The skin is one of the first organs to show evidence of HIV infection. Opportunistic infections, neoplasms, dermatoses, and pruritus involving skin and mucosa occur in over 90% of HIV-infected individuals. The successful treatment of skin manifestations will do much to improve the quality of life, comfort and appearance of those living with HIV and AIDS.

Introduction 
By the end of 2002, it was estimated that there were 42 million people living with the human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS). An estimated 5 million people acquired HIV in 2002. More than 90% of new infections occur in developing countries. The skin is one of the first organs to show evidence of HIV infection, and mucocutaneous disorders are a common indication for initial HIV testing. This is particularly distressing to patients, not only because of the discomfort but also because of their fear that the diagnosis may be obvious to the public. Opportunistic infections, neoplasms, dermatoses, and pruritus involving skin and mucosa occur more commonly as the immune function deteriorates, and affect over 90% of HIV-infected individuals. With the use of highly active antiretroviral therapy (HAART), the incidence and severity of many such diseases have decreased. However, in developing countries where few sufferers receive these drugs, the management of each of the common skin manifestations is particularly challenging.

Eosinophilic pustular folliculitis 
Eosinophilic pustular folliculitis (EPF) is a chronic dermatosis occurring in individuals with advanced HIV disease. The condition ‘pruritic papular eruption of HIV disease’ appears to be the same entity as EPF. Microbiology is negative. However, the disorder is thought to be secondary to Pityrosporum infection or to the Demodex folliculorum mite. It is also possible that sebum may be the target antigen of an autoimmune process.1 
The pruritus in EPF is intense. Small, red, oedematous, perifollicular papules or pustules occur symmetrically above the nipple line on the chest, proximal arms, head and neck. The lesions have the appearance of small insect bites (Figure 1). Scratching often alters primary lesions (Figure 2), and secondary bacterial infections can occur. The diagnosis may be further confounded, as many patients at this stage in their disease may also get hypersensitivity reactions to insect bites (papular urticaria). However, the distribution of the lesions helps to elucidate the diagnosis, and histological examination confirms it. 
Treatment reflects the many possible aetiologies. High-potency topical corticosteroid preparations may reduce the formation of new EPF lesions and may cause established lesions to resolve. Sedating antihistamines are most effective for symptomatic control of pruritus. Permethrin cream applied daily may be helpful. Ultraviolet B or psoralen with ultra­violet A (PUVA) may be efficacious in some cases. Prednisone given at an initial oral dose of 70 mg and tapered over a 1- or 2-week period is most useful in treating the cutaneous lesions. If symptoms recur after discontinuation of prednisone, the course can be repeated or prednisone 60 mg can be given 1 day per week. Oral itraconazole, 200 mg per day, is effective therapy and usually gives symptomatic relief within 2 weeks. The dose may be increased to 400 mg per day if the response is inadequate. Oral isotretinoin is reported to be highly effective, usually at doses of 40 mg twice daily until lesions resolve. The dose should then be tapered to 40 mg daily for several weeks, and then to 20 mg daily. Metronidazole 250 mg three times daily for 3 weeks may be helpful.2

Psoriasis 
The risk of developing psoriasis (Figure 3) is increased three-fold by HIV infection. Topical agents, namely coal tar products, dithranol, corticosteroids, vitamin D analogues, or retinoids, are usually effective in the management of limited psoriasis. For more widespread disease, phototherapy with ultraviolet B or PUVA is safe and efficacious, as are retinoids (etretinate and acitretin), methotrexate, hydroxyurea and cyclosporin.

Seborrhoeic dermatitis 
Seborrhoeic dermatitis (Figure 4) is the most common dermatosis occurring in HIV disease, presenting in the usual areas of the scalp, face, presternum, back and flexures. It is thought to be due to overgrowth or an abnormal reactivity to Pityrosporum yeasts. 
The aim of therapy is to remove scales and crusts, inhibit yeast colonisation, control secondary infection, and reduce erythema and itching. The scalp can be treated by washing daily with shampoos containing selenium sulphide, ketaconazole, zinc pyrithione, salicylic acid or coal tar. Crusts or scales can be removed by overnight application of salicylic acid in water-soluble bases such as aqueous cream. Corticosteroid scalp applications or creams, with or without 2% precipitated sulphur, may alleviate erythema and itching.
For the face, low-potency corticosteroids such as 1% hydrocortisone are usually sufficient. These may be mixed with 2% precipitated sulphur or with an imidazole, as in some proprietary compounds. For the flexures, imidazole and hydrocortisone mixtures are best. Treatment of the trunk usually requires potent topical corticosteroids. Oral itraconazole, which has activity against Pityrosporum ovale, may be used at a dose of 100 mg for up to 3 weeks, and may result in long-term remission in some patients. Lithium succinate 5% cream with or without hydrocortisone has been useful in some cases.3 

