Acne Vulgaris and Acne Rosacea

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[edit] Acne Vulgaris and Acne Rosacea

Frank Parker

James C. Shaw


[edit] ACNE VULGARIS

Acne vulgaris, commonly referred to as “acne,” is a multifactorial inflammatory disorder of the pilosebaceous units over the face, chest, and back areas where the greatest concentrations of these skin appendages are found. It is the most common cause of pustular reactions of the skin.


[edit] Epidemiology and Etiology

Acne occurs during the life of nearly every human being. Very mild cases go unnoticed, while severe cases result in significant physical and psychologic problems. Several factors play a role as individuals enter puberty: (1) androgenic stimulation of the sebaceous glands and increased serum production; (2) abnormal keratinization in the pilosebaceous canal with obstruction to sebum flow (comedones); and (3) proliferation of anaerobic bacteria, Propionibacterium acnes, which lead to rupture of the pilosebaceous unit, extravasation of sebum, and bacteria into the dermis, resulting in inflammatory papules, pustules, and cysts.


[edit] Pathophysiology

Weak and strong androgens stimulate the pilosebaceous units at the time of puberty to enlarge and produce large amounts of sebum (an oily substance composed in part of large quantities of triglycerides, diglycerides, and monoglycerides). The vast majority of patients secrete normal amounts of androgens from the ovaries, testes, and adrenal glands, but in occasional instances an underlying endocrine problem (polycystic ovarian syndrome, adrenal hyperplasia, adrenal or ovarian tumors) may cause acne. At the same time the increased sebum production is seen, the keratinization process in the pilosebaceous canal is disrupted with impaction and obstruction of the outflow of sebum (comedo formation—open blackheads and closed whiteheads). The wall of the closed comedo may rupture, spilling the follicular contents into the dermis. This leads to the development of inflammatory papules, pustules, and large cysts because under the influence of increased sebum production large numbers of P. acnes proliferate (sebum is the substrate for the P. acnes); these bacteria are chemotactic, bringing in neutrophils, which cause the inflammatory response. Stress may accentuate acne. Dietary factors seem to play little or no role in the pathogenesis.[1]


[edit] History

The comedones, papules, and pustules that evolve on the face, chest, and back early in puberty occur at the usual time of onset; but acne can occur in patients in their second and third decade. In women, cosmetics with oily bases may aggravate acne. A history of irregular menses or hirsutism should lead to an evaluation of possible endocrine disorder. Potent topical or large doses of corticosteroids can also induce an acneiform eruption.


[edit] Physical Examination and Clinical Features

In noninflammatory acne, comedones (plugged follicles—blackheads and whiteheads) are usually present in large numbers over the forehead, nose, cheeks, and occasionally in the ears and on the lower face, chest, and back. Inflammatory acne is classified as papular (mild, moderate, severe) or nodular (mild, moderate, severe) on the basis of size of lesions and degree of involvement[2] (Plate 25). Pustular components can be present in papular and nodular types. The term cystic acne has been recently discouraged because these lesions are not cysts but are large inflammatory nodules. True cysts can form in the wake of severe acne lesions, but this is uncommon. Acne scars can be discrete “ice-pick” scars or larger depressed areas. Some individuals develop hypertrophic scars or keloids in response to acne.

Several variants of acne vulgaris that are worth noting include the following:

  • Acne fulminans: A rare, acute, severe variety of acne with widespread nodular lesions that contain large quantities of necrotic material that may break down, leaving eroded areas over the face and back accompanied by systemic findings of fever, leukocytosis, and arthralgias.
  • Acne due to drugs: Several medications, including androgens, corticosteroids, and medications with halogens (iodides, bromides, anticonvulsants, and lithium), may lead to acne or exacerbate preexisting acne.
  • Gram-negative folliculitis: A true bacterial infection that usually presents during the course of treatment with antibiotics or isotretinoin for acne. A sudden worsening of acne-like lesions is typical and requires culture for diagnosis and appropriate antibiotic coverage.


[edit] Differential Diagnosis

Rosacea may be confused with acne, but a history of flushing, the presence of telangiectases, and lack of comedones should help distinguish this condition. Flat warts on the face also should be in the differential diagnosis, but the lack of pustules and comedones help identify warts. Bacterial folliculitis can be diagnosed by Gram's stain and cultures of the pustules. Occasionally, acne is confused with adenoma sebaceum (angiofibroma), which consists of fleshy, red papules over the central face associated with tuberous sclerosis.


