Skin Disorders Guide

Diagnostic Hallmarks

1. Distribution- face and shoulders
2. Pustules are intermingled with comedones and inflammatory papules

Clinical Presentation

A wide variety of lesions are found in acne, only a portion of which are pustules. Open comedones (blackheads) consist of a pigmented keratinous plug firmly lodged at the orifice of a sebaceous follicle. The reason for the black color is not fully understood, but it most likely occurs because of the deposition of melanin granules in the multiple layers of compacted keratinocytes that make up the plug.

Closed comedones are dome-shaped 1-2-mm papules. They are skin-colored rather than black. The central follicular orifice is often so small as to be clinically inapparent. These, too, occur because of a keratinous plug in the outlet of a sebaceous follicle, but in these lesions the plug lies below the surface of the skin at a point too deep to pick up color from the surface melanocytes.

Pustules situated on an inflammatory base occur when the plugged duct of an androgen-driven sebaceous follicle ruptures with extrusion of the keratin plug and retained bacterial, keratinous, and sebaceous materials into the surrounding dermis. This extrusion causes a brisk foreign body inflammatory response. Thus, acne “white heads” initially contain mostly a solid white keratin core and only subsequently accumulate enough neutrophils to become a true pustule.

Inflammatory papules without an overlying pustule occur when the follicular rupture and induced inflammatory response occur at a level too deep to result in a visible pustule. Inflammatory cysts and pseudocysts 1-2 cm in diameter develop when the process is unusually intense and occurs even deeper at the level of the sebaceous gland itself. Such cystic lesions are often fluctuant and painful. Moreover, as opposed to the other lesions of acne, they heal with scar formation.

Most instances of pustular acne begin at puberty. Acne lesions at this early age generally consist of comedones and small pustules, these are usually found on the forehead and upper cheeks. During the late teen years, the mix of lesions shifts toward larger, more inflammatory pustules and papules. These lesions generally occur on the lower cheeks, chin, and jaw line. Inflammatory lesions may also develop over the shoulders and upper arms. The diagnosis of acne is made on the basis of history and clinical examination.

Clinical Presentations

Acne conglobata is the name used for the presence of multiple, deep, cystic, scarring lesions over the face and upper trunk. It occurs predominantly in individuals with genetically malformed sebaceous follicles. One indication of this structural abnormality is the presence of multiple, closely spaced twin comedones in the skin adjacent to cysts. Some individuals with severe acne conglobata have associated fever, leukocytosis, and arthralgia.

Drug-induced acne is caused by certain medications. The administration of phenytoin (Dilantin) to individuals already prone to acne worsens the severity and duration of what is otherwise typical-appearing acne vulgaris. Administration of corticosteroids can cause an acne-like folliculitis in which small pustules without keratin plugs develop in considerable profusion on the chest, back, and shoulders. Comedones and cysts are not found. Ingestion of large amounts of iodine also leads to the presence of an acneiform eruption.

Chloracne is the name used for contactant-induced acneiform lesions. This eruption can be induced through occupational exposure to tars, cutting oils, and chlorinated hydrocarbons and through the use of petrolatum pomades as hair dressings. The use of the herbicide Agent Orange in Vietnam led to the development of such “chloracne” in many soldiers. Babies occasionally develop a few acne lesions during the first month or so of life, presumably as a result of maternal hormonal stimulation.

Acne excoriee des jeunes filles occurs when individuals neurotically pick at acne lesions. Because of this chronic picking, minor acne lesions are kept inflamed and active for weeks or even months at a time. The excoriated papules eventually heal with hypopigmentation and, sometimes, frank scarring.

Course and Prognosis

Generally, the peak activity of acne is in the middle to late teen years, with steady improvement ensuing in the early 20’s. Occasionally, however, disease activity continues into the fourth decade. Women seem particularly prone to this long-lasting form of acne.

Hormonal factors play an important role in the course of acne. Acne, in general, seems to be more severe in men, and cystic lesions, which are common in men, are only rarely found in women. In women, a monthly peak of acne activity often occurs during the week prior to their menses. Acne tends to improve during the latter half of pregnancy, but rebound worsening sometimes occurs following parturition and cessation of lactation.

It is difficult to predict the future severity of acne at the time a young patient is first seen. The presence of cysts and a family history of scarring acne are, however, bad prognostic signs.

When acne is untreated, individual small papules and pustules resolve spontaneously in 7-10 days. Resolution of these lesions does not result in scarring even when some relatively modest degree of picking is carried out. Larger papules and all cysts require several weeks to resolve. Subsequent postinflammatory hyperpigmentation and hyperopigmentation may persist for months. Scarring is occasionally found at the site of deep-seated papules and is almost invariably present following resolution of cystic lesions.

Pathogenesis

Acne is a disease of complex genetic and hormonal factors. Identical twins tend to have acne of equal severity and similar type. Parents who have had troublesome acne tend to have children with a similar problem. The differences in severity of acne among siblings and, within families, from one generation to the next suggest, however, that genetics simply provides a permissive setting for the other factors.

Stimulation of the sebaceous glands by androgenic hormones appears to be a necessary factor for induction of acne in both men and women. Thus acne does not occur until puberty when such hormonal stimulation first begins to develop, and castrated men and oophorectomized women do not develop acne. Serum androgen levels may be slightly elevated in men and women with cystic acne, but it seems likely that the hyperresponsiveness of the sebaceous follicle to normal hormone levels is the more important hormonal factor. The significance of androgenic factors in women is underscored by the regular presence of acne in patients with polycystic ovarian disease and in those with sterol hydroxylase deficiencies.

Hormonal stimulation leads to increased sebaceous gland size and to increased sebum output. The presence and severity of acne correlate in a general way with production levels of sebum; but high sebum flow rates alone, in the absence of follicular plugs, do not cause acne.

