flesh-colored, flat-topped papules usually located on the face. On close inspection, the flat wart is seen to have a sharp right-angled edge and a finely textured surface, whereas a closed comedone has a dome-shaped, smooth surface ( Fig. 12.5 ).

Steroid acne is caused by use of corticosteroids and is distinguished from acne vulgaris by its sudden onset (usually within 2 weeks of starting high-dose systemic or potent topical corticosteroid therapy) and appearance (uniform, 2- to 3-mm, red, firm papules and pustules) ( Fig. 12.6 ). Steroid acne caused by topically applied agents occurs most often on the face. With systemic corticosteroids, the eruption is most prominent on the upper trunk.

Pustular acne vulgaris can be confused with bacterial folliculitis or rosacea. In bacterial folliculitis , hairs are visible in some of the pustules and a bacterial culture is positive, usually for Staphylococcus aureus or, less often, a Gram-negative organism. Rosacea is distinguished from acne vulgaris by the presence of a background blush of erythema and telangiectasia, and the absence of comedones. Rosacea also usually occurs later in life.

Angiofibromas, a skin manifestation of tuberous sclerosis, are often incorrectly diagnosed as acne. Clinically, the lesions appear as firm, pink papules that are clustered primarily in the center of the face, are persistent, and are, of course, resistant to acne therapy. Keratosis pilaris, when it affects the facial cheeks, is distinguished from acne by its minute, rough, uniform papules on the background of “red” (e.g., prominent skin vasculature) skin and by its lack of comedones. Keratosis pilaris is a chronic condition and relatively unresponsive to acne treatments.

Laboratory and Biopsy

The diagnosis is almost always made clinically. Occasionally, a bacterial culture is indicated to rule out infection. A biopsy is not indicated but would show an occluded pilosebaceous unit along with inflammation ( Fig. 12.7 ).

Therapy

Four categories of medication have proved efficacious in the treatment of acne: topical agents, systemic antibiotics, systemic retinoids, and hormonal agents. The type of acne guides the choice of treatment. For the majority of patients, systemic retinoids and hormonal therapy are not required.

Systemic retinoids

The oral retinoid isotretinoin became available commercially in September 1982 for use in the treatment of patients with severe acne ( Fig. 12.8 ). This potent vitamin A analog decreases follicular keratinization, sebum production, and intrafollicular bacterial counts. Side-effects are common. Almost all patients experience chapped lips and dry skin, and extracutaneous complications also occur; for example, increased levels of liver enzymes and plasma lipids. Most importantly, systemic retinoids are teratogenic . It is mandatory that female patients not be pregnant when taking isotretinoin. Special consent forms, strict birth control measures, and monthly pregnancy tests are required for women taking isotretinoin. A consent form acknowledging the risk of depression and suicide while on isotretinoin is required for both men and women. There is also a controversial link of isotretinoin to inflammatory bowel disease. Because of these restrictions, the drug is recommended mainly for the treatment of selected patients with severe, therapy-resistant papular/pustular acne or scarring nodular acne ( Fig. 12.9 ). The drug should be prescribed only by physicians who are familiar with its use and participate in a national risk management program ( www.ipledgeprogram.com ).

Isotretinoin is teratogenic.

Course and Complications

With therapy, the prognosis for acne is good, if not excellent. The patient should understand that most therapies provide control of the disease rather than cure, and that improvement does not occur overnight. The only potential cure, other than time, for acne is isotretinoin. If improvement has not been noted after 2 months, more intensive therapy can be prescribed, including increased concentrations of the topical agents, increased dosage of the oral antibiotic, or change in the antibiotic therapy. Continued improvement in the disease is expected with continued therapy. Many patients can discontinue systemic antibiotics after 3 to 6 months, but most require prolonged (often lasting for years) maintenance therapy with topical agents. However, bacterial resistance to antibiotics is becoming more frequent, thereby limiting the usefulness of long-term antibiotic therapy for acne. If acne is not responding to systemic antibiotics and topical therapies, then referral to a dermatologist is warranted. Isotretinoin induces prolonged remissions, if not “cures,” in many patients.

Acne remits spontaneously with time, to a degree that varies widely. For individual patients, there is no way to predict in advance when they will “outgrow” their acne. The goal of therapy is to keep the condition under control as long as it is active.

The major complication of acne is its psychosocial ramifications, which can be devastating for some patients. Patients with severe cystic acne may even be socially ostracized. In an ironic quirk of timing, acne occurs at a time of life when personal appearance is a prime concern and self-consciousness is at its peak. Regardless of the severity of the acne, for patients seeking help (even those with apparently mild disease), the disease is important and deserves serious attention. Patients are not impressed with soothing advice that trivializes their disease and reassures them that they will eventually “outgrow” it.

In addition to the cosmetic liability of active lesions, scars further compound and perpetuate a poor self-image in some patients long after the acne has remitted. Scars are difficult to treat. Dermabrasion, laser “resurfacing,” chemical peels, and surgery have all been employed, with varying results. Because scars are more easily prevented than treated, the emphasis in acne is on early and aggressive medical therapy.

Pathogenesis

Multiple factors are involved in the pathogenesis of acne. The three most significant are:

• 1.

  Androgenic hormones . Under androgen stimulation, sebaceous glands enlarge and increase their sebum production. Before puberty, the responsible androgens are secreted by the adrenal gland. During puberty, the addition of gonadal androgens provides further sebaceous gland stimulation.

• 2.

  Follicular obstruction . For acne to occur, outlet obstruction of the follicular canal is required. All acne lesions begin with a microcomedone. This obstruction occurs because of accumulation of adherent keratinized cells within the canal, forming an impaction. The cause of follicular obstruction is not known, but may also be influenced by androgens.

• 3.

  Bacteria . Proximal to the follicular outlet obstruction, sebum and keratinous debris accumulate. This provides an attractive environment for the growth of anaerobic bacteria, specifically Propionibacterium acnes . These bacteria produce lipase enzymes that hydrolyze the sebaceous lipids, resulting in the release of free fatty acids, which are presumed to cause inflammation. P. acnes play other roles in the pathogenesis of acne (e.g., these bacteria are chemotactic for neutrophils). Regardless of the mechanism, the therapeutic benefit of antibiotics supports the notion that bacteria play a pathogenetic role in acne.

Definition

Candidiasis represents an inflammatory reaction in the skin resulting from infection of the epidermis with Candida albicans . Clinically, the infection appears as a “beefy red” erythematous area with surrounding satellite papules and pustules ( Fig. 12.10 ). The pustules, when present, help in the diagnosis. In this section, candidiasis of the skin is discussed. Mucous membrane infection is discussed in Chapter 22 .