In fixed drug eruptions, red plaques or blisters form at the same site each time a drug is taken; residual postinflammatory hyperpigmentation usually persists. Typical lesions occur on the face (especially the lips), hands, feet, and genitals. Typical inciting drugs include sulfonamides, tetracycline Some Trade Names: ACHROMYCIN V, TETRACYN, TETREX, NSAIDs (especially phenazone derivatives), barbiturates, and carbamazepine Some Trade Names, TEGRETOL.
Most prescription creams used to lighten the skin contain hydroquinon and bleaching agents which are so dangerous to health and skin.
Most prescription creams used to lighten the skin contain hydroquinon and bleaching agents which are so dangerous to health and skin.
Bleaching creams
Bleaching or skin lightening creams or ointments are widely used worldwide either to attempt to remove localised dark patches (e.g. melasma or postinflammatory hyperpigmentation) or as a fashion trend aiming to reduce normal melanin in the skin.
What do bleaching creams contain?
Bleaching creams may contain a variety of ingredients. Some of these are more effective than others. In many areas, unregulated products are sold, often without listing their contents or they are labelled incorrectly. They may be safe but completely ineffective, or the chemicals may result in side effects and toxicity.
Skin lightening agents may include:
What are the risks and side effects?
The risks depend on which ingredient is being applied to the skin, in what concentration, over what area, and for how long it is used.
Hydroquinone
Hydroquinone is an effective skin lightening agent. It is no longer available in some parts of the world because of the damaging affects of longterm use. The recommended concentration over the counter is 2%, but up to 4% is available from a dermatologist in some countries. It should be used daily for no more than 6 months.
Its initial effect of inhibiting pigmentation is lost with prolonged application and sun stimulation.
Exogenous ochronosis is the main risk of continued use. This results in an irregular blue-black staining affecting sun-exposed skin and nails. It is due to deep deposition of the same pigment that occurs in alkaptonuria (endogenous ochronosis). Exogenous ochronosis may also occur from phenol, quinine or resorcinol.
Ochronosis may also result in loss of elasticity of the skin and impaired wound healing.
In some subjects, excessive use of hydroquinone in combination with certain foods in the diet (fish, eggs, offal, beans) can result in an unpleasant fish odour in the body secretions such as sweat and urine (trimethylaminuria).
Hydroquinone is sometimes given another name, such as:
Monobenzyl ether of hydroquinone is a strong derivative of hydroquinone that almost always causes nearly irreversible complete depigmentation of the skin (white patches).
Topical retinoids
Tretinoin is the main topical retinoid that has been used in skin lightening products. It thins the skin, increasing the penetration of other agents. as well as having a direct effect in reducing melanisation. It is a prescription medication because of potential risk in pregnancy. It can be quite irritating and may cause contact irritant dermatitis.
Botanicals
New active skin lightening compounds isolated from plants are being added to modern cosmetics. They appear to inhibit the production of melanin without being toxic to the melanocyte (tyrosinase inhibitors). It is not yet known which preparations are the most effective. Active ingredients include:
Other agents
Other agents in use for their skin lightening effect include:
Unregulated skin lightening creams may include many other ingredients. These may be relatively safe (e.g. lemon juice), toxic (e.g. camphor), irritating (e.g. detergents) or likely to provoke allergy (e.g. hair dye). Complications may include:
Topical corticosteroids
Topical corticosteroids lighten the skin by the following mechanisms.
In New Zealand and many other countries, stronger topical corticosteroids are regulated and can only be obtained with a doctor's prescription. However products containing betamethasone valerate, fluocinonide and clobetasol propionate can be purchased over the counter from a pharmacy or from drug vendors in a market place in some places such as Nigeria.
Potent topical steroids have a wide range of local side effects including skin thinning and atypical fungal infections (tinea incognito). When used over large areas for prolonged periods, they may risk serious internal disease from hypopituitarism. Steroid addiction syndrome results in folliculitis and steroid rosacea.
Mercury
Mercury was used as mercurious chloride, oxide and ammoniated mercury in many cosmetics and toiletries in the early part of the 20th century, before it was realised it caused toxicity. It is still found in some skin lightening creams because mercury inactivates the enzyme that leads to the production of melanin.
Longterm application of mercurial products to the skin makes the skin and nails darker, because the mercury is deposited in the epidermis, hair follicles and dermis.Mercury poisoning results in acute and chronic toxicity including acrodynia, as well as neurological and kidney damage.
DNA Clinical Treatment Protocol:
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Wearing a sunscreen is a must. The sunscreen must be "broad spectrum" (i.e. it blocks both UVA and UVB). A single day of excess sun can undo months of treatment.
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Hyperpigmentation has multiple causes and may be focal or diffuse. Most cases are due to an increase in melanin production and deposition.
