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Management of ACNE VULGARIS in General Practice

By Dr. Atul M. Kochhar MD, DNB, MNAMS, Consultant Specialist, Department of Dermatology & STD, Maulana Azad Medical College & Lok Nayak Hospital, New Delhi

Introduction

We all remember our school days, when a single ‘pimple’ was the end of the world and the face seemed to be ‘pockmarked’. Every over-the-counter ‘panacea’, every magic remedy was tried faithfully but nothing seemed to be effective. The information available was full of myths and everybody dismissed it as a trivial disease. Afflicted teenagers bound themselves with their self imposed massive restrictions regarding food, drinks and lifestyle.

Today Acne vulgaris, or the common acne, is recognized as a multifaceted skin disorder of the hair follicles and sebaceous glands. It is manifested by comedones, follicular papules and pustules, and cysts and nodules. The lesions are found in areas of greatest concentration of the sebaceous glands---the face, neck, and upper trunk.

No single disease causes more psychic trauma in young people, decreases their self-esteem and significantly affects their social interaction skills than Acne vulgaris. Studies have suggested a significant change in how people with acne perform academically, and a study in Britain showed that almost twice the number of acne patients were unemployed compared with those without acne.

Acne affects people of all ages, but it is most common among adolescents. At least 95% (according to some studies : 100%) of teenagers have acne, and the disease affects 85% of persons between the ages of 17 and 24 years. But the disease may persist into adulthood affecting 3% of people up to the age of 45.

Adult women, in particular, may be affected and may experience premenstrual flares. However, severe acne tends to be more common in adolescent males than in people of other age-groups.

Genetic factors : A genetic influence is confirmed by a very high concordance between monozygotic twin of severity of acne and sebum excretion rate. Also patients with persistent acne have a strong family history of persistent acne in contrast to patients with adolescent acne.

Pathophysiology Of ACNE

At least four factors are important in the development of acne:

• Follicular plugging : Plugging of the hair follicle with abnormally cohesive desquamated cells
• Sebaceous gland hyperactivity : increased sebum production by the sebaceous glands
• Colonization and Proliferation of the sebaceous follicles with bacteria (especially Propionibacterium acnes)
• Inflammation
  The earliest change occurs in the hair follicle, when the follicular canal becomes blocked with abnormally keratinized desquamating cells. This plug starts above the opening of the sebaceous gland into the follicular canal and causes gradual expansion of cells and sebum within the canal. The plug then becomes visible at the skin surface as a white papule ("whitehead," or closed comedone). If the opening of the follicular canal dilates, this plug protrudes from the canal and turns a dark color ("blackhead," or open comedone) The reason for the color change is unknown, but melanin and lipid oxidation are among possible causes. These are not filled with dirt, which can be reassuring for the patients.
  
  Increased androgenic influence (or perhaps increased end-organ responsiveness) produces sebaceous gland hyperplasia and seborrhea Though, the sebum production increases during adolescence (particularly in boys, because of androgen stimulation), this alone does not cause acne. Plasma testosterone levels are not abnormally high in males with acne while in females they may be normal or raised (albeit to a fraction of the concentration in the males.) The disease is thought to ease off in the 20s, perhaps because of decreasing levels of the hormone dehydroepiandosterone (DHEA).
  
  Bacteria, most importantly Propionibacterium acnes ( and to a lesser extent P.granulosum), are present in increased numbers in persons who have acne. Much of the inflammation that eventually occurs arises from the action of enzymes produced by the bacteria. These enzymes hydrolyze sebum into free fatty acids, which stimulate the inflammatory process by diffusing through the follicular walls and causing inflammation and follicular destruction. Keratin freed from the injured follicles produces a granulomatous response in the dermis. ( It is possible that Staphylococcus epidermidis also contributes to the lipolysis). Chemotactic factors are released by this reaction, attracting neutrophils. As the follicular wall becomes inflamed, an erythematous papule appears at the skin surface. With increased sebum production, obstruction and bacterial colonization, the follicular unit ruptures, spilling its contents into the dermis. The inflow of neutrophils causes the formation of pustules. Continuation of severe inflammation leads to formation of nodules and subsequent cysts.
  
  Comedo formation results from an abnormality of the keratinization of the follicular mouth. Follicular damage occurs mainly in follicles with large sebaceous glands and weak hair growth and in follicles that have small blocked openings. Fatty acids are freed by hydrolysis from triglycerides in the sebum along with bacterial esterases from Propionibacterium acnes high in the follicles.
  
  Adult women who present with acne in conjunction with hirsutism, alopecia or menstrual disturbances should be examined for the possibility of ovarian or adrenal hyperandrogenism. Basic screening tests include measurement of free testosterone and dehydroepiandrosterone sulfate (DHEA-S) levels and the luteinizing hormone/follicle-stimulating hormone (LH/FSH) ratio. An elevated serum free testosterone level indicates a hyperandrogenous state of adrenal or ovarian origin; an increased DHEA-S level suggests adrenal hyperandrogenism and an LH/FSH ratio of greater than 3 suggests polycystic ovary syndrome Polycystic ovary syndrome should be suspected in women with oligomenorrhea, hirsutism, and acne. This common disorder affects 6% of women. Hyperinsulinemia appears to have a role in this syndrome, and new treatment options that also suppress insulin production are available .Consultation with an endocrinologist may be helpful in treating these conditions.