The presence of a follicular plug is an important and necessary factor for the development of an acne lesion in any given follicle. Such blockages are caused by the accumulation of compacted, dead, cornified cells within the orifice of the follicle. Several hypotheses exist to explain the formation of these plugs- genetic malformation of the follicle, stimulation of follicular keratinization by bacteria present in the follicle, or hormonal effects on the follicle wall. Such information as is available favors the first of these.

Once a blockage is present in a follicle, bacteria, mostly the omnipresent Propionibacterium ames, causes lipolysis of the sebum with consequent formation of free fatty acids. It is hypothesized that these acids, bits of keratin, and bacterial proteins are then extruded through a distended and, subsequently, disrupted follicular wall. Once within the dermis, they call forth an intense neutrophilic inflammatory infiltrate that leads to the formation of pus.

The various therapeutic modalities address the roles played by hormonal stimulation, follicle plugging, and bacterial induction of inflammation.

Therapy

Mild acne (comedones and small pustules) can be treated with topical preparations that, because of their exfoliating effect, “peel out” the plugged follicular orifices. Benzoyl peroxide lotion, gel, or cream in a 5% concentration can be applied once nightly after normal facial washing. If no peeling effect is noted at the end of the first week, the frequency of application is increased to twice daily, or the strength is increased to 10%. Mild redness and chapping are expected effects of this therapy during the first few weeks of application. This reaction becomes less troublesome during the second month of treatment, even though the therapeutic effect continues. Benzoyl peroxide not only unplugs follicles by the induction of peeling but also reduces the number of P. acnes through oxidative destruction of the organisms.

Topically applied tretinoin (Retin-A) is both a little more effective and a little more irritating than benzoyl peroxide. The gel or cream in a 0.025% concentration is applied each evening. The strength and frequency of applications can be modified for the use of benzoyl peroxide. The effect of Rectin-A on follicular plugs is two fold- it removes plugs through the induction of postinflammatory peeling and it “dissolves” the plugs by way of its disruptive effect on the cement-like substance that binds the keratinized cells together.

A number of alternate approaches for the induction of peeling exist. These include:

• the application of sulfur, salicylic acid, and resorcinol in an alcohol vehicle
• natural or artificially administered ultraviolet light
• mechanical scrubbing of the face with various abrasive products and
• the use of cryotherapy in the form of liquid nitrogen spray or carbon dioxide slush.

All of these methods result in peeling thus help to free plugged follicles. No one approach is pcrior to benzoyl peroxide or retinoic acid.

Patients with more severe acne (inflammatory papules,large,pustules, and cysts) almost always require the addition of antibiotics either applied topically or administered systemically. Orally administered tetracycline in a dosage of 1000 mg has historically been the antibiotic of choice. This approach has an excellent record of safety and efficacy.

Alternatively, topically applied 1.5-2.0% erythromycin (A/T/S, Benzamycin, Emgel, Erycette, T-Stat) or 1 % clindamycin (Cleocin-T) can result in a degree of improvement roughly equal to that obtained with 500 mg of orally administered tetracycline. With anyone of these three preparations, 75% of patients will be substantially improved by the end of 6-8 weeks of treatment. For those who fail on this regimen, other orally administered antibiotics are usually substituted. Erythromycin, because of its low cost and freedom from side effects, is usually tried first. The dosage used is 1.0 g/day. Minocycline (Minocin) and doxycycline (Vibramycin) given as 100 mg once or twice daily are at least as efficacious as erythromycin. The former is very expensive and occasionally causes disturbance in vestibular function and cutaneous discoloration, the latter, though inexpensive, may cause a photosensitivity reaction.

Mechanical extrusion (acne surgery) of the follicular keratinous plugs is carried out by many physicians. Such manipulation can be temporarily helpful, but its usefulness in the long run is much less clear. Patients often object to this manipulation because of discomfort and the unsightly appearance that remains for hours after the procedure. I do relatively little acne surgery, instead allowing patients to (carefully!) open and squeeze out the plugs themselves at home. Chronic picking and/or squeezing is, however, discouraged, since repeated manipulation creates additional inflammation and prolonged healing times. Neither acne surgery by the physician nor gentle extrusion by the patient causes scarring; scarring is directly related to the depth and severity of the inflammation in the acne lesion itself.

Dietary therapy is sometimes advised. Anecdotal reports of its usefulness are numerous, but the few controlled studies available suggest that it is of little help. Most investigators believe that oil-based cosmetics should be used as little as possible. I am less sure about this, though results of animal studies suggest that these cosmetics have some propensity for the induction of corned one formation.

Many acne patients, particularly those over age 20 years, experience a flare of their acne during periods of stress. Usually, little can be done to lessen this problem, but counseling, tranquilizers, or antidepressants are occasionally indicated.

Blockage of the androgen effect on the sebaceous glands can be achieved through the use of estrogens. The estrogens are usually administered in the form of birth control pills. Oral contraceptives used for the control of acne probably need to contain 50 mg of estrogen. Brands such as Ortho-Novum, Norinyl, and Demulen are good choices, as the progestational agents they contain are among the least sebotropic.

Patients with severe acne unresponsive to the therapeutic regimens described above can be treated with isotretinoin (Accutane). Use of this retinoid in a dose of 40-80 mg/day for a 4-month period leads to very impressive improvement. Unfortunately, the side effects are troublesome and the cost is high. Nevertheless, this approach leads to highly satisfied patients 95% of the time. Moreover, for most patients, no further medical treatment is likely to be necessary for at least the subsequent 12 months.

Tags:acne, acne vulgaris, acneiform lesions, blackheads, Lesions, papules, Postular Disease, pseudocysts pustules