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Obstetrics & Gynecology 1999;94:537-542
© 1999 by The American College of Obstetricians and Gynecologists
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ORIGINAL RESEARCH

Effect of Human Immunodeficiency Virus Infection on Serum Beta2-Microglobulin Levels in Pregnant Women

ARLENE D. BARDEGUEZ, MD, EDWARD CONNOR, MD, RICHARD STEPHENS, PhD, THOMAS N. DENNY, BART HOLLAND, PhD and JAMES OLESKE, MD, MPH

From the Departments of Obstetrics, Gynecology and Women’s Health, Pediatrics, and Preventive Medicine and Community Health and the Pediatrics AIDS Clinical Trials Unit, New Jersey Medical School, Newark, New Jersey.

Address reprint requests to: Arlene D. Bardeguez, MD Department of Obstetrics, Gynecology and Women’s Health New Jersey Medical School 185 South Orange Avenue, MSB-E506 Newark, NJ 07103 E-mail: bardegad{at}umdnj.edu


   Abstract
Top
Abstract
Materials and Methods
 Results
 Discussion
 References
 
Objective: To assess serum ß2-microglobulin levels in human immunodeficiency virus (HIV)-infected and uninfected pregnant women, variations of serum ß2-microglobulin levels during pregnancy and postpartum, factors that might influence ß2-microglobulin levels in pregnant women, and the association between ß2-microglobulin and perinatal HIV-1 transmission.

Methods: We assayed 374 stored (-70C) serum samples from pregnant women enrolled in the Newark perinatal HIV-1–transmission study and 18 nonpregnant women for ß2-microglobulin using a microparticulate enzyme immuno assay. The Student t test, Wilcoxon rank test, binomial test, and Spearman correlation coefficient were used for statistical analysis, with P < .05 considered statistically significant. A linear regression model was used to assess the effect of independent variables on serum ß2-microglobulin levels.

Results: There were no significant differences (P = .16) in serum ß2-microglobulin levels between pregnant and non-pregnant HIV-negative women (1.07 ± 0.35 versus 0.99 ± 0.18 mg/L) ß2-Microglobulin levels did not vary throughout pregnancy and postpartum, irrespective of HIV serostatus. Substance abuse did not alter ß2-microglobulin levels. Human immunodeficiency virus infection caused significant increases of this surrogate marker, but it could not discriminate among disease stages. ß2-Microglobulin levels at delivery were lower among women who delivered HIV-infected infants.

Conclusion: Human immunodeficiency virus infection was associated with increased serum ß2-microglobulin levels in pregnant women and was the most significant correlate of increases of that marker. Pregnancy and substance use during pregnancy did not influence levels of serum ß2- microglobulin significantly.

Immune system activation has a great effect on the pathogenesis of human immunodeficiency virus (HIV) disease.1 Activated CD4 lymphocytes are infected more readily with HIV than are nonactivated cells. Immune activation of chronically HIV-infected cells can trigger transition to active viral replication.2 Single or serial determinations of immune system activation markers such as serum neopterin and ß2-microglobulin have been used to determine disease stage, identify individuals at higher risk of disease progression, and evaluate efficacy of antiretroviral therapies.3,4 Reliability of those markers can be influenced by race, gender, and behavioral patterns.5–8 To optimize clinical application of surrogate markers, we must evaluate their prognostic value in different HIV-infected populations.

ß2-Microglobulin is a subunit of the class I major histocompatibility complex found on the surface of all nucleated cells, including lymphocytes. Serum levels show production of the peptide during cellular turnover, and increases usually indicate generalized lymphoid activation.3 Increased serum ß2-microglobulin levels have been used as an independent predictor of progression to AIDS among seropositive homosexual men and as a marker of increased mortality among seropositive black women.9–11 Temporal changes in serum ß2-microglobulin levels after initiation of antiretroviral therapy can be used to evaluate therapeutic efficacy.4,12 Using ß2-microglobulin to monitor HIV disease progression has multiple advantages, including reduced cost, the feasibility of using frozen specimens, and the capability of many laboratories to do the assay, because of its high reproducibility.