Clinical Features & Classification Of ACNE

Acne is a polymorphic disease, occurring to a larger extent on the face (99%), and to a lesser extent on the back(60%) and chest (15%). It is frequently accompanied by seborrhea. Non-inflammatory lesions are more common in the younger patients

‘Leeds classification’ is a research oriented classification system which divides Acne into ten subtypes but for treatment purposes it can be classified into three categories – based on morphology : comedonal, inflammatory, and nodulo-cystic. Within each category, acne can be further divided into mild, moderate, or severe, based on the number of lesions and the amount of skin involved.

Comedonal acne consists predominantly of open or closed comedones with generally few, if any, inflammatory lesions. Inflammatory acne consists of comedonal lesions plus inflamma-tory lesions, such as erythematous papules and pustules. By comparison, nodulocystic acne comprises extensive comedonal lesions and inflammatory papules and pustules, plus nodules and cysts or abscesses.

ACNE Variants

There are many acne variants. All these and their clinical features are summed up in TABLE 1

Differential diagnosis

Acne uvlgaris is a clinical diagnosis and usuall y there is no difficulty in differentiating itn from other similar conditions.The differential diagnosis of acne includes rosacea, perioral dermatitis, gram-negative folliculitis, and steroid-induced acne. More are also summed up in TABLE 2

Rosacea occurs predominantly in middle-aged, fair-skinned persons. The patient may report flushing of the face associated with the drinking of hot liquids. The lesions are never comedonal but rather papulopustular and clustered over the cheeks, nose, forehead, and chin. Telangiectasia develops as the condition progresses. Treatment with topical agents, such as metronidazole 0.75% or 1%, clindamycin 1% lotion, or sodium sulfacetamide 10%/sulfur 5%, may be effective, especially for mild cases. More severe papulopustular disease sometimes requires oral antibiotics.

Perioral dermatitis occurs primarily in young women and adolescents and is characterized by erythema, scaling, and papulopustular lesions that are most commonly clustered around the nasolabial folds, mouth, and chin. The cause is unknown, but perioral dermatitis may behave more like rosacea than like acne vulgaris. A 2-month course of oral antibiotics is usually effective.

Gram-negative folliculitis, although rare, can occur after long-term treatment of acne with oral antibiotics. Affected patients may have an increased carrier rate of gram-negative bacteria in the anterior nares and may experience sudden onset of superficial pustules around the nose, chin, and cheeks. Treatment involves growing cultures of samples taken from the lesions or the anterior nares and instituting appropriate antibiotic therapy for the gram-negative organisms.

Topical or oral corticosteroid therapy sometimes causes steroid-induced acne. The lesions, which generally develop within 2 to 5 weeks after therapy is started, are usually uniform in size and flesh-colored, pink, or red. They often appear in a symmetric distribution on the neck, chest, and back. Corticosteroids should be discontinued, and treatment should be started with topical agents, such as benzoyl peroxide or sodium sulfacetamide/sulfur lotions.

Myths & Misperceptions

Diet and Acne

There are a number of misconceptions associated with acne. In the past chocolates, soft aerated drinks, or junk food have been implicated as has been dirty skin. Today there is no concrete evidence that food causes acne. Following the strictest diet will not by itself clear acne.

On the other hand, a few people insist that their acne seem to worsen when they eat certain foods, particularly chocolates, fried food and chillies. These people should be advised to avoid the foods that clearly aggravate their acne.

Stress, may also be a factor, though that has not been proven.

Treatment of Acne Vulgaris

Effective treatment of acne vulgaris can prevent emotional and physical scarring and reduce psychosocial burden A rational therapeutic decision requires a careful analysis of the risks and benefits of treatment and therapy varies according to the severity of the disease.

Counseling about the natural course and care of acne, is a must. Frequent washing of oily hair and skin is desirable, as is a hairdo in which the hair is not touching the face. Children and their parents may be taught the use of the comedo extractor, extracting only those blackheads that come out easily and doing about 10 at one sitting. Squeezing, rubbing, and picking are discouraged. The person with acne should eat a balanced diet; avoid undue stress, fatigue, and perspiration.

Since acne vulgaris is associated with increased sebum excretion, obstruction of the pilosebaceous duct, and alteration of the lipid composition of the skin surface, treatment generally attacks one or more of these areas.

Topical medication is generally adequate in clearing comedonal acne, while inflammatory acne usually requires the addition of oral medication. Systemic antibiotics are used most frequently and can be highly effective. Newer formulations of combined oral contraceptives are also helpful in modulating sebum production in the female patient. This is effective because of the medication's estrogen content. Some researchers have found oral contraceptive therapy to be particularly effective in preventing the common premenstrual flare of acne The use of anti-androgens in a topical medication base is a possible helpful future development.

Severe nodulocystic acne that does not respond to topical retinoids and systemic antibiotics may be treated with isotretinoin. However, the side effect profile of this medication is extensive, and physicians should be well-versed in its potential adverse effects. Topical corticosteroids are not helpful in treating acne and may, in fact, make it worse.