Focal hyperpigmentation is most often postinflammatory in nature, occurring after injury (eg, cuts and burns) or other causes of inflammation (eg, acne, lupus). Focal linear hyperpigmentation is commonly due to phytophotodermatitis, which results from ultraviolet light combined with furocoumarins in limes, celery, and other plants.
Hyperpigmentation also has systemic and neoplastic causes.
Melasma (chloasma): Melasma consists of dark brown, sharply marginated, roughly symmetric patches of hyperpigmentation on the face (usually on the forehead, temples, and cheeks). It occurs primarily in pregnant women (melasma gravidarum, or the mask of pregnancy) and in women taking oral contraceptives. Ten percent of cases occur in non-pregnant women and dark-skinned men. Melasma is more prevalent and lasts longer in people with dark skin.Because all cases are associated with sun exposure, the mechanism probably involves overproduction of melanin by hyperfunctional melanocytes. Other than sun exposure, aggravating factors include:
In women, melasma fades slowly and incompletely after childbirth or cessation of hormone use. In men, melasma rarely fades.
Treatment depends on whether the pigmentation is epidermal or dermal; epidermal pigmentation becomes accentuated with Wood's light or can be diagnosed with biopsy. Only epidermal pigmentation responds to treatment. First-line of therapy includes a combination of DNA Skin Care Product which is earmarked at the bottom of this page.
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Lentigines: Lentigines (singular: lentigo) are flat, tan to brown oval spots. They are commonly due to chronic sun exposure (solar lentigines; sometimes called liver spots) and occur most frequently on the face and back of the hands. They typically first appear during middle age and increase in number with age. Although progression from lentigines to melanoma has not been established, lentigines are an independent risk factor for melanoma. They are treated with cryotherapy or laser.
Nonsolar lentigines are sometimes associated with systemic disorders, such as Peutz-Jeghers syndrome (in which profuse lentigines of the lips occur), multiple lentigines syndrome (Leopard syndrome), or xeroderma pigmentosum.
Diffuse hyperpigmentationdue to systemic disorders: Common systemic causes include Addison's disease (see Adrenal Disorders: Addison's Disease), hemochromatosis (see Iron Overload: Primary Hemochromatosis), and primary biliary cirrhosis (see Fibrosis and Cirrhosis: Primary Biliary Cirrhosis (PBC)). Skin findings are nondiagnostic as to cause.
Drug-induced hyperpigmentation: Changes are usually diffuse but sometimes have drug-specific distribution patterns or hues (see Table 1: Pigmentation Disorders: Hyperpigmentation Effects of Some Drugs and Chemicals ). Mechanisms include:
Focal hyperpigmentation frequently follows drug-induced lichen planus (also known as lichenoid drug reactions).
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Hyperpigmentation Effects of Some Drugs and Chemicals | |
Substance | Effect |
Drugs | |
Amiodarone Some Trade Names CORDARONE | Slate-gray to violaceous discoloration of sun-exposed areas; yellowish-brown deposits in the dermis |
Antimalarials | Yellow-brown to gray to bluish black discoloration of pretibial areas, face, oral cavity, and nails; drug-melanin complexes in the dermis; hemosiderin around capillaries |
Bleomycin Some Trade Names BLENOXANE | Flagellate hyperpigmented streaks on the back, often in areas of scratching or minor trauma |
Cancer chemotherapy drugs, including busulfan Some Trade Names MYLERAN, cyclophosphamide Some Trade Names CYTOXAN dactinomycin Some Trade Names COSMEGEN , daunorubicin Some Trade Names CERUBIDINE , and 5- fluorouracil Some Trade Names ADRUCIL (5-FU) | Diffuse hyperpigmentation |
Desipramine Some Trade Names NORPRAMINImipramine Some Trade Names TOFRANIL | Grayish blue discoloration on sun-exposed areas; golden-brown granules in upper dermis |
Hydroquinone Some Trade Names CLARIPEL ELDOQUIN SOLAQUIN | Bluish black discoloration of ear cartilage and face after years of use |
Phenothiazines, including chlorpromazine Some Trade Names THORAZINE | Grayish blue discoloration on sun-exposed areas; golden-brown granules in upper dermis |
Tetracyclines, particularly minocycline Some Trade Names MINOCIN | Grayish discoloration of teeth, nails, sclerae, oral mucosa, acne scars, face, forearms, and lower legs |
Heavy metals | |
Bismuth | Blue-gray discoloration of face, neck, and hands |
Gold | Blue-gray deposits around the eyes (chrysiasis) |
Mercury | Slate-gray discoloration of skinfolds |
Silver | Diffuse slate-gray discoloration (argyria), especially in sun-exposed areas |