Abstract

Women and children are the fastest growing segment of the U.S. population to have human immunodeficiency virus (HIV) infection. In 1997, approximately 20,000 American children were infected with HIV, and a quarter of them had acquired immune deficiency syndrome (AIDS). By the year 2000, AIDS will be one of the five leading causes of death among American children and among children worldwide. Cases tend to cluster in geographic areas where the disease is most prevalent: New York City, Newark, NJ, and Miami, FL.1 Most of the children are black (57%) or Hispanic (26%). More than 90% of children in the United States infected with HIV acquired their infection from their mothers (vertical transmission). Infection can occur by intrauterine transmission across the placenta, at the time of delivery, or in the postpartum period through breastfeeding. Available evidence suggests that the majority of infections occur close to the time of or during delivery. Some studies suggest higher rates of perinatal transmission in women who seroconvert during pregnancy and those with advanced disease, low peripheral CD41 T-lymphocyte counts, prolonged rupture of membranes, and high viral load as evidenced by HIV p24 antigenemia, quantitative viral culture, or RNA concentration. In vaginal deliveries, a first-born twin is at greater risk of HIV infection than the second-born twin. Prevention of transmission by cesarean section has not been proven. Vertically acquired infection now accounts for virtually all new infections in children. The risk of perinatal transmission of the virus is 25%. This is reduced to 8% with zidovudine treatment of the pregnant woman from the second trimester onward.2 Transmission from contaminated blood, blood components, or clotting factor concentrates is now rare in the United States because of exclusion of infected donors, viral inactivation treatment of clotting factor concentrates, and the availability of recombinant clotting factors. However, this mode of transmission has remained a problem in developing countries. A child can also acquire HIV from sexual abuse by an HIV-infected adult. Routes of HIV transmission in adolescents are similar to those of adults. The clinical characteristics of AIDS in children are different from those in adults. In 1987, the Center for Disease Control (CDC) published a classification system for children infected with HIV. Additional knowledge about the progression of the disease among children prompted a revision of the classification in 1994. Table 1 shows the 1994 pediatric HIV classification into clinical categories. Table 2 shows the immunologic categories based on age-specific CD41 T-lymphocyte counts and percent of total lymphocytes. Tables 3 and 4 list the clinical categories. Although this pediatric classification system was established for surveillance of HIV infection, its clinical categories are used to define the progression of the disease. Table 5 outlines the diagnosis of HIV infection in children. These tables were reproduced from the 1997 Red Book (24th edition) of the American Academy of Pediatrics. A skin eruption may be the presenting sign of HIV infection in a child. Included in this review are the most common reported ones as well as rare conditions that the author had seen and treated. Table 6 lists the categories of cutaneous manifestations. The severity of cutaneous manifestations correlates with the immune status of the patients. Researchers3 divided 21 HIV-infected children arbitrarily into three groups based on CD41 cell counts to determine the relationship between T-cell numbers and skin manifestations. The group of patients with CD41 cell counts less than 200/mm had severe and often multiple categories of cutaneous manifestations that were not amenable to conventional treatment. This subset of patients followed a grave clinical course manifested by severe bacterial and opportunistic infections. They also tended to have poorer prognoses, contributing to their rapid demise. Patients with CD41 cell counts between 200 and 500/mm and those with more than 500/mm had transient types of cutaneous manifestations that were more amenable to topical therapy. In patients with CD41 cell counts greater than 500/mm, skin involvement was less frequently noted than in the other two groups. From the State University of New York, Health Science Center at Brooklyn, Brooklyn, New York, USA. Address correspondence to Teresita A. Laude, MD, Department of Dermatology, Box 46, State University of New York, Health Science Center at Brooklyn, 450 Clarkson Ave., Brooklyn, NY 11203, USA.

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