- HIV detection is the first step in the laboratory workup.
- Nonquantitative detection of HIV is the first step in diagnosing infectivity. In adults and older children, enzyme-linked immunosorbent assay (ELISA) and Western blot assay are used initially to detect HIV-specific antibodies; however, because maternal antibodies are present in neonatal blood, these tests are not used for diagnosis in patients younger than 2 years. DNA polymerase chain reaction (PCR) and/or viral culturing is the standard detection method in infants and young children.
- HIV DNA PCR detects the HIV-1 provirus within mononuclear cells by using oligonucleotides directed at highly conserved regions of the virus genome. This test can be performed within 24 hours of infection and has a sensitivity and specificity of 95% and 97%, respectively. Although it is more sensitive than viral cultures, their diagnostic performances are equivalent.
- Viral cultures are obtained by cocultivating potentially infected and uninfected mononuclear cells together to promote viral replication. Every few days, the culture is assayed for HIV p24 antigen. Positive results with 2 sequential p24 antigen detection assays indicate infection. This technique requires 7-14 days on average, but it may require as long as 28 days.
- An ELISA HIV antibody test, followed by a confirmatory Western blot test, should be used to diagnose HIV infection in older children and adults.
- Many new rapid HIV antibodies tests exist, and some have impressive sensitivities and specificities. The Single Use Diagnostic System (SUDS), however, is the only rapid HIV antibody test that is commercially available in the United States. In some studies, SUDS has been reported to have a false-positive rate approaching 50%, which makes its use difficult to justify.
- The viral load can be quantified by using several HIV assays. These assays should not be used until the diagnosis of HIV has been confirmed with a nonquantitative method because these tests may falsely indicate low viral loads in individuals who are HIV negative. A 5- or 3-fold change in the viral load is needed to reliably indicate a significant change in children younger than 2 years or in those older than 2 years, respectively.
- Reverse transcriptase PCR (RT-PCR) and nucleic acid sequence–based amplification (NASBA) of plasma RNA reveal a viral load that is 2-fold that obtained with the branched-chain DNA (bDNA) method. The former methods are sensitive only to HIV-1 subtype B viruses, whereas the bDNA method is sensitive to other HIV-1 subtypes.
- Initial infection is associated with high viral loads, especially in the neonate. In adults and adolescents with nonvertically acquired infections, the viral load rapidly decreases 6-12 months after the primary viremia. Neonates have high viral loads that persist throughout infancy. In children with vertically acquired infections, the load slowly declines after they are aged 1 year. Persistently high viral loads in patients older than 1 month and failure of the viral load to decrease after they are aged 1 year are associated with a poor prognosis.
- Viral resistance may be present.
- Both primary and secondary mutations can develop. Primary mutations alter the effectiveness of antiretroviral therapy (ART). Secondary mutations improve virus survival.
- Both genotypic and phenotypic assays can be performed. Genotypic assays are fast and available, but they reveal only known mutations, and they cannot be used to predict complex interactions when multiple antiretroviral drugs (ARDs) are used together. Phenotypic assays are not readily available, require more time to obtain results, and are expensive; however, they can be used to detect complex interactions between ARDs and quasispecies, perform in vitro drug trials, and measure ART inhibitory concentrations.
- Genotype or phenotype assays performed prior to the start or a change in therapy can help in preventing drug resistance.
- Both genotype and phenotype assays may not be useful to detect minor quasispecies, and treatment failure occurs despite the use of these techniques.
- Serum electrolytes should be monitored on a regular basis because nephrotoxicity may be induced by medications or HIV infection.
- Gastrointestinal function should be monitored.
- Liver function can be impaired as a result of medication or HIV or opportunistic infections. Transaminase levels should be monitored.
- Pancreatitis can be the result of medication or HIV or opportunistic infections. Amylase and lipase levels should be monitored.
- Parotitis is not uncommon, and amylase levels should be followed if parotitis is suspected or if a history of parotitis is present.
- Quantitative immunoglobulin levels should be followed periodically.
- Hyperimmunoglobulinemia is associated with disease progression.
- Hypoimmunoglobulinemia is observed in end-stage disease and is associated with a poor prognosis.
- Hematologic laboratory values may be assessed.
- The CD4 lymphocyte count is a surrogate marker for disease progression and should be followed closely. The CD4 count should be obtained prior to therapy. A rapid decrease in the CD4 count, especially in infants younger than 1 year, is a poor prognostic sign and should prompt the initiation or alteration of therapy.
- Consumptive thrombocytopenia is a common finding in children with HIV infection and may be observed in 10% of patients at initial diagnosis.
- Anemia occurs in as many as 20% of patients at diagnosis and occurs in as many as 80% of patients at some time. Anemia can have many etiologies in HIV infected individuals and requires a workup as described in Medical Care.
- A high mean corpuscular volume (MCV) is most commonly caused by zidovudine and can be used to verify compliance. Other medications also cause a high MCV, as well as vitamin B-12 and folate deficiencies.
- Pancytopenia results from folate deficiency, pharmaceutical use, and infections with viruses such as parvovirus B19.
- Neutropenia is observed in 10% of early asymptomatic HIV infections and in 50% of patients with AIDS.
- Blood smears may reveal large ovalocytes and hypersegmented polymorphonucleocytes in folate deficiency.
- Brain CT scanning may demonstrate white matter degeneration, atrophy, and/or basal ganglia calcifications with progressive HIV encephalopathy.
- Renal ultrasonography
- HIV nephropathy increases renal size and echogenicity, with a loss of cortical medullary differentiation.
- Renal cysts are observed with an increased incidence.
- Renal CT scanning
- Stasis of urine within the pyramids is observed in HIV nephropathy.
- This finding, combined with characteristic renal ultrasound findings, is rather specific for HIV nephropathy.
- Renal scintigraphy with technetium-99m-mercaptoacetyltriglycine (99mTc MAG3)
- Delayed elimination of the tracer and increased residual activity consistent with tubular dysfunction is observed in HIV nephropathy and is correlated with creatinine clearance.
- Delayed uptake and elimination of tracer indicates end-stage disease.
- Renal gallium scanning: Increased signal indicates inflammation in HIV nephropathy and is correlated with proteinuria.
- Abdominal ultrasonography: Calcifications within the liver, spleen, or kidney are observed with Pneumocystis carinii pneumonia (PCP) and MAC, Bartonella, and Histoplasma infections.
- Abdominal CT scanning: Mesenteric adenopathy can be observed with MAC infections.
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