ointments, which are greases such as white or yellow soft paraffin. They are more occlusive on the skin than creams, and this keeps the skin hydrated,
pastes, which are suspensions of fine powder in an ointment and will stay where they are placed on the skin. Their main use is to apply noxious chemicals that should be confined to one area of the skin,
creams, which are emulsions of water with a grease. They are less greasy than ointments, are absorbed more quickly into the skin and are often used as a vehicle for active ingredients,
lotions, which are any kind of liquid. They are less messy for use on wet surfaces and hairy areas and their main advantage is a cooling effect,
gels, which can be hydrophilic or hydrophobic and have a high water content. They are combined with an active ingredient, particularly for use on the face or scalp.Atopic and contact dermatitis
Dermatitis is a term used to describe eczematous inflammation of the skin. It has significant underlying genetic influences, but is triggered by external factors.
Atopic dermatitis (eczema)
The pathogenesis of atopic dermatitis is determined by a combination of genetic, environmental, pharmacological and immunological factors. There are two forms of atopic dermatitis. The extrinsic type (70–80% of cases) is associated with a food or aero-allergen. There is an association with other atopic disorders such as asthma and hay fever. It is associated with IgE-mediated sensitisation, with eosinophilia in the peripheral blood and with a raised plasma IgE concentration. In atopic individuals, circulating mononuclear cells have a reduced ability to produce interferon γ, which normally inhibits both IgE production and the proliferation of T-helper type 2 (Th2) lymphocytes. The function of regulatory T-cells is also abnormal. Keratinocytes produce cytokines that stimulate eosinophil activation and adhesion to vascular walls. The intrinsic form of atopic dermatitis also involves immune dysregulation, but there is no IgE excess or eosinophilia.
As a result of the changes in immune regulation in atopic individuals, Th2-cells proliferate. Dominance of either a Th1 or Th2 response is partially programmed in early life, with exposure to microbial antigens promoting the normal Th1 dominance. Th1-cell responses are induced by infections, and suppress the development of Th2-cells. It is possible that the increasing use of antibacterial drugs in childhood may partially explain the rise in atopic dermatitis (Chs 38 and 39).
Affected skin is red, scaly and extremely dry, often affecting the flexures. The dryness is a consequence of the inflammation, but the permeability barrier function of the skin is also impaired, resulting in increased transepidermal water loss. There may be vesicles and weeping with crusting over the skin surface. Scratching produces excoriation and thickening of the skin. The affected skin is infiltrated with activated T-cells, with selective recruitment of Th2-cells, and eosinophils. Increased carriage of Staphylococcus aureus on the affected skin may also maintain inflammation by activating T-cells and macrophages.
Contact dermatitis
immunological sensitisation involving a delayed hypersensitivity response (Ch. 39). Once the skin has been sensitised, the potential for further reaction persists indefinitely. Sensitisation can arise in response to topical application of drugs.Other types of dermatitis
These include nummular (discoid) eczema, photosensitive dermatitis and seborrhoeic dermatitis.
Treatment of atopic dermatitis
Emollients (substances that soften the skin) are helpful as hydrophobic agents that seal the surface of the skin and reduce water loss. Paraffin derivatives are most effective but are greasy and not well accepted by most people. Alternatives, such as aqueous creams, are more cosmetically acceptable.
Avoidance of irritants, such as soaps, detergents, alcohols and astringents. Wet dressings may help to prevent skin fissuring and reduce scratching.
Topical corticosteroid ointment (Ch. 44) is effective, but a low-potency corticosteroid should be chosen if there is continuous use, to minimise unwanted effects. The anti-inflammatory effect of these drugs makes them the mainstay of treatment, but diminished effectiveness with prolonged use (tachyphylaxis) limits their long-term value. Tachyphylaxis may be delayed by twice-weekly application of a more potent corticosteroid.
Topical calcineurin inhibitors, such as tacrolimus (Ch. 38), directly or indirectly reduce activation of many of the inflammatory cells involved in the pathogenesis of the dermatitic lesions, including T-cells, dendritic cells, mast cells and keratinocytes. Local burning is the major unwanted effect, and skin malignancy has been reported. Tacrolimus is more effective than a potent corticosteroid for moderate to severe eczema.
Sedative antihistamines (Ch. 39) at night assist sleep, although they have little effect on itching. A topical formulation of the tricyclic antidepressant doxepin (see Ch. 22) is available to treat itch. It is uncertain whether its antihistamine activity is the major mode of action.
Immunosuppressant therapy with azathioprine, ciclosporin or mycophenolate mofetil (Ch. 38) can be tried for treatment-resistant dermatitis. Apart from unwanted effects the main problem is rapid relapse when treatment is stopped.
Phototherapy with natural sunlight is helpful, but sweating can increase pruritus. Narrow-band ultraviolet B (UVB) radiation is a useful alternative.
Psoriasis
Psoriatic skin lesions are produced by a very rapid proliferation of epidermal cells. Cell turnover time is decreased from about 28 days to 3–4 days, which prevents adequate maturation. Instead of producing a normal keratinous surface layer, the skin thickens, forming a silvery scale with dilated upper dermal blood vessels. Psoriatic plaques (psoriasis vulgaris, accounting for 90% of cases) are usually found on the elbows, knees, lower back, buttocks and scalp. Various subtypes of psoriasis present with different clinical manifestations. An inflammatory arthritis occurs in up to 25% of people with psoriasis (see Ch. 30).
There is a genetic component to psoriasis, which interacts with unknown environmental factors to produce an immune reaction in the dermis. Antigen-presenting cells in the dermis mature after contact with the antigen, migrate to regional lymph nodes and activate T-cells. T-cells then proliferate and enter the circulation and extravasate into the skin at sites of inflammation, assisted by local chemokine production. In the dermis, interaction with the initiating antigen results in Th1 immune responses, with secretion of cytokines such as interferon γ, interleukin (IL)-12 and IL-23 and tumour necrosis factor α (TNFα). The cytokines stimulate cell proliferation and impair maturation of keratinocytes, and produce vascular changes in the skin.
Psoriasis can be provoked or exacerbated by several drugs, including lithium, chloroquine, hydroxychloroquine, β-adrenoceptor antagonists, non-steroidal anti-inflammatory drugs and angiotensin-converting enzyme inhibitors.
There are several treatments for the skin lesions, both topical and systemic, but none produce long-term remission. Increasingly, combinations of treatments have been found to be more effective than one agent alone.
Topical therapy
These reduce scaling and itching and may be sufficient in mild psoriasis (see atopic dermatitis, above). They can also be used with a keratolytic.
Keratolytics
Keratolytics such as salicylic acid break down keratin and soften skin, which improves penetration of other treatments. Salicylic acid ointment is most frequently used.
Vitamin D analogues
Vitamin D regulates epidermal proliferation and differentiation. It also has immunosuppressant properties. Vitamin D analogues (e.g. calcipotriol, calcitriol) are clean and simple to apply and are particularly useful for chronic plaque psoriasis, although complete clearing of the plaques is unusual. Ointment has a greater emollient effect than has cream, but is messy to apply. Calcipotriol should not usually be used on the face, where it often causes irritation; calcitriol may be better tolerated on this site, although it is less effective elsewhere. Excessive use of vitamin D analogues can lead to hypercalcaemia, but this is not a problem at recommended dosages. The ease of use of these compounds makes them a popular choice if a keratolytic is insufficient.
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