ACNE VULGARIS

Acne vulgaris is a disorder of pilosebaceous unit which predominantly affects the peribubertal population and clinically manifests as comedones , papules , nodules, pustules, and cysts and heals with scars.


PATHOGENESIS
Although the exact cause of the acne is unknown ,several interrelated pathogenic mechanisms are incriminated .
I. Increased sebum production
II. Follicular epidermal hyperproliferation
III. Microbial colonization
IV. Release of inflammatory mediators

I) INCREASED SEBUM PRODUCTION
• Sebaceous gland activity is controlled by androgens and though most patients with acne have normal levels of circulating androgens , their sebaceous glands are unusually sensitive to androgens due to an enhanced end organ sensitivity .
• This is related to increased activity of an enzyme 5-α reductase , which converts testosterone to more potent DHT , which binds to specific receptors in the sebaceous glands increasing sebum production .


II) FOLLICULAR EPIDERMAL HYPERPROLIFERATION
• INDUCED
1. DHT
2. Reduced levels of linoleic acid: in sebum of acne patients
3. P.acne
4. Cytokines: like IL: 1 which are themselves produced by ductal epithelium
• RESULTS IN
1. Retention of sebum , encouraging growth of microbes , triggering a vicious cycle
2. Rupture of distended follicle ,releasing proinflammatory chemicles into the dermis , stimulating intense inflammation

III) MICROBIAL COLONIZATION
• ORGANISM IMPLICATED :
1. Propionium bacterium species especially P.acnes
2. Malassezia furfur
3. Staph epidermidis

• ROLE OF PATHOGENESIS
1. Tiggers a type IV inflammatory response
2. Produce extracellular enzymes , which attract inflammatory cells.
3. Induced follicular epidermal hyperproliferation

IV) RELEASE OF INFLAMMATORY MEDIATORS:
1. Distended follicles ruptures, releasing inflammatory chemicals into dermis that leads to intense inflammatory reaction.
2. Cytokines released from ductal epithelium triggers an inflammatory cascade.
3. Extracellular enzymes released by microbes attract these inflammatory cells.

FACTORS MODIFYING ACNE:

• GENETIC PREDISPOSITION:
– Acne vulgaris is familial but exact mode of inheritance is unknown.
– Patients with severe cystic acne often have a positive family history; identical twins often have greater chances of same severity of acne.

• DIET:
– Although diet is believed to play a very little role is aggravating acne or cause acne at all. Some recent studies though provide evidence that a diet that is rich in dairy products or diet with a high glycemic index plays some role in aggravation of acne.
– No diet restriction to be practiced until there is solid evidence to support the claim.
– Diet restrictions can be done for other health reasons like obesity or PCOD but never for acne vulgaris.

• COSMETICS:
– Acne is frequent in females who tend to use oil based cosmetics for a longer period of time.
– Not cleaning up the residual cosmetic product from the skin after usage.

• MENSTRUAL CYCLE:
– most of the females complain of increased acne just before menstruation, this can be implicated to premenstrual edema of pilosebaceous gland.

EPIDEMIOLOGY:

– PREVALENCE: an extremely common skin condition with at least milder forms affecting almost all adolescent.
– Age: onset at 12-14 years of age, earlier in females m
– Gender: both sexes are affected equally, nodulocystic acne being more common in males.

CLINICAL FEATURES:

MORPHOLOGY:
– Most patients with severe acne have a greasy skin with patulous follicular openings.
– Eruptions are polymorphic, with comedones, inflammatory lesions and scars, all present on skin at same time.

COMEDONES:
– These are pathognomonic of acne vulgaris.
– Types: open comedones ( black heads): due to plugging of pilosebaceous orifice by keratin and sebum on skin surface. The black color is due to melanin and lipid oxidation.
Closed comedones ( white heads): are due to sebum and keratin plugging the pilosebaceous ducts. Some of these are extremely deep seated called submarine comedones, and are seen by stretching the skin, these respond poorly to medical treatment.

INFLAMMATORY LESIONS:
– These are either small papules with an erythematous halo to superficial deep pustules and tender, fluctant nodules.
SCARS:
– Lesions of acne that heal with scarring.
– These can be: depressed scars: ice pick scars: deep pits and boxcar scars: which can be superficial or deep. Hypertrophic and keloidal scars.

SITES OF PREDILECTION:
– Predominantly on face and upper part of trunk, chest and sometimes shoulder.

VARIANTS:

1. ACNE CONGLOBATA: severe variant of acne, more frequent in males. Characterized by polyporous comedones, intercommunicating abscess, cysts and sinuses loaded with serosanguinous fluid or pus.

2. ACNE FULMINANS: acute onset, presented as crusted ulcerated lesions.

3. DRUG INDUCED ACNEIFORM ERUPTIONS: steroids, OCPs, antitubercular drugs, anticonvulsants and halides are associated with acneiform eruptions. Lesions are monomorphic with papules and sometimes pustules.

4. ACNE EXCORIEE: seen in young girls who prick their otherwise mild acne.

DIAGNOSIS:

– Patient in adolescent.
– Skin is greasy with prominent follicular openings.
– Eruptions of papules, pustules , nodules, cysts and scarring.

DIFFERENTIAL DIAGNOSIS:

1. ROSACEA: motly seen in middle aged females and comedones are absent with sparing of periorificial area.
2. FOLLICULITIS: comedones absent, distribution is perifollicular around terminal hair.

TREATMENT:

– LOCAL HYGIENE: regular gentle cleansing with mild soap and water. Avoid using oil based cosmetics but water based cosmetics can be used.
– RETINOIDS: drugs available are; retinoic acid, adapalene, isoretinoin and tazarotene. RA available as 0.025% , 0.05%, 0.1% cream and gel. Newer formulations include microsphere or polymer formulations that are less irritating. These are indicated in active disease and are effective against both comedones and inflammatory acne. Retinoids act by normalizing follicular keratinization by increasing epidermal turnover and increasing dehiscence of stratum corneum.
– BENZOYL PEROXIDE: A powerful antimicrobial and also has anti inflammatory effect. Indicated in mild acne and also along with antibiotics. Used in both inflammatory and noninflammatory.
– TOPICAL ANTIBIOTICS: most frequently used are clindamycin and erythromycin.
– SYSTEMIC TREATMENT: antibiotics such as doxycycline and minocycline. ANTIANDROGENS act by decreasing sebum production. ISORETINOIN can be used for severe acne and acne conglobata.

PHYSICAL MODALITIES OF TREATMENT:

• INTRALESIONAL CORTICOSTEROIDS: for active disease injection of long acting steroids into nodules. For hypertrophic scar long acting steroid in recalcitrant hypertrophic scar or keloid.
– CRYOTHERAPY: freezing with liquid nitrogen speeds up resolution of recalcitrant nodulocystic lesions.
– LASER THERAPY: usually fractional lasers such as CO2 lasers used.
– PHOTODYNAMIC TREATMENT: red light and a photosensitizer like aminolevulinic acid.
– DERMABRASION.

Contributor – Dr. Yagika Pareek