Abstract and Introduction Disorders of hyperpigmentation are difficult to treat, particularly in dark-skinned individuals.
The goal is to reduce the hyperpigmentation without causing undesirable hypopigmentation or irritation in the surrounding normally pigmented skin.
The psychosocial impact caused by these disorders must be considered.
Although there are many effective therapeutic modalities available, there are potentially significant side-effects associated with treatment.
The most commonly used treatment is topical hydroquinone.
There are other phenolic agents, such as N-acetyl-4-cystaminylphenol (NCAP), that are currently being studied and developed.
The non-phenolic agents, which include tretinoin, adapalene, topical corticosteroids, azelaic acid, arbutin, kojic acid, and licorice extract, are also used for hyperpigmentation disorders.
Hyperpigmentation is a common and distressing problem caused by various inflammatory skin disorders, such as eczema, allergic contact dermatitis, and irritant contact dermatitis Acne is also a frequent cause.
Papulosquamous disorders in general commonly predispose a patient to postinflammatory hyperpigmentation.
Melasma is a common form of non-inflammatory hyperpigmentation.
Sun exposure often reverses the results of therapy, compromising the lengthy treatment process.
Consequently, the first line of therapy for hyperpigmentation is a broad-spectrum sunscreen used in conjunction with a phenolic agent such as a hydroquinone, or with a non-phenolic agent such as tretinoin, azelaic acid, or kojic acid.
There are hundreds of sunscreen formulations with different UV absorbing chemicals in various concentrations.
The UVB and UVA absorbing chemicals used in the formulation of topical sunscreens include para-aminobenzoic acid-related products, salicylates, cinnamates, benzophenones, zinc oxide, and titanium oxide.
Almost all sunscreen products contain a mixture of one or more UVB absorbing chemicals.
Hydroquinone and related compounds reduce the production of melanin by their inhibition of the enzyme tyrosinase.
Topical corticosteroids also inhibit tyrosinase activity and affect endoplasmic reticulum secretory function of melanocytes.
Agents such as salicylic acid and glycolic acid act to remove melanin in the epidermis by their peeling action.
Tretinoin, which has a mild peeling effect, acts in a similar manner.
It may also inhibit tyrosinase.Full Article