In the United States, approximately 7000 HIV-infected women give birth annually. Most of those women belong to racial or ethnic minority groups and acquired their infections through intravenous (IV) drug use or heterosexual exposure.13 Our current knowledge of the effect of pregnancy on surrogate markers used to monitor HIV disease progression is limited. This study was designed to assess ß2-microglobulin levels in HIV-infected and uninfected pregnant women, variations of ß2-microglobulin levels during pregnancy and postpartum, factors that might influence ß2-microglobulin levels in pregnant women, and the association between ß2-microglobulin and perinatal transmission.


   Materials and Methods
Top
Abstract
 Materials and Methods
Results
 Discussion
 References
 
We assayed stored (-70C) samples from women enrolled in the Newark perinatal HIV-transmission study between September 1, 1989, and June 1, 1992, for ß2-microglobulin. We also measured ß2-microglobulin levels in serum samples from 18 HIV-1–negative, non-pregnant women between ages 28 and 50 (mean [± standard deviation {SD}] 37 ± 9 years) without histories of substance use. Human immunodeficiency virus status of participants was confirmed by enzyme-linked immunosorbent assay and Western blot positivity for HIV antibody. Women who were HIV-1–positive were assigned to clinical categories based on the 1993 revised classification for HIV infection in adolescents and adults.14 Clinical evaluation and toxicology, immunologic, and virologic studies were done for each participant during pregnancy and postpartum. Demographic and clinical information, including information about use of HIV-related therapies, was collected at each study visit. Substance abuse was defined as use of cocaine, marijuana, opiates, methadone, or benzodiazepines as evidenced by a positive history or a positive urine test at any study visit. Human immunodeficiency virus–infected pregnant women were classified as transmitters (infant was HIV-infected) or nontransmitters (infant was HIV-negative). Infants with two positive HIV polymerase chain reaction (PCR) or HIV culture assays at two different visits or with persistent HIV antibody after age 18 months were classified as HIV-infected. A child was considered HIV-negative if two virologic assays were negative and at least one of those was done after age 6 months, or if the child had seroreversion by age 18 months.

All virologic and immunologic assays, including lymphocyte phenotyping, p24 antigen, HIV culture, and HIV-PCR, were done in an AIDS Clinical Trials Group–certified laboratory. Detailed description of the methodology for those assays was published previously.15,16 Serum ß2-microglobulin levels were measured using an automated microparticle enzyme immunoassay technology (IMX ß2-microglobulin; Abbott Laboratories, Abbott Park, IL), which combines an antigen-antibody reaction with an enzyme-rate reaction. The lowest level of ß2-microglobulin detectable using this assay is 5 µg/L. Ninety-five percent of specimens from healthy individuals have values no more than 1.9 mg/L in our laboratory. The coefficients of variation among repetitive samples and among different laboratories range between 6.6 and 7.3% and 7.3 and 9.2%, respectively.

SAS 6.09 software (SAS Institute, Cary, NC) was used for statistical analysis. For data analysis, the serum samples were grouped by time obtained, as follows: less than 20 weeks, 26 ± 2 weeks, 36 ± 2 weeks, delivery ± 3 days, 4–8 weeks postpartum, and 6 months ± 4 weeks postpartum. For each subject there was an average of three serum samples available for analysis. The Student t test was used to assess differences in ß2-microglobulin levels between pregnant and nonpregnant HIV-1–negative women and between HIV-1–positive and HIV-1–negative women with or without histories of positive toxicologic findings. {chi}2 analysis was used to assess the association between HIV-1 seropositivity and positive toxicologic findings. If significant associations were observed between pregnancy, HIV status, and toxicology using {chi}2 tests or the two-tailed Fisher exact test, stratified analysis was considered justified. The binomial test was used to assess the consistency of increases in ß2-microglobulin levels in HIV-positive patients. The Spearman correlation co-efficient was used to assess the correlation between ß2-microglobulin concentrations and absolute CD4 or CD8 counts, p24 antigen, and HIV-1 culture. The Wilcoxon score test was used to evaluate the relationship between maternal ß2-microglobulin and perinata l HIV-1 transmission. Except for the {chi}2 tests, all tests were two-tailed. Because of the potential for problems with multiple comparisons, consistency of findings was emphasized throughout the analysis. Special attention was paid to findings in which P was < .001, but findings in which P was < .05 also were noted, for completeness.

