- Email: [email protected]
Prevalence of hepatitis B and C in pregnant women who are infected with human immunodeficiency virus
American Journal of Obstetrics and Gynecology (2005) 193, 1270–3
www.ajog.org
Prevalence of hepatitis B and C in pregnant women who are infected with human immunodeficiency virus Patricia Santiago-Munoz, MD,* Scott Roberts, MD, MS, Jeanne Sheffield, MD, Barbara McElwee, BSN, RNC, WHCNP, George D. Wendel Jr, MD Department of Obstetrics and Gynecology, The University of Texas Southwestern Medical Center, Dallas, TX Received for publication March 1, 2005; revised June 1, 2005; accepted June 30, 2005
KEY WORDS Hepatitis B virus Hepatitis C virus Human immunodeficiency virus Pregnancy Co-infection
Objective: The purpose of this study was to evaluate the prevalence of hepatitis B and hepatitis C virus co-infection among pregnant women who are infected by human immunodeficiency virus and who attend an obstetric complications prenatal clinic. Study design: A de-identified research obstetric human immunodeficiency virus database was reviewed regarding patient demographic characteristics, risk factors for infection, history of sexually transmitted diseases, and initial CD4 count. Results: Four hundred fifty-five women who are infected with human immunodeficiency virus with 572 pregnancies were delivered over 11 years. The overall prevalence of human immunodeficiency virus and hepatitis B or C virus co-infection in our population was 6.3%. More specifically, 1.5% was co-infected with hepatitis B virus, and 4.9% was co-infected with hepatitis C virus. Patients with hepatitis virus were more likely to use intravenous drugs (52% vs 18%; P ! .01) and alcohol (38% vs 5%; P ! .01). Co-infected patients were older (28 vs 25.6 years; P Z .04), but there were no racial differences. Median baseline CD4 counts in hepatitis B virus co-infected patients were significantly lower (310 cells/mm3) than those in either hepatitis C virus co-infected patients (453 cells/mm3) or patients who were not co-infected with human immunodeficiency virus (414 cells/mm3). Conclusion: One of 16 pregnant women who were infected with human immunodeficiency virus was co-infected with hepatitis B or hepatitis C virus. Hepatitis B co-infections appear to be associated with more compromised immune status in our cohort. Ó 2005 Mosby, Inc. All rights reserved.
Estimates for the prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections in the United States are 0.4% and 1.8%, respectively.1,2 Data are limited regarding the estimates of these prevalences Presented at the Twenty-Fifth Annual Meeting of the Society for Maternal Fetal Medicine, Reno, Nevada, February 7-12, 2005. * Reprint requests: Patricia Santiago-Munoz, MD, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9032. E-mail: [email protected] 0002-9378/$ - see front matter Ó 2005 Mosby, Inc. All rights reserved. doi:10.1016/j.ajog.2005.07.002
in pregnancy: 0.5% to 1.5% for HBV and 1% for HCV.3,4 Absent from the obstetric literature is a description of HBV and HCV prevalence in pregnant women who are infected with human immunodeficiency virus (HIV) in the United States. The HIV-infected pregnant cohort represents a unique population. Risk factors that are associated with HIV infection are also associated with HBV and HCV infection. One study from sub-Saharan Malawi, Africa, described the prevalence of persistent HBV as
Santiago-Munoz et al 13% and HCV as 16.5% in HIV-infected pregnant women. In this region, HBV and HCV are highly endemic and are not associated with HIV co-infection.5 These prevalences were in agreement with other reports from highly endemic areas.6-9 The aim of this study was to describe the seroprevalence of HBV and HCV co-infections in HIV-infected pregnant women who attended an inner city obstetric complications clinic in the United States. Liver disease that is caused by chronic HBV and HCV is currently an important cause of morbidity and death among HIVinfected patients.10
