SEBACEOUS GLAND DISORDERS

Sebaceous glands are saccular dermal structures to produce sebum, which usually drains into hair follicle via sebaceous ducts. Sebaceous secretions are androgen dependent, most prominent during puberty and fetal life (constitute vernix caseosa along with desquamated s.corneum).

Acne vulgaris is a very common disorder of sebaceous glands in adolescents, characterized by recurrent pathognomonic lesions (comedones) with/without secondary papules, pustules or nodulo-cystic lesions.

Etiopathogenesis: Acne denotes blockade of sebaceous ductal openings into hair follicular canal, leading to distension and rupture of sebaceous glands and microbial degradation of sebum. Though exact cause is not established, four factors are important:

a. Sebaceous gland hypertrophy and increased sebum production in adolescence due to androgenic hormones.

b. Abnormal keratinization of follicular epithelium (? hereditary or hormonal), blocking sebaceous ducts by a keratin plug.

c. Back pressure in sebaceous ducts, leading to distension and rupture of sebaceous glands into dermis with inflammatory reaction and secondary lesions

d. Contributing microbial degradation of sebum—a lipoid substance, by colonizing flora of sebaceous follicles, i.e. Propionibacterium acne, anaerobic diphtheroids and Staph. epidermidis.

Pathognomonic Comedone is a non-inflamed dilated follicular sac filled with keratinized material and sebum.

Clinically, acne is most common in adolescents, in males, in persons with oily/hyperhidrosis skin, during hot and humid weather and in pre-menstrual phase.

Comedones appear as tiny papules (1-3 mm) with a central dot denoting pilosebaceous orifice on skin. These lesions are of two types—open comedones or black heads, where blackish keratin plug is visible through open and patulous pilosebaceous orifice and closed comedones or white heads, where follicular opening is visible only as a tiny whitish dot in the center of macule.

Secondary lesions are inflammatory, due to rupture of sebaceous glands, microbial degradation of sebum and external trauma, e.g. pinching or scratching, presenting as papules, nodules, pustules or nodulocystic lesions.

As sebaceous glands are concentrated over face and upper chest, most lesions are also seen in these regions. Most lesions heal with minimal transient scarring and hyperpigmentation, unless secondary changes are present.

Management: Acne is not preventable (except perhaps by Tretinoin), though lesions may be controlled and scarring may be prevented by j udicious use of following measures:

a. Regular cleansing of skin with mild soap/water and avoidance of greasy creams or oil applications. Squeezing of comedones should be strictly avoided, as it may rupture sebaceous ducts to induce inflammation.

b. Topical therapy for minimum 4-6 weeks with:

- Comedolytic agents, e.g. benzyl peroxide or tretinoin. Tretinoin—a retinoic acid derivative, is the most effective drug for non-inflammed comedones, by reducing keratinization in sebaceous follicles. It should be applied as 0.025-0.5% cream/gel once a day after face wash, starting with low concentration.

- Topical antibiotics, e.g. clindamycin 1% or erythro­mycin 2% for inflamed lesions, to inhibit growth of P. acne. Simultaneous use of comedolytic agents improves penetration of these drugs.

c. Systemic antibiotic therapy with erythromycin or tetracycline is indicated in severe acne with extensive secondary lesions.

d. Other agents of some benefit in severe cases include- Anti-androgens (cyproterone acetate with ethinyl estadiol) in post-menopausal females or Oral isotretinoin-a retinoic acid derivative (0.5-1.0 mg/ kg/d for 3-4 months).

e. Surgical intervention with aspiration and intralesional instillation of steroids may be necessary in painful nodulocystic lesions. Dermoabrasion to minimize scarring is indicated only after active phase is over, beyond the adolescence.

D/D: Other common causes of acne in childhood include:

a. Drugs, e.g. steroids, INH, phenytoin, phenobarbitone, iodine compounds (halogen acne),

b. Transient neonatal acne, due to placental transfer of androgens, and

c. Tropical acne, due to intense hot and humid climate.

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