The Duncan multiple-range test was used to determine whether there were significant differences in mean serum ß2-microglobulin concentrations at different HIV disease stages. Linear regression analysis was done to determine the relative importance of the covariates in predicting increases in serum ß2-microglobulin levels. Pair-wise interactions between covariates were considered by including in the model the product of two covariates as an additional explanatory variable.


   Results
Top
Abstract
 Materials and Methods
 Results
Discussion
 References
 
Seventy-four HIV-1–positive and 90 HIV-1–negative pregnant women were enrolled in the perinatal HIV-transmission study. The mean (± SD) age of study participants was 26 ± 5 years, but seropositive women were slightly older than seronegative controls (27.8 ± 5 and 25.1 ± 5 years, respectively; P = .001). Women in both groups were comparable with regard to gravidity, marital status, level of education, and racial-ethnic distribution. Overall, the racial-ethnic distribution of participants was 87% black (142 women), 9% Hispanic (15 women), and 4% white (seven women). Heterosexual transmission with an HIV-infected partner was the most common exposure category. Fifty-one women (69%) were asymptomatic, ten (13%) were symptomatic, and 13 (18%) had AIDS. The mean absolute CD4 counts of asymptomatic and symptomatic subjects and subjects with AIDS were 592 ± 244, 344 ± 121, and 128 ± 81, respectively. Twelve women used zidovudine for medical indications during pregnancy. Six of those were receiving zidovudine before their initial study visits. Although 72 women (44%) in the cohort were substance users, only 24 (32%) of the 74 HIV-infected women currently were using drugs or had histories of IV drug use. Using {chi}2 analysis, we found a significant association between substance use and HIV-1 status (P = .001). Therefore, substance use was controlled in all further analyses of serum ß2-microglobulin concentration in pregnant subjects.

A total of 374 serum samples were assayed for ß2-microglobulin: 204 from HIV-positive pregnant women, 152 from HIV-negative pregnant women, and 18 from nonpregnant controls. To assess the effect of pregnancy itself, mean (± SD) serum ß2-microglobulin concentrations in HIV-negative, non–substance user pregnant (n = 89), and nonpregnant women (n = 18) were compared. There were no significant differences in serum ß2-microglobulin concentrations between those groups (1.07 ± 0.35 versus 0.99 ± 0.18 mg/L, respectively; P = .16), suggesting that pregnancy per se does not affect serum ß2-microglobulin concentration. The influence of HIV infection on serum ß2-microglobulin concentration was assessed by comparing concentrations in HIV-infected and uninfected pregnant women. Levels of ß2-microglobulin were increased significantly in the former (1.92 ± 1.21 versus 1.21 ± 0.53 mg/L; P = .005). The effect of HIV infection also was assessed in pregnant substance users. Levels were 1.88 ± 0.95 mg/L for HIV-positive women with positive toxicology and 1.16 ± 0.73 mg/L for HIV-negative women with positive toxicology (P = .008). In our cohort, HIV infection during pregnancy caused significant increases in serum ß2-microglobulin concentrations, independent of substance use status. Thus, HIV infection appears to be the strongest correlate of increased ß2-microglobulin levels during pregnancy.

