Page 256 - AIDSBK23C

Page 256

Zidovudine therapy in an HIV-infected mother has been shown to reduce the rate of
perinatal transmission of HIV by two-thirds, and no association with birth defects has been
reported from zidovudine therapy. Zidovudine decreases viral load and decreases the risk for
perinatal transmission in late gestation and/or at the time of delivery.[183] Such therapy
includes antenatal maternal oral administration of zidovudine starting at 14 to 34 weeks gestation
and continuing throughout the pregnancy, intravenous maternal zidovudine therapy during labor
and delivery, and oral administration of zidovudine to the infant within 12 hours after birth and
continuing for 6 weeks following delivery.[180,185] However, even an abbreviated regimen of
zidovudine is efficacious in reducing the risk for perinatal transmission of HIV.[293] Anemia
and neutropenia occur in HIV-uninfected infants during the first 3 months of life following
maternal prophylaxis to prevent transmission of HIV, and this anemia is greater in ART-exposed
infants.[1042]
There appear to be two patterns of progression to AIDS with perinatal HIV infection. In
about 10 to 25% of infections the infants and children manifest severe immunodeficiency with
failure to thrive and encephalopathy in the first two years of life, with mortality of nearly 100%
from AIDS by 4 years of age.[1043] Rapid progression of perinatally acquired HIV-1 may be
predicted by a number of factors. These include positive HIV-1 culture or polymerase chain
reaction (PCR) assay during the first week of life, <30% CD4+T-lymphocytes at birth, and any
or all of the following noted at birth: hepatomegaly, splenomegaly, lymphadenopathy.[1044]
Specific infectious diseases, severe bacterial infections, progressive neurologic disease, anemia,
fever, cardiomyopathy, growth failure, hepatitis, and persistent oral candidiasis are all findings
that correlate with shortened survival.[233]
In the remaining 75 to 90% of cases, children with HIV infection have a much slower
progression to AIDS over 10 years or more, often remaining asymptomatic through adolescence,
and their morbidity and mortality more closely resembles adult AIDS.[1043] From a pediatric
standpoint, long-term nonprogressors or slow progressors may be defined as children reaching
the age of 10 years without ART therapy (single or dual nucleosides only), without AIDS
defining illness and with CD4 counts above 25%. In one study of such children, half showed
deterioration in CD4 counts beginning at puberty while half remained stable. Thymic output did
not predict this difference in course.[1045]
HIV-infected children, however, with hepatomegaly, splenomegaly, lymphadenopathy,
parotitis, skin diseases, and recurrent respiratory infections tend to have longer survival.
Children with lymphoid interstitial pneumonitis tend to have a survival intermediate between the
above two groups. About half of children with perinatally acquired HIV infection are alive at
age 9.[79] In any case, increased HIV viral replication is noted in the first 3 to 16 weeks of life,
similar to acute HIV infection in adults. A higher viral load at this time suggests a more rapid
pattern of progression.[1043]
In developed nations, most of the mothers of infants with HIV infection have acquired
HIV infection as injection drug users or as sexual partners of drug users, but increasing numbers
of mothers have acquired HIV heterosexually. In addition, some sexually abused children have
contracted AIDS, with symptoms often not appearing until adolescence. Transfusion-associated
AIDS in the early 1980's accounted for about 10% of pediatric cases and transfusion of blood
products for hemophilia about 5%. In places where screening of blood products for HIV has
been employed, these percentages have decreased substantially. Death has occurred in over 75%
of reported pediatric AIDS cases, usually with opportunistic infections similar to adult AIDS
patients, but with a clinical course, on overall average, shorter than that of adult patients.[233]