[edit] Management

The principles of therapy involve reversing the following etiologic factors that induce the acne lesions: decrease sebaceous activity, decrease P. acnes population, decrease follicular occlusion and inflammation, and decrease androgen stimulation of sebaceous glands.[3]


[edit] Topical Therapy
  • Comedolytics: Retinoic acid (tretinoin, Retin-A, Avita), adapalene (Differin), and azaleic acid (Azalex) are comedolytic agents available as gels, creams, or solutions in varying concentrations. They are applied to the affected areas once a day beginning with the weakest preparations to avoid its two major side effects, skin irritation and scaling. Although comedolytic agents are used mainly for comedonal acne, they are also beneficial in inflammatory acne.
  • Antiseptics: Benzoyl peroxide, an effective antibacterial agent, as well as a comedolytic agent, is most useful to treat inflammatory acne. It is available as an over-the-counter lotion base and in a gel base in 2.5%, 5%, and 10% concentrations as prescription items. Irritation may follow the use of benzoyl peroxide and allergic sensitization may occur. The preparation is usually applied once a day. At times it may be useful to use both comedolytics and benzoyl peroxide (inflammatory and comedonal acne).
  • Antibiotics: Topical antibiotics including erythromycin and clindamycin are effective in decreasing theP. acnes skin population. These preparations in solution, lotion, and gel are used twice a day, often in conjunction with comedolytics or benzoyl peroxide. Topical antibiotics are not quite as effective as systemic antibiotics, but they do alleviate the many side effects of oral antibiotics.


[edit] Systemic Therapy
  • Antibiotics: Tetracycline and erythromycin are effective in controlling mild to moderate papular or nodular inflammatory acne. Tetracycline 500 mg twice daily, or erythromycin 500 mg twice daily (or E.E.S. 400 mg three times daily) is commonly used. Gastrointestinal upset is common with both drugs, and tetracycline must be taken on an empty stomach. Alternatives include minocycline 100 mg/day and doxycycline 100 mg twice daily. Both of these drugs can cause photosensitivity. Sulfa drugs, although reportedly used in acne, have a high incidence of allergic reactions and should be avoided if possible. All of these drugs can cause candidal vaginosis. The length of treatment depends on the response but frequently requires up to 3 months before significant improvement is observed.
  • Systemic retinoids: Isotretinoin (Accutane) is a useful therapy in severe nodular acne that is unresponsive to other treatment regimens. The medication produces remarkable clearing in 95% of these patients, but it also provides persistent remissions in 85% of patients. The drug, usually given in doses of 0.5 to 1.0 mg/kg per day for 3 to 4 months, has many side effects characteristic of chronic hypervitaminosis A, including cheilitis, xerosis, epistaxis, eye irritation, myalgias, and bony hyperkeratosis. Accutane is a potent teratogen and is contraindicated during pregnancy. Dose-related elevations in serum triglycerides and night blindness also occur. Because of these potential problems, the medication should be given by those familiar with the use of this drug with frequent monitoring of complete blood count (CBC), serum chemistries (occasionally liver function test abnormalities are seen), and fasting blood lipids. Women of childbearing age must be on birth control measures (both birth control pills and barrier methods) and be monitored for pregnancy before and during treatment (usually at 2 and 4 weeks and then monthly).
  • Hormonal therapies: Adult women with acne or hirsutism present unique problems that go beyond the scope of this text. However, the selected use of hormonal treatments can be helpful in these women. Treatment options include ovarian androgen suppression with oral contraceptives, androgen receptor blockers (spironolactone, flutamide), and adrenal androgen suppression with corticosteroids.[4]


[edit] ROSACEA

Acne rosacea, commonly called rosacea, is a chronic inflammatory disorder of the blood vessels and pilosebaceous units of the face that occurs most often in middle-aged adults.


[edit] Pathophysiology

The cause of this condition is not completely understood.[5] Some studies suggested a role for the follicular mite Demodex. Other aggravating factors that have been incriminated but not well proved include ingestion of foods that cause flushing (hot liquids, caffeine-containing beverages, alcohol, spicy foods), stress, and sunlight.


[edit] History

Middle-aged adults are primarily affected. Erythema develops first, followed by telangiectasia, associated with increasing blushing and flushing over the central face and at times the neck and chest. Flushing is an important symptom, often precipitated by heat, hot foods, alcohol, and caffeine-containing beverages. Papules and pustules develop over the central face, nose, and chin. Eye symptoms of burning, itching, and irritation may also occur, as well as a history of chalazia.