The effect of substance use on serum ß2-microglobulin concentration among pregnant women also was evaluated. There was no difference in serum ß2-microglobulin concentration when HIV-negative substance users were compared with nonusers (1.16 ± 0.73 versus 1.24 ± 0.36 mg/L; P = .67). There were no significant differences in serum ß2-microglobulin concentrations between HIV-infected substance users and nonusers. Temporal variations in serum ß2-microglobulin levels were monitored throughout pregnancy. Across the six time categories, ß2-microglobulin levels did not vary substantially (Table 1Go). In fact, in the HIV-negative group, as well as in the HIV-positive group, no more than a single SD separated the highest and lowest ß2-microglobulin levels. However, in six of six time categories, the ß2-microglobulin level was higher in HIV-positive subjects than in HIV-negative subjects (P = .016, binomial test).


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  		Table 1. Serum ß2-Microglobulin Levels During Pregnancy and Postpartum in Relation to Human Immunodeficiency Virus Serostatus
 
There was a statistically significant negative correlation (r = -0.378, P = .001) between ß2-microglobulin levels and absolute CD4 lymphocyte count. There was a weak but significant positive correlation (r = .195, P = .001) between ß2-microglobulin levels and absolute CD8 lymphocyte count. There was no significant correlation between ß2-microglobulin levels and positive, qualitative HIV culture or p24 antigen. To assess the correlation between ß2-microglobulin levels and stages of HIV disease, data were censored and one randomly selected result was used for each subject. Human immunodeficiency virus–infected pregnant women (n = 48) had significantly higher ß2-microglobulin levels than did uninfected pregnant women (n = 41) (1.92 ± 1.21 versus 1.21 ± 0.53 mg/L, P = .001) or uninfected nonpregnant counterparts (n = 18) (0.99 ± 0.18 mg/L). Serum ß2-microglobulin concentrations could not discriminate between pregnant women with different stages of HIV disease. Serum ß2-microglobulin levels in asymptomatic and symptomatic pregnant women and pregnant women with AIDS were 1.79 ± 1.36, 2.02 ± 0.65, and 2.20 ± 1.06 mg/L, respectively. There was a statistically significant difference (P < .05) in serum ß2-microglobulin levels between pregnant women with advanced disease (women who were symptomatic or had AIDS) and HIV-negative pregnant or nonpregnant women. However, there was no significant difference in serum ß2-microglobulin between HIV-positive asymptomatic pregnant women (1.79 ± 1.36 mg/L) and HIV-negative women, irrespective of pregnancy status (1.21 ± 0.53 and 0.99 ± 0.18 mg/L, respectively). To assess further the relative importance of individual variables with regard to predicting increases in serum ß2-microglobulin in pregnancy, multiple linear regression analysis was used. The most powerful correlate of ß2-microglobulin level was HIV infection, which accounted for 27% of the serum ß2-microglobulin level (P = .001). Human immunodeficiency virus seropositivity was more powerful than stage alone, which accounted for 22% of serum ß2-microglobulin level, but once HIV seropositivity was in the model, stage of disease added little predictive power (P = .4344). CD4 lymphocyte counts less than 500/mm3 or 200/mm3 accounted for only 8% (P = .085) and 4% (P > .50) of ß2-microglobulin levels, respectively. Thus, in the regression analysis, only HIV status was a significant determinant of serum ß2-microglobulin levels, whereas HIV disease stage, toxicology status, and CD4 lymphocyte count less than 500/m2-m3 or 200/mm3 were not associated significantly with ß2-microglobulin levels. We also assessed the strength of interactions of several variables in the prediction of serum ß2-microglobulin concentrations. Pair-wise interactions between covariates were considered by including the product of two covariates in the model as an additional explanatory variable. Human immunodeficiency virus–1 infection remained the most significant variable. Substance use had a trivial independent effect on the ß2-microglobulin value, decreasing the level by 0.006 mg/L.

Eight of 66 infants were classified as HIV-infected, for a perinatal HIV-1–transmission rate of 12%. ß2-Microglobulin levels were known for 22 nontransmitters and five transmitters at delivery. The mean (± SD) serum ß2-microglobulin levels for those groups were 2.14 ± 1.51 and 1.18 ± 0.28 mg/L, respectively (P = .03).


