Anemia is a common manifestation of HIV infection, occurring in approximately 30% of patients with asymptomatic infection and in as many as 75% to 80% of those with AIDS. Anemia has been associated with decreased quality of life and decreased survival. We performed a cross-sectional study nested within a multicenter prospective cohort study to describe the prevalence of anemia in 2056 HIV-infected and 569 HIV-negative women as well as to define the demographic, clinical, immunologic, and virologic correlates of anemia among HIV-infected women. A total of 37% of HIV-positive women and 17% of HIV-negative women had hemoglobin levels < 12 g/dl (p < .001). Factors associated with anemia in HIV-positive and HIV-negative women included mean corpuscular volume (MCV) < 80 fl (p < .001) and black race (p < .001). Among HIV-infected women, multivariate logistic analyses revealed that African American race (p < .0001), MCV < 80 fl (p < .0001), CD4 count < 200 per microliter (p <.0001), higher HIV RNA in plasma (p = .02), current use of ZDV (p = .01), and history of clinical AIDS (p = .004) were all independent predictors of anemia. These data indicate that worsening parameters of HIV disease are associated with anemia among HIV-infected women. Black women and women with low MCV values are at increased risk for anemia independent of HIV status.

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Most diagnostic tests are not dichotomous (negative or positive) but, rather, have a range of possible results (very negative to very positive). If the pretest probability of disease is high, the test result that prompts treatment should be any value that is even mildly positive. If the pretest probability of disease is low, the test result needed to justify treatment should be very positive. Simple decision rules that fix the cutpoint separating positive from negative test results do not take into account the individual patient's pretest probability of disease. Allowing the cutpoint to change with the pretest probability of disease increases the value of the test. This is primarily an issue when the pretest probability of disease varies widely between patients and depends on characteristics that are not measured by the test. It remains an issue for decision rules based on multiple test results if these rules fail to account for important determinants of patient-specific risk. This tutorial demonstrates how the value of a diagnostic test depends on the ability to vary the cutpoint, using as an example the white blood cell count in febrile children at risk for bacteremia.

Hypogammaglobulinemia (HGG) frequently occurs in recipients after types of (SOT). The incidence and significance of HGG in HIV+ recipients of SOT are just being explored. We reported that 12% of the recipients in the SOT in multi‐center HIV‐TR (HIV‐TR) Study developed moderate or severe HGG at 1 year. In LT recipients, this was associated with serious infections and death. We have now further characterized the decreased antibodies in HIV+ SOT recipients who developed HGG. We measured the levels of pathogen‐specific antibodies and poly‐specific self‐reactive antibodies (PSA) in relation to total IgG levels from serial serum samples for 20 HIV+ SOT recipients who developed moderate to severe HGG following SOT. Serum antibody levels to measles, tetanus toxoid, and HIV‐1 were determined by EIA. Levels of PSAs were determined by incubating control lymphocytes with patient serum, staining with anti‐human IgG Fab‐FITC, and analysis by flow cytometry. Levels of PSA were higher compared to healthy, HIV‐uninfected controls at pre‐transplant baseline and increased by weeks 12 and 26, but the changes were not significant. Likewise, anti‐HIV antibody levels remained unchanged over time. In contrast, antibody levels against measles and tetanus were significantly reduced from baseline by week 12, and did not return to baseline, even after 2 years. For HIV patients who develop moderate to severe HGG after transplant, the reduction in IgG levels is associated with a significant decrease in pathogen‐specific antibody titers, while PSA levels and anti‐HIV antibodies are unchanged. This may contribute to infectious complications and other clinical endpoints.