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Acne Vulgaris By Dr. Hala- Al- Salman M.B.Ch.B., F.I.B.M.S. Acne is a disorder of the pilosebaceous unit characterized by comedones, papules, pustules, nodules, cyst and scars. Prevalence: Nearly all teenagers have some acne (100% of boys and 90% of girls). Starting between 12-14 years, earlier in females. It’s a disease of adolescence, but it may continue up to the age of 30. The severe form of acne occurs more frequently in male, but the disease tend to be more persistent in females. Etiology: Many factors combine to cause acne, causing chronic inflammation around the pilosebaceous follicles. 1. Genetics: Acne is familial in about half of the cases. 2. Sebum: Sebum excretion is increased, but this alone need not cause acne, patients with acromegaly or Parkinson's disease have increase sebum excretion but no acne and sebum remain high after acne has improved. 3. Hormonal: Androgens (from testes, ovaries & adrenals) are the main stimulant of sebum excretion. Other hormones e.g. thyroid and growth hormone have minor effect. In acne, the sebaceous glands respond excessively even to the normal level of these hormones (increased target organ sensitivity), 50% of females with acne have raised testosterone level. 4. Poral occlusion: Both genetic and environmental factors (e.g. some cosmetics) cause the epithelium to overgrow the follicular surface. The follicles then retain sebum which has increased concentration of bacteria and free fatty acid. Rupture of the follicles is associated with intense inflammation and tissue damage. 1 5. Bacteria: Propionibacterium acne, a normal skin flora break down triglyceride, releasing free fatty acid, produces chemotactic substance and lead to inflammation. Clinical picture: Site: Face, shoulders, upper chest and back. Seborrhea (greasy skin) is often present. Lesion: 1. Non- inflammatory: consist of: *Open comedones (black head), caused by plugging of the pilosebaceous orifice by keratin and sebum. * Closed comedones (white head), caused by overgrowth of the follicle opening by surrounding epithelium. 2. Inflammatory: characterized by papules, pustules, nodules and cysts. Acne conglobata: severe form of acne with abscesses, cyst and intercommunicating sinuses that contain thick fluid and pus. Course: Acne clear by the age of 23-25 years in 90% of patients, but some 5% of females and 15 of males still need treatment in their thirties or even forties. Variants: 1. Infantile / Neonatal acne: It follow transplacental stimulation of the child' sebaceous gland by maternal androgen. 2. Mechanical: Excessive scrubbing, picking and rubbing can rupture the occluded follicles. 3. Hormonal: - Polycystic ovaries syndrome. - Congenital adrenal hyperplasia. - Androgen secreting tumors (adrenals, ovaries or testes). 2 4. Drug induced: - Corticosteroid (topical or systemic), cause papulopustular lesion rather than comedones, sudden onset, in non-teenager ( Acniform ). - Gonadotrophine, oral contraceptive, lithium, iodide, bromide, anti T.B., anticonvulsant. 5. Acne cosmetica / Exogenous acne: Tar, chlorinated hydrocarbons, oil and oily cosmetics can cause or exacerbate acne ( comedones predominate ). 6. Excoriated acne: Occurs most commonly in girls, due to obsessional picking or rubbing leaving discrete denuded areas. 7. Acne fulminans: Rare variant of severe acne, associated with fever and high ESR. 8. Late onset acne: Occurs mainly in females, often limited to the chin. Nodular and cystic lesions predominate. Severity of acne: Depend on the number and the types of the lesion: 1. Mild. 2. Moderate. 3. Severe. Complications: 1. Disfiguring scars; pitted or hypertrophic and keloid. 2. Hyperpimentation: transient, but it can persist. 3. Psychological depression. Differential Diagnoses: 1. 2. 3. 4. Rosacea. Pyogenic folliculitis. Hidradenitis suppurativa. Pseudofolliculitis barbae. 3 Treatment: I. Local: 1. Regular gentle cleansing with soap and water to remove surface sebum. Antibacterial cleanser are also useful e.g. chlorhexidine. 2. Benzyle peroxide (2.5%, 5%& 10%), has antibacterial and effective for inflammatory lesion. 3. Retinoid (vitamin A drevatives). Tretinoin 0.05%, Adapalene 0.1%, Tazarotene 0.1%. Normalize follicular keratinization, effective against comedones. Side effects: irritation& photosensitivity. It should not used in pregnancy. 4. Azeliac acid: Bacteriocidal, anti-inflammatory, and inhibit comedones formation. 5. Sulphur. 6. Local antibiotics: clindamycin, erythromycin, and sulfacetamide. 7. Cosmetic camouflage (cover-up). II. Systemic: 1. Antibiotics: * Oxytetracycline and tetracycline: (250mg 4X daily), for not less than 3 months, taken on empty stomach. The dose then tapered to maintenance dose of 250-500mg daily. * Minocycline: 50mg X2, or 100mg once, more lipophilic than tetracycline, so it concentrate better in the sebaceoud glands. (expensive). * Doxycycline: 100mg once or twice daily, (cheaper). * Erythromycin: second line antibiotic, used in woman who might become pregnant, drawback is the development of resistant p.acne. * Trimethoprim: third line drug. * Ampicillin. 2. Hormonal: - Combined antiandrogen-oestrogen in women with persistent acne. - Contraceptive with high androgen content. 4 3. Systemin retinoid: isotretinoin (13-cis-retinoic acid) (Ro-accutane / Retane). - Inhibit sebum secretion. - Inhibit growth of p. acne. - Inhibit acute inflammatory process. Uses: - Nodulo-cystic acne. - Unresponsive to other measures. Dose: 0.5-2mg.kg. for 4-6 months. Highly teratogenic, full blood count, liver function, lipid profile, and urine analysis should checked routinely. The female should start contraceptive 2 months before its use and 3 months after stooping the drug. Side effects: 1. Depression, some time lead to suicide. 2. Dry skin, dry and inflamed lips and eyes, epistaxis, facial erythema, muscle ache, hyperlipidaemia, and hair loss. Diet: There is little evidence that any dietary constitute, except iodide, cause acne.(Nuts, chocolate). Dermabrasion, laser, collage injection to smooth out facial scars. Rosacea Affect the face of adult, usually females. Peak incidence is in the thirties and forties, but can be seen in younger or older age groups. Cause: Unknown, seen in those who flush easily in response to warmth, spicy food, alcohol, or embarrassment. Demodex folliculorum mite in the hair follicles may have a pathogenic role, but this has not been proved. 5 Clinically: The cheeks, nose, centre of forehead and chin are most commonly affected. The periorbital and perioral area are spared. There is intermittent flushing, followed by a fixed erythema and telangiectasia. Discrete domed inflamed papules, papulopustules and rarely nodules develop later. There are no comedones or seborrhea (unlike acne). The lesion is usually symmetrical. The course is prolonged with exacerbation and remission. Complications: 1. Eye complication: blepharitis, conjunctivitis and keratitis. 2. Rhinophyma: hyperplasia of the sebaceous gland and connective tissue of the nose. Differential Diagnoses: 1. 2. 3. 4. 5. Acne. Seborrheic dermatitis. SLE (butter fly erythema). Photodermatitis. Flushing associated with menopausal symptoms. Treatment: 1. 2. 3. 4. 5. 6. Tetracyclines. Erythromycine. Metronidazole 0.75% gel. Systemic metronidazole. Zinc sulphate (oral 5mg/kg). Sunscreen. 6