Non-inflammatory acne is characterized by both open and closed comedo formation. Closed comedones, or whiteheads, are typically small-approximately 1mm-skin-colored papules with no apparent follicular opening.
Open comedones, or blackeads, are dome-shaped papules with a conspicuous dilated follicular outlet. This opening is filled with an inspissated core of shed keratin. Melanin deposition and lipid oxidation within the debris may be responsible for the black coloration. Ice-pick-type scarring may result from comedones alone.
The inflammatory lesions of acne originate with comedo formation but then expand to form papules, pustules, nodules and cysts of varying severity. Erythematous papules range from 1 to 5mm in diameter. Pustules tend to be approximately equal in size and are filled with sterile, white pus. As the severity of lesions progresses, nodules form and become markedly inflamed, indurated and tender.
The cysts of acne are deeper and filled with a combination of pus and serosanguineous fluid. In patients with severe nodulocystic acne, these lesions frequently coalesce to form massively inflamed complex plaques that can include sinus tracts (conglobate lesions).
Acne fulminans is the most severe form of cystic acne and is characterized by the abrupt onset of nodular and suppurative acne in association with variable systemic manifestations.
Osteolytic bone lesions may accompany the cutaneous findings: Systemic manifestations include fever, arthralgias, myalgias, hepatosplenomegaly and severe prostration.
Treatment depends on clinical severity and includes topical, intra-lesional or oral corticosteroids, oral isotretinoin and oral antibiotics. Dapsone in conjunction with isotretinoin was reportedly beneficial.
Severe eruptive nodulocystic acne without systemic manifestations is termed acne conglobata.
Acne mechanica occurs secondary to repeated mechanical and frictional obstruction of the pilosebaceous outlet. Comedo formation is the result. Well-described mechanical factors include rubbing by helmets, chin straps, suspenders and collars and scarfs.
Acne excoriee, occurs primarily in young women. Typical comedones and inflammatory papules are neurotically excoriated, leaving crusted erosions that may scar. Linear erosions suggest self-mutilation, and underlying psychiatric component should be suspected. Patients with an anxiety disorder, obsessive-compulsive disorder or personality disorder are particularly at risk.
Acne lesions or eruptive acneiform lesions can be seen as a side effect of a number of medications, including anabotic steroids (e.g. danazol, testosterone), corticosteroids, corticotropin, phenytoin, lithium, isoniazid, iodides, bromides, azathioprine, PUVA, monomorphous eruption of inflammatory papules and pustules is often observed in drug-induced acne.
Cutting oils, petroleum-based products, and coal tar derivatives. Comedones dominate the clinical picture, with varying numbers of papules, pustules and cystic lesions distributed in exposed as well as typically covered areas.
Chloracne, the term used to define occupational acne caused by exposure to chlorinated aromatic hydrocarbons.
The following agents, found in electrical conductors and insulators, insecticides, fungicides, herbicides and wood preservatives.
Neonatal acne occurs in more than 20% of healthy newborns. Lesions appear at about 2 weeks of age and generally resolve within the first 3 months of life. Typically, small inflamed papules arise on the cheeks and across the nasal bridge.
If acne presents at 3-6 months of age, it is classified as infantile. Clinically, comedo formation is much more prominent than in the neonatal from and may lead to pitted scarring. The pathogenesis of infantile acne reflects the hormonal imbalances.
I- Topical treatment
Tretinoin (all-trans-retinoic acid) was the first topical comedolytic agent used for the treatment of acne. Its mechanism of action involves normalizing follicular keratinization, it aids in the expulsion of existing comedones and prevents the formation of new ones. Tretinoin has been shown to have significant anti-inflammatory properties.
Benzoyl peroxide (2.5-10%) is a potent bacteriocidal agent that reduces P. acnes within the follicle. It is particularly effective when used in combination with other therapies. In contrast to topical antibiotics, microbial resistance to benzoyl peroxide has not been reported.
Topical antibiotics, clindamycin and erythromycin represent the two most commonly utilized antibiotics and the formulations vary from creams and gels to solutions and pledgets.
Salicylic acid is a widely used comedolytic and mild anti-inflammatory agent.
Azelaic acid is a naturally occurring dicarboxylic acid found in cereal grains. It is available as a topical cream, which has been shown to be effective in inflammatory and comedonal acne. By inhibiting the growth of P. acnes, azelaic acid reduces inflammatory acne. Azelaic acid is applied twice daily. In addition, it may help to lightened postinflammatory hyperpigmentation.
Oral erythromycin and tetracycline, or its derivatives doxycycline and minocycline, are usually prescribed for moderate to severe inflammatory acne unresponsive to topical combinations, primary mechanism of action of these agents is suppression of the growth of P.acnes, thereby reducing bacterial production of inflammatory factors.
Hormonal therapy is an established second-line treatment for female patients with acne.
a) The progestational antiandrogen cyproterone acetate is currently used. The standard formulation combines cyproterone acetate 12 mg with ethinyl estradiol (35 µg or 50 µg) in an oral contraceptive formulation.
b) Spironolactone functions as both an androgen receptor blocker and an inhibitor of 5-reductase. In doses of 50-100 mg twice daily. Side effects are dose-related and include potential hyperkalemia, irregular menstrual periods, breast tenderness, headache and fatigue.
Since 1971, isotretinoin (13-cis-retinoic acid), for patients with severe, nodulocystic acne refractory to treatment, including oral antibiotics.
Isotretinoin is best absorbed from the gastrointestinal tract when it is taken with a fatty meal.
The oral retinoid acts upon the sebaceous gland, prohibiting maturation of the basal cells leads to sebaceous gland atrophy. It reduces sebum production by up to 90%. As a result, P. acnes, which are dependent on the glycerol resulting from the hydrolysis of sebum triglycerides, are unable to thrive. Normalization of follicular of follicular keratinization also occurs, and this initial step in acnegenesis is significantly inhibited.
Dosing of isotretinoin 0.5-2.0 mg/kg/day for 16-20 weeks is recommended., with a total cumulative dose of 120-150 mg/kg, have been shown to reduce the risk of relapse.
The side effects of isotretinoin are numerous. These include cheilitis, dryness of the oral and nasal mucosa, generalized xerosis, and skin fragility. Alopecia. Xerophthalmia is common.
Teratogenicity is a serious potential complication
when isotretinoin is used in women of childbearing age.
Elevated serum triglyceride levels. Increased levels of transaminases.
Comedo extraction can improve the cosmetic appearance.
For deep and inflamed cystic lesions, intralesional injection of corricosteroid. Larger nodulocystic lesions may require incision and drainage prior.
Low-concentration chemical peels are also beneficial for the reduction of comedones. The -hydroxy acids (including glycolic acid), salicylic acid and trichoroacetic acid are the most common peeling agents.
One of the most distressing consequences of acne vulgaris is scaring. Surgical treatment should be aimed at the type of scarring present. Dermabrasion, laser resurfacing and deeper chemical peels.
Filler substances used include bovine and human collagen hyaluronic acid and autologous fat. Punch grafting is an option for patients with "ice-pick" scaring.