   Discussion
Top
Abstract
 Materials and Methods
 Results
 Discussion
References
 
Serum elevations of ß2-microglobulin level have been associated with generalized immune system activation and advanced HIV disease.3,10 Our study confirmed that serum ß2-microglobulin concentrations are in creased significantly in HIV-infected pregnant women compared with seronegative counterparts.17 We found HIV infection to be the strongest correlate for increased ß2-microglobulin levels during pregnancy. Contrary to other immunologic markers such as CD4 lymphocyte counts, pregnancy per se did not appear to influence serum ß2-microglobulin concentration,18 because there were no significant differences in serum ß2-microglobulin levels of HIV-negative pregnant and nonpregnant women. No significant variation of serum ß2-microglobulin levels with gestational age or between pregnant and postpartum samples was found. Elevation of serum ß2-microglobulin concentrations precedes the accelerated CD4 lymphocyte loss and the viral load increase seen in women with AIDS.19 Those observations highlight the potential use of ß2-microglobulin levels in addition to CD4 lymphocyte counts to monitor disease progression in HIV-infected pregnant women.

In the United States, most HIV-infected women have histories of drug use or currently use drugs. The effect of substance use on ß2-microglobulin levels has been a subject of controversy.7,8 Understanding the interaction among pregnancy, HIV infection, and substance use is clinically relevant and the interaction has not been studied previously. We observed a modest increase in serum ß2-microglobulin levels among HIV-negative substance users, but the effect of substance use on serum ß2-microglobulin level was vershadowed by the effects of HIV infection, and no significant increase in serum ß2-microglobulin level was detected when HIV- positive drug users and HIV-positive non–drug users were compared. We do not know the reason for this nonspecific increase in ß2-microglobulin levels, but it could explain the low reliability of this marker as a predictor of HIV disease progression previously reported among drug users.7,8

Like Hofmann et al and others,3,9,10 we found a negative correlation between CD4 lymphocyte counts and ß2-microglobulin levels and no correlation between serum ß2- microglobulin levels and HIV disease stage. That discrepancy can be explained by the fact that ß2-microglobulin levels are a marker of immune system activation. Therefore, concomitant infections, immunizations, or therapy could alter the degree of immune system activation in an individual, independent of disease stage. We also must acknowledge specific issues in our study such as the possibility of a type II error due to sample size, the fact that 60% of women with AIDS were taking zidovudine, and variation in the biologic response of the host to HIV infection. Zidovudine use in this cohort was limited to women with clinical indications for antiretroviral treatment. The effect of antiviral therapy on the reliability of this surrogate marker should be studied in larger cohorts with therapeutic intervention.

Contrary to observations published previously,20,21 in our cohort, women with HIV-infected children had significantly lower serum ß2-microglobulin levels at delivery than did those who did not transmit HIV infection. Those reports concerned HIV-infected women from underdeveloped countries in which concomitant infections could increase immune system activation and perinatal HIV transmission. Limited sample size or zidovudine use could have influenced our observations. Other groups have reported greater variability in serum ß2-microglobulin concentrations among heterosexual cohorts. The reliability of this surrogate marker is decreased significantly in cohorts with unknown seroconversion,22 as is usually observed in HIV-infected pregnant women. Therefore, the ability of this marker to predict the risk of perinatal HIV transmission deserves further evaluation.


   Footnotes
 
Supported by grants USAMRDC 70090001 from the Department of Defense, ACTG 125883-01 from the National Institute of Allergy and Infectious Diseases, and U64-CCU202219-08 from the Centers for Disease Control and Prevention.

PII S0029-7844(99)00343-9

Received October 13, 1998. Received in revised form March 24, 1999. Accepted March 25, 1999.


   References
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Abstract
 Materials and Methods
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 Discussion
 References
 
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4. Bass HZ, Hardy WD, Mitsuyasu RT, Taylor JM, Wang YX, Fischl MA, et al. The effect of zidovudine treatment on serum neopterin and ß2-microglobulin levels in mildly symptomatic, HIV type 1 seropositive individuals. J Acquir Immune Defic Syndr 1992;5:215–21.