Xerosis and ichthyosis 
Xerosis and acquired ichthyosis are very common in HIV-infected individuals, occurring in up to 30% of those with advanced disease.2 The individual should avoid using soap, which removes the skin’s natural oil. Bathing with bath oils in the water, washing with emulsifying ointment or aqueous cream instead of soap, and applying an emollient with lactic acid, glycolic acid, salicylic acid or urea are all helpful. 

Photosensitivity 
Photosensitivity in HIV-infected individuals often occurs as an acute drug-induced reaction, usually to cotrimoxazole, or as a chronic photodermatitis. The aim of management is to reduce ultraviolet radiation exposure and to treat the dermatitis with topical, intralesional or systemic steroids and antipruritics. Mild topical steroids may be applied to the face and potent topical steroids may be used on affected areas on the body and limbs, followed after 10 minutes by sunscreen cream or lotion with sun protection factor of at least 20. The person should avoid going out between 1000 and 1500 hours, when ultraviolet A radiation is more intense. Wearing a hat and long-sleeved shirt further reduces ultraviolet exposure. 

Oral candidiasis 
Oral candidiasis (Figure 5) occurs in the majority of HIV-infected individuals during the course of HIV disease. 
Nystatin suspension, pastilles or lozenges, or the topical application of miconazole gel four times daily may be sufficient therapy. Treatment should be continued for 14 days in the first instance. However, if lesions persist beyond this time, treatment should be continued until 48 hours after the lesions have resolved. For more severe cases, ketoconazole 200 mg daily, fluconazole 50-100 mg daily or itraconazole 100 to 200 mg daily may be used. When the infection is resistant to both fluconazole and itraconazole, parenteral amphotericin B is offered. 

Viral warts 
Viral warts caused by the human papillomavirus (HPV) are more common in HIV infection, particularly on the face, inside the mouth and around the perineal area, presenting clinically as verrucae or condylomata acuminata.
Women with condylomata acuminata should have the uterine cervix evaluated for the presence of HPV changes, including malignancy. Cryotherapy with liquid nitrogen is a common and efficacious treatment for most warts. They may also be curetted or surgically excised, particularly large anogenital warts. Electrodesiccation of condylomata acuminata after local anaesthesia is also effective. A carbon dioxide laser can be used for resistant warts; infectious viruses have been identified in the vapour during laser or electrocoagulation of warts, so a surgical mask should be routinely used. 
Topical podophyllin resin is effective, especially for anogenital warts, and purified podophyllotoxin is approved for treatment of genital and perineal warts. Intralesional bleomycin may eradicate verrucae but may lead to extensive tissue necrosis. Topical 5-fluorouracil, sometimes in combination with salicylic acid, is helpful.4 Podophyllin, bleomycin and 5-fluouracil are contraindicated in pregnancy.
Salicylic acid and lactic acid may be used, especially for children. Trichloroacetic acid may be applied once every 2 weeks to genital warts, if podophyllin resin is contraindicated. Retinoic acid has been used for flat warts, and formalin soaks 3% to 10% have proved efficacious for mosaic warts. Cantharidin, which causes blistering, is also effective for some warts. Interferon-a has been used intralesionally for refractory genital warts, and imiquimod 5% cream (Aldara®), which stimulates the release of cytokines, can be used topically for persistent warts. 

Herpes zoster 
Herpes zoster in HIV infection may affect more than one dermatome and may become disseminated. Aciclovir, 800 mg five times daily for 1 week, is the treatment most commonly used. Famciclovir, valaciclovir and foscarnet are also effective. Analgesia (non-opiate) and bed rest are essential. Postherpetic neuralgia may be treated with amitriptyline, carbamazepine or gabapentin.

