Cutaneous Manifestations of HIV: A Primer

Advances in Skin & Wound Care, Apr 2004 by Trent, Jennifer T, Kirsner, Robert S

PURPOSE:

To provide physicians and nurses with an overview of the characteristics and treatments for skin lesions associated with HIV/AIDS.

TARGET AUDIENCE:

This continuing education activity is intended for physicians and nurses with an interest in identifying and managing skin lesions in patients with HIV/AIDS.

OBJECTIVES:

After reading the article and taking the test, the participant will be able to: 1. Identify the characteristics of skin lesions associated with HIV/AIDS. 2. Identify treatment options for skin lesions associated with HIV/AIDS.

ADV SKIN WOUND CARE 2004:17:116-29.

Since its emergence in the early 1980s, human immunodeficiency virus (HIV) infection has had a major impact on the field of dermatology.1 Skin diseases that were once rare have become commonplace. Because skin is among the organs where HIV disease and immunosuppression typically manifest, accurate diagnosis of skin eruptions is critical.

Cutaneous lesions may be the first sign of HIV infection or acquired immunodeficiency syndrome (AIDS). In patients with known HIV disease, skin diseases and skin-related signs of internal disease may be associated with significant morbidity and even mortality. Because certain skin manifestations of HIV infection are associated with levels of immune suppression, immune deterioration can be detected by monitoring skin disease2 (Table T).

HIV is associated with a variety of infectious and noninfectious diseases. The purpose of this article is to discuss a cross-section of these conditions and their cutaneous manifestations.

VIRAL INFECTION

Human herpesvirus 1 and 2

Classic human herpesvirus (HHV) 1 and 2, known as herpes simplex virus (HSV) types 1. and 2 (HSV-1, HSV-2), lead to orolabial and genital herpes, respectively.2-3 However, significant crossover and novel areas of presentation have increased over the years. This is, in part, a result of a change in sexual practices. Transmission of HSV can occur via direct sexual contact. In addition to the morbidity of these conditions, early recognition, education, and treatment are critical because HSV facilitates infection with HIV, as well as activates and promotes replication of HIV.3,4

Clinically, HSV presents as grouped vesicles on a red base that may progress to deep ulcerations and necrosis.1-6 In patients with HIV, HSV lesions occur more often, are more frequently atypical, and have a prolonged and recalcitrant course;2,4 they may even become chronic. Lesions commonly appear in the mouth and esophagus and on genitalia, perianal areas, and distal fingers.

Diagnosis can be made based on histopathology, which reveals epidermal balloon degeneration with intraepidermal vesicles and eosinophilic intranuclear inclusion bodies. It can be confirmed with Tzanck smear, by visualization of multinucleated epidermal (giant) cells, viral culture, and scrum antigen detection.1-6

The mainstay of treatment for HIV-associated HSV has been acyclovir.1-6 Patients with HIV are usually treated with higher doses, for longer periods, and with lifelong suppressive therapy. Patients with HTV and orolabial herpes can be treated with acyclovir, 400 mg orally 5 times a day or 5 mg/kg intravenously (IV) every 8 hours for 7 days. Patients who need suppressive therapy can take 400 mg of oral acyclovir twice a day. Patients with HTV and their first episode of genital herpes can be treated with 200 mg of acyclovir orally 5 times a day for 10 days, and recurrent herpes can be treated with 200 mg of acyclovir orally 5 times a day for 5 days. If IV acyclovir is needed, it can be given at 5 mg/kg every 8 hours for 7 days. Suppressive therapy includes 400 mg of acyclovir orally twice daily. Patients on suppressive therapy have been shown to have lower viral loads and a survival advantage.

A high prevalence (6.4%) of acyclovir resistance is seen among patients with HlV disease. This occurs via a mutation in thymidine kinase, necessitating the use of IV foscarnet, 40 mg/kg every 8 to 12 hours for 2 to 3 weeks, along with topically applied cidofovir 1% used once a day.4

Patients with HlV-assodated HSV have also been effectively treated with valacydovir and famciclovir. For orolabial herpes, the typical oral valacydovir dosage is 1 gram 3 times a day for 7 days. Famciclovir may be given orally at 500 mg twice a day for 7 days for treatment or 500 mg twice a day for suppression. Genital herpes can also be treated with oral valacydovir: 1 gram twice a day for 10 days for primary HSV-2 infection, 500 mg twice a day for 5 days for recurrent lesions, or 1 gram daily for suppression. Oral famciclovir may be used for genital herpes, at dosages of 500 mg twice a day for 7 days or 250 mg twice daily for suppression.

Varicella-zoster virus

Varicella-zoster virus (HHV-3) affects about 25% of patients with HIV.3 Transmission can occur via respiratory droplets and direct contact. Primary varicella infection presents with successive crops of vesicles on red base, which start on the head and face and subsequently spread to the rest of the body. In patients with HIV, the lesions may be more painful, severe, and prolonged. After lying dormant within the dorsal root ganglions, reactivation may occur and present as zoster or shingles, which is characterized by dermatomal distribution of vesicles on a red base.' Patients with HIV experience numerous episodes that last longer, disseminate more frequently, and are more painful. The vesicles often become chronic ulcerative, necrotic, or verrucous.1-3,5,6 Progressive neuronal inflammation and necrosis leads to severe pain (postherpetic neuralgia), which increases as the infection travels down the nerve.