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6. Lucey DR, McCarthy WF, Blatt SP, Melcher GP, Hendrix CW. Racial differences in serum ß2-microglobulin in persons with human immunodeficiency virus infection. J Infect Dis 1993;167: 1259–60.[Medline]

7. Fernandez-Cruz E, Desco M, Garcia-Montes M, Longo N, Gonzalez B, Zabay JM. Immunological and serological markers predictive of progression to AIDS in a cohort of HIV-infected drug users. AIDS 1990;4:987–94.[Medline]

8. Flegg PJ, Brettle RP, Robertson JR, Clarkson RC, Bird AG. ß2- Microglobulin levels in drug users: The influence of risk behavior. AIDS 1991;5:1021–4.[Medline]

9. Hofmann B, Wang YX, Cumberland WG, Detels R, Bozorgmehri M, Fahey JL. Serum beta 2-microglobulin level increases in HIV infection: Relation to seroconversion, CD4 T-cell fall and prognosis. AIDS 1990;4:207–14.[Medline]

10. Fahey JL, Taylor JM, Detels R, Hofmann B, Melmed R, Nishanian P, et al. The prognostic value of cellular and serologic markers in infection with human immunodeficiency virus type 1. N Engl J Med 1990;322:166–72.[Abstract]

11. Kerlikowske KM, Katz MH, Allen S, Wolf W, Hudes ES, Karita E, et al. ß2-Microglobulin as a predictor of death in HIV-infected women from Kigali, Rwanda. AIDS 1994;8:963–9.[Medline]

12. Jacobson MA, De Gruttola V, Reddy M, Arduino J, Strickland S, Reichman RC, et al. The predictive value of changes in serologic and cell markers of HIV activity for subsequent clinical outcome in patients with asymptomatic HIV disease treated with zidovudine. AIDS 1995;9:727–34.[Medline]

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14. 1993 Revised classification system for HIV infection and expanded surveillance case definition for AIDS among adolescents and adults. MMWR 1992;41(no. RR-17):1–19.

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16. Palumbo PE, Burchett S. Diagnosis of HIV infection and markers of disease progression in infants. In: Pizzo PA, Wilfert CM, eds. Pediatric AIDS. Philadelphia: Lippincott Williams & Wilkins, 1998:67–87.

17. Mikyas Y, Aziz N, Harawa N, Gorre M, Neagos N, Nogueira M, et al. Immunologic activation during pregnancy: Serial measurement of lymphocyte phenotype and serum activation molecules in HIV infected and uninfected women. J Reprod Immunol 1997;33:157–70.[Medline]

18. Biggar RJ, Pahwa S, Minkoff H, Mendes H, Willoughby A, Landesman S, et al. Immunosuppression in pregnant women infected with human immunodeficiency virus. Am J Obstet Gynecol 1989; 161:1239–44.[Medline]

19. Salazar-Gonzalez JF, Martinez-Maza O, Nishanian P, Aziz N, Shen LP, Grosser S, et al. Increased immune activation precedes the inflection point of CD4 T cells and the increased serum virus load in human immunodeficiency virus infection. J Infect Dis 1998;178: 423–30.[Medline]

20. Bredberg-Raden U, Urassa W, Urassa E, Lyamuya E, Msemo G, Kawo G, et al. Predictive markers for mother-to-child transmission of HIV-1 in Dar es Salaam, Tanzania. J Acquir Immune Defic Syndr 1995;8:182–7.

21. Jackson JB, Kataaha P, Hom DL, Mmiro F, Guay L, Ndugwa C, et al. Beta2-microglobulin, HIV-1 p24 antibody and acid-dissociated HIV-1 p24 antigen levels: Predictive markers for vertical transmission of HIV-1 in pregnant Ugandan women. AIDS 1993;7:1475–9.[Medline]

22. Immunologic marker paths for seroconversion: Single determinations of immunoglobulin A and ß2-microglobulin are not adequate to estimate time of HIV infection. Multicohort Analysis Project Workshop. Part II. AIDS 1994;8:923–33.[Medline]





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