Acne vulgaris

                               

Though the acne or pimples are very common among adolescence or young adults, it is better classified as a disease rather than a physiological phenomenon due to inflammatory component and scarring it can cause.

It is a common disease with more than 90% of the people experiencing it sometime or other in their lifetime. Age of onset is between 14-17 years among girls and 16-19 among boys.

Severity of acne is usuallny more among males due to androgen activity. Genetic factors influence the susceptibility to acne.

Causes

1.     Alteration in the pattern of keratinization within the sebaceous follicle

2.     Level of circulating sex hormones, especially androgens

3.     Quantity and quality of sebum production

4.     Colonization by follicular microbial flora

5.     Immunological factors

6.     Environmental factors

Alteration in the pattern of keratinization

The comedones which are the primary lesions of acne are formed by increased production as well as accumulation of keratin in the sebaceous follicles. The stimulus for this may be androgens or the irritating effect of sebum. It is found that the prepubertal girls with inflammatory and comedonal acne have significantly higher levels of androgens. The acceleration in the sebum secretion or its composition may irritate keratinocytes of infundibulum leading to release of inflammatory substances.

The hyperkeratinization leads to decreased barrier function which in turn makes it susceptible to inflammatory agents. Horny plug debris become inflammatory and trigger acne. Increased hydration of comedones causes obstruction of sebum outflow. This mechanism is the cause of tropical acne and premenstrual flare of acne.

Circulating sex hormones

Androgens increase sebum secretion and cause sebaceous gland hyperplasia while estrogens suppress sebaceous gland activity. When there is increased androgen-estrogen ratio there is increase in acne.

Quality and quantity of sebum

Excess sebum secretion and sebaceous gland hypertrophy is seen in acne patients. At the same time there is difference in the composition of sebum too is responsible for inflammation. High levels of wax esters and squalene are found in sebum of acne patients.

Follicular microbial flora

The resident bacterial flora like P.acnes, P.granulosum, p.ovale and Staphylococcus epidermidis play important role in the production of acne. Lipases released by these bacteria cause follicular hyperkeratosis and even rupture of follicles. The materials thus released attract neutrophils and inflammation sets in.

Immunological factors

Various immunological phenomena take place in acne prone skin the details of which are beyond the scope of this article.

Environmental factors

A hot and humid environment aggravates acne due to ductal hydration. The occupations involving exposure to such environments make the persons with pre existing acne more susceptible to acne flares. Emotional stress and strains of various types are known to worsen the condition while natural light often improves acne. External applications of oils, pomades and other comedogenic chemicals cause acneiform eruptions.

Diet plays a role in pathogenesis of acne. Sugar rich diet causes hyperinsulinemia which results in androgen synthesis leading to comedone formation. Diet induced hyperinsulinemia increases insulin like growth factor (IGF-1) causing unregulated growth of follicular epithelium, sebum production and synthesis of androgens from gonads.

Similarly, this insulin like growth factor (IGF-1) is increased on intake of milk and diary products. Milk contains IGF-1 and induces endogenous production as well. Milk also contains androgens. Iodine and low omega fatty acids content of milk also seems to be responsible for acne formation in high glycemic load diet.

Sequence of events

Microcomedo is the first lesion formed due to increased keratinization leading to blockage of sebaceous canal resulting in retension of sebum and initiation of inflammatory reaction. Increase in bacterial flora increases inflammation. Further retention of sebum and release of enzymes causes rupture of the gland. The spread of sebum in dermis adds to the inflammation causing areas of accumulation of fluid, pus and glandular debris. Scar forms on healing the pattern of which is determined by the size and pattern of lesion and individual susceptibility.

Clinical features

The lesions of acne are seen on face, chest, back, shoulders and upper arms. Comedones or the early lesions of acne are chiefly of two types-open and closed. Open comedones represent follicles with dilated follicle.the black dot is caused by oxidization of melanin, transmission of light through compacted epithelium and presence of certain lipids. Closed comedones are small papules without surrounding erythema. There are several subtypes like macrocomedones, sandpaper comedones and submarine comedones all of which do not easily respond to topical therapies.

Grading of acne

Grade 1(mild): comedones, occasional papules

Grade 2(moderate): comedones, many papules, a few pustules

Grade 3(severe): predominantly pustules, nodules and abscesses

Grade 4(cystic): mainly cysts and abscesses ,widespread scarring

Oily skin is always associated feature and seborrhoeic dermatitis also may coexist. Premenstrual flare and postmenstrual improvement is common. Sequelae include hyperpigmentation and various types of scars.

Psychological impact of acne

Patients with severe acne and scarring have shown wide range of psychological abnormalities like depression, suicidal ideation, anxiety, embarrassment, body dysmorphic disorder and social inhibition.

Treatment

Aims of treatment

1.     To reduce follicular bacterial population , reduce lipases

2.     To remove follicular obstruction

3.     To reduce inflammation

4.     To reduce sebaceous gland activity by blocking androgen stimulation.

General measures

1.     Avoid usage of acnegenic drugs, oils, cosmetics.

2.     Stress control.

3.     Rule out hormonal abnormalities.

4.     Regular face wash with proper cleansing agents.

5.     Dietary restrictions as per the personal observation, balanced diet.

Treatment modalities

1.     Mild involvement: Benzoyl peroxide/salicylic acid/azelaic acid topically.

2.     Mild to moderate involvement: Benzoyl peroxide/ tretinoin/adapalene/tazarotene/clindamycin  topically.

3.     Moderate to severe involvement:

a.     Oral antibiotics like doxycycline, minocycline, lymecycline, azithromycin etc.

b.     Isotretinoin

4.     Cystic acne:

a.     Aspiration of cyst or intralesional injection of steroid.

b.     Systemic antibiotics.

c.      Dapsone.

d.     Isotretinoin

5.     Adjunctive therapies like comedo extraction, chemical peels, microdermabrasion, laser and light therapies.

6.     Acne surgeries like draining cysts, punch grafts, resurfacing with laser, cryosurgery, dermarollers, fillers.

[ Reference: IADVL textbook of dermatology]