[edit] Physical Examination

Typically papules and pustules are superimposed on a ruddy complexion and telangiectases most pronounced over the central face (see Plate 7). Sebaceous and fibrous enlargement of the nose (rhinophyma) may eventually ensue. Comedones are not present. In severe cases the pustular component may lead to cystic and granulomatous nodules. Ten percent of patients may have ocular complications, including blepharitis, conjunctivitis, chronic chalazia, and keratitis, that may impair vision. Some patients present with only ocular findings.


[edit] Laboratory Studies

The diagnosis is based on clinical findings. Laboratory findings are not helpful, and skin biopsy is seldom required.


[edit] Differential Diagnosis

Rosacea may be confused with acne vulgaris, but the former is found in older individuals, lacks comedones, and is accompanied by blushing and telangiectasis. Lupus erythematosus, photodermatitis, and seborrhea may be confused with the vascular element of rosacea, but none of these have pustules. The flushing component of rosacea might cause one to consider the carcinoid syndrome. Perioral dermatitis is considered a variant of rosacea seen in young women. It consists of papules and pustules around the mouth and nose. Steroid rosacea is a papulo-pustular eruption that mimics rosacea but is associated with the use of potent topical corticosteroids.


[edit] Management
[edit] Nonpharmacologic.

Trigger factors in rosacea include sunlight, emotional stress, hot liquids, spicy foods, certain vasoactive foods (cheeses, chocolate, alcohol, especially red wine), and all of these should be avoided if possible. Daily use of sunscreens can help with the most common trigger factor: ultraviolet light.


[edit] Pharmacologic
[edit] Topical Therapy.

Topical metronidazole (Metrogel, Metrocreme), 0.75% twice a day, often can control the condition without oral antibiotics. At times both tetracycline and topical metronidazole are needed. Topical sulfur-containing materials (Sulfacet-R) are also useful. Topical steroids should be avoided, especially fluorinated potent steroids, as they may exacerbate the problem and indeed can induce steroid rosacea.


[edit] Systemic Therapy.

Low-dose tetracycline or erythromycin, 250 to 1000 mg/day, controls the papules and pustules, but the erythema and telangiectasis are resistant to therapy. The use of antibiotics must be continued lifelong, and some patients require tetracycline 250 mg two to three times a week to suppress the condition. Flushing can be treated with low doses of clonidine.[6]


[edit] Surgery.

Severe telangiectasias can be treated with tunable dye laser. Rhinophyma can be treated with removal of the excess sebaceous and collagenous material with scalpel, electrosurgery, or laser technique.


[edit] Hidradenitis Suppurativa

Hidradenitis suppurativa is a chronic, suppurative, acne-like eruption occurring primarily in the axillae, inguinal and intergluteal folds, and inframammary areas. Frequently patients with hidradenitis suppurativa also suffer from severe acne (acne conglobata). The precise pathophysiology of this condition is not certain, but whereas early theories linked the apocrine glands to this disease, more recent evidence shows a histologic process identical to that seen in acne vulgaris. Mild cases exist, but the more familiar presentation is that of large draining nodules with sinus tract formation and fibrosis in the affected areas. The presence of double comedones is characteristic in early stages. Treatment is usually difficult. Standard therapy to control inflammation includes systemic antibiotics in maximal acne doses, occasional use of systemic corticosteroids, oral isotretinoin, and local care as needed with incision and drainage. Surgical excision of large areas of involvement is curative, and in severe cases, may be the only successful treatment approach.


[edit] REFERENCES

  1. JJ Leyden: New understandings of the pathogenesis of acne. J Am Acad Dermatol 1995; 32 (part 3):S15 - S25.
  2. PE Pochi, AR Shalita, JS Strauss,et al.: Report of the consensus conference on acne classification. J Am Acad Dermatol 1991; 24:495 - 500.
  3. JJ Leyden: Therapy for acne vulgaris. N Engl J Med 1997; 336:1156 - 1162.
  4. JC Shaw: Antiandrogen and hormonal treatment of acne. Dermatol Clin 1996; 14:803 - 811.
  5. JK Wilkin: Rosacea: pathophysiology and treatment. Arch Dermatol 1994; 13:359 - 362.
  6. JK Wilkin: The red face: flushing disorders. Clin Dermatol 1993; 11:211 - 223.
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