Herpes simplex infections 
Recurrent herpes simplex virus (HSV) infection is one of the most common opportunistic infections in HIV disease. Lesions may become persistent and erosions may progress to become painful ulcers. Chronic HSV infections can also present as proliferative lesions of the epidermis.2 Viral culture, Tzanck smear or biopsy of the lesion help to confirm the diagnosis. 
Aciclovir 400 mg is usually given five times daily for 5 days. Famciclovir 500 mg may be given twice daily for 7 days, or valaciclovir 500 mg twice daily for 5 days. These agents can be offered to treat reactivated infection or to suppress reactivation. Intravenous aciclovir is usually administered for severe infections, or intravenous foscarnet or cidofovir for infections caused by aciclovir-resistant HSV.

Molluscum contagiosum 
Molluscum contagiosum virus (MCV) infection commonly occurs on the face and anogenital region. In the immunocompetent host, lesions resolve spontaneously, usually within 1 year. Clinically, molluscum contagiosum presents as small, skin-coloured papules or nodules with a characteristic central umbilication. However, giant mollusca (>1 cm) do occur.
Therapeutically, the most efficient approach towards MCV infection is correction of the underlying immunodeficiency. With the use of HAART, MCV infection regresses or resolves completely. If correction of immunodeficiency is not possible, treatment is directed at controlling the number and bulk of lesions. Liquid nitrogen cryotherapy is the most convenient therapy, and usually must be repeated every 2-4 weeks. Curettage, followed by light electrodesiccation to control bleeding, is also effective. Topical applications of cantharidin, tretinoin, podophyllin, trichloro­acetic acid, tincture of iodine, silver nitrate or phenol, and intravenous and topical cidofovir or intralesional interferon-a may all be helpful. Treatment may be augmented by chemical peels.4 

Kaposi’s sarcoma 
Kaposi’s sarcoma (KS) (Figure 6) is a multifocal neoplastic process, arising from vascular and lymphatic endothelium. AIDS-associated KS is most common in homosexual men and has been associated with human herpesvirus 8. The lesions are pink, purple or brown in colour, initially appearing as patches and then becoming more elevated as plaques, papules or nodules. Lesions can occur anywhere on the skin or mucous membranes and about 20% involve the viscera.5 
Individual lesions of KS may be excised or treated with cryotherapy or lasers. Cytotoxic drugs such as vinblastine, bleomycin, interferon-a, interleukin-2 and recombinant granulocyte-macrophage colony-stimulating factor may be injected intralesionally. Radiation therapy plays a major role in the management of both solitary and disseminated mucocutaneous KS. Extensive disease can be treated with cytotoxic drugs such as chlorambucil, vinblastine or dactinomycin. Systemic low-dose interferon-a in combination with cytotoxic therapy or antiretroviral drugs has shown promising results.5,6 

Adverse cutaneous drug eruptions 
The incidence of adverse cutaneous drug eruptions is high in HIV infection. Antiretroviral drugs are not exempt from the group of causative agents, and have been associated with a variety of cutaneous reactions. Patients may also develop cutaneous eruptions in response to drugs used for the prophylaxis of opportunistic infection; for example, exanthematous eruptions, urticaria, Stevens-Johnson syndrome and toxic epidermal necrolysis can be associated with the use of cotrimoxazole. 
Among the most common and challenging of these eruptions are those associated with nevirapine, including Stevens-Johnson syndrome and toxic epidermal necrolysis, and the exanthematous reaction associated with cotrimoxazole. With nevirapine, the rash usually occurs within the first 8 weeks. The incidence is less if the drug is introduced at a low dose and increased gradually. If the rash is mild or moderate, nevirapine may be continued without interruption, but the dose should not be increased until the rash resolves. Systemic antihistamines, topical mild or moderately potent corticosteroids, and emollients may provide symptomatic relief. If the rash is severe or accompanied by blisters, oral lesions, conjunctivitis, oedema, general malaise or hypersensitivity reactions, the drug should be discontinued immediately and permanently. Further treatment of these eruptions should be at a centre specialised in the management of such reactions. 
For minor exanthematous reactions to cotrimoxazole, withdrawal of the drug and symptomatic therapy with emollients, moderately potent topical corticosteroids and systemic antihistamines are all that is necessary. For more severe reactions, potent topical steroids and prednisolone, 40-60 mg/day, should be offered. Successful desensitisation has been accomplished in individuals with previous exanthematous or urticarial reactions to cotrimoxazole, and desensitisation in persons with previous Stevens-Johnson syndrome has also been reported. 

Conclusion 
The use of HAART has prolonged the life and improved the health and well-being of HIV-infected individuals. Successful treatment of skin manifestations will also do much to improve the quality of life, comfort and appearance of those living with HIV and AIDS.