Page 257 - AIDSBK23C

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FAILURE TO THRIVE.-- Poor growth may be seen in up to half of children infected
with HIV. The decrease in growth continues over time, and appears to involve lean body mass.
This effect may be present from birth, since it is noted that infants born to HIV-infected mothers
(even those who do not acquire HIV) have a significantly lower mean birth weight and length.
Micronutrient deficiencies, and vitamin A deficiency, may play a role, but dietary
supplementation does not correct deficits in lean body mass or height. The levels of HIV-1 RNA
are higher in children with poor growth.[1046]

PULMONARY FINDINGS.-- Pulmonary problems include Pneumocystis jiroveci
(carinii) pneumonia (PCP), which occurs in more than half of pediatric patients with AIDS and
has a high mortality rate in infants less than 2 months of age. Approximately 12% of infants
with perinatally acquired HIV infection develop PCP in the first year of life. More than a third
of pediatric AIDS patients die from PCP. Recurrent bacterial infections are common and
account for about 20% of deaths from AIDS in children.[1047] The histopathology is similar to
that seen in adults. Prophylaxis is recommended for all infants with perinatal HIV exposure,
beginning at 4 to 6 weeks of life, and continuing throughout the first year of life if HIV infection
is confirmed. Despite prophylaxis, PCP may still occur.[307] The risk for PCP is increased
when the CD4 count is declining or when maternal CD4 counts are lower, but does not appear to
be related to HIV-1 RNA levels.[1048]
Cytomegalovirus pneumonia can complicate HIV infection in infants being ventilated for
suspected Pneumocystis pnemonia. High dose corticosteroids for treatment of Pneumocystis
pneumonia may further immunocompromise these infants contributing to the development of
CMV pneumonia. Ganciclovir may be used empirically until CMV disease is excluded.[1049]
Lymphoid interstitial pneumonitis (LIP) is not characteristic of adult AIDS but is seen at
some point in about 20 to 30% of all children with AIDS. LIP rarely causes death and affected
children may have a better prognosis than that of HIV-infected children with AIDS-defining
opportunistic infections and neoplasms. It usually develops when passively acquired maternal
antibody begins to disappear. Corticosteroid therapy may be useful in treatment of LIP.[1050]
Bacterial pneumonias can be seen in the late stage of pediatric AIDS. Cytomegalovirus infection
of the lungs is also common and may be associated with pulmonary failure and death.
Mycobacterial and fungal infections are uncommon.[419,642]
A polyclonal B-cell lymphoproliferative disorder (PBLD) can affect the lungs in children
with HIV infection, as well as other organ sites including liver, spleen, lymph nodes, and
kidneys. Thus, hepatosplenomegaly and lymphadenopathy may be present. The lungs can
demonstrate nodular infiltrates. PBLD is a more florid example of pulmonary lymphoid
hyperplasia (PLH) characterized by lymphoid follicles with or without germinal centers
surrounding bronchioles. With PBLD, there are nodular infiltrates of polyclonal B-lymphocytes
and CD8+ T-lymphocytes.[646]

CNS FINDINGS.-- The most common neurologic finding in pediatric AIDS is a
progressive encephalopathy, or progressive HIV-related encephalopathy (PHE), which appears
to be caused by direct CNS infection by HIV. PHE may affect 30 to 60% of children with AIDS.
Neurologic signs can occur before complications of immune suppression appear. In children,
neurologic symptoms related to PHE include acquired microcephaly, acquired symmetric motor
deficits such as paresis or pathologic reflexes, and a failure to attain age-appropriate milestones