Material and methods Study population Patients who were eligible for this study were drawn from an obstetric complications clinic that specializes in infectious diseases. Participation in this clinic includes all patients in the Parkland Health and Hospital System who were known to be HIV-infected before or during pregnancy. The prevalence of HIV infection in our general obstetric population is approximately 0.4% to 0.5%. Parkland Hospital, which is a county-supported tertiary care center in Dallas County, Tex, delivers approximately 15,000 to 16,000 women annually, and serves a predominantly young, indigent Hispanic population. Institutional Review Board approval was obtained before this study was performed. Our study cohort consisted of all HIV-infected pregnant women who were followed in this prenatal clinic over the course of 11 years. The study involved 455 individual patients consecutively who were seen from January 1, 1993, to December 31, 2003, some of whom had O1 delivery during this time period. Patients with HIV infection who were cared for in the infectious disease clinic followed an evidence-based treatment protocol. In addition to routine prenatal laboratory evaluations, pregnant HIV-infected patients were tested for HBV and HCV infection at the initial visit. At intake, CD4 cell count, HBV surface antigen (HBsAg), HBV anti-core antibodies (anti-HBc immunoglobulin G and M), and HCV antibodies were obtained. If hepatitis serologic test results returned positive, the appropriate confirmatory tests were ordered. HIV viral loads were not collected consistently until the latter part of this longitudinal study and were not included in our final analysis. Demographic information and details concerning risk factors for infection such as alcohol abuse, intravenous drug use, and history of sexually transmitted diseases were collected. All pregnant women who were found to be infected with HBV or HCV underwent appropriate counseling and treatment, if warranted.
1271
Laboratory tests Presence of anti-HIV antibodies was determined by enzyme-linked immunosorbent assay screen (Abbott Laboratories, Abbott Park, Ill). All positive tests were retested in duplicate and confirmed by indirect immunofluorescence assay (Fluorognost HIV-1; Sanochemia Pharmazeutika, Vienna, Austria). This test is an in vitro, qualitative assay for the detection of antibodies to HIV-1 in human serum or plasma and has been found to be highly concordant with the Western blot. It is O99.98% specific and O99.7% sensitive in the detection of anti– HIV-1. There is no stated false-positive rate for indirect immunofluorescence assay.11 HBV surface antigen and HBV core immunoglobulin G and immunoglobulin M antibodies were determined by enzyme-linked immunosorbent assay. HCV antibody was identified by enzymelinked immunosorbent assay. For the purpose of this study, we defined asymptomatic HBV carriage as having a reactive HBsAg, reactive anti-HBc immunoglobulin G, and non-reactive antiHBc immunoglobulin M. HBV natural immunity was defined as nonreactive HBsAg, and a reactive anti-HBc immunoglobulin G. Positive HCV status was defined as having a reactive anti-HCV result. No co-infection was defined by the absence of anti-HCV and anti-HBsAg.
Statistical analysis All data for the study, including both demographic characteristics and laboratory results, were abstracted from a de-identified research HIV database that was reviewed for the purpose of documenting the prevalence of HBV or HCV infection in this population of pregnant patients. A de-identified database is one in which a particular patient cannot be recognized because key identifying characteristics, such as name and medical record numbers have been removed. Continuous data were analyzed with the Student t and Wilcoxon rank sum tests. Discrete data were analyzed with chi-square tests. Risk factors for chronic HBV, HCV, and a history of HBV infection were analyzed with logistic regression.
Results Between January 1, 1993, and December 31, 2003, a total of 455 women with HIV infection were followed and were delivered of 572 pregnancies through the infectious disease complications clinic. All of these women were included in our study cohort. The overall prevalence of HIV and HBV or HCV co-infection among pregnant women tested in this population was 6.3% (29/455 women). More specifically, 1.5% (7/455 women) were co-infected with HBV, and 4.9% (22/455 women) were co-infected with HCV. No women were
1272 Table
Santiago-Munoz et al HBV or HCV co-infected cohort versus no hepatitis co-infected HIV cohort
Variable
HBV or HCV (n Z 29)
Age (y)* Race n (%) Black White Hispanic Other Median CD4 count (cells/mm3) Alcohol abuse n (%) Injection drug use n (%) Sexually transmitted diseases n (%)
28 G 6.0 20 (69.0%) 5 (17.2%) 4 (13.8%) 0 415 11 (37.9%) 15 (51.7%) 21 (72.4%)
No co-infection (n Z 426) 25.6 G 6.1 289 51 77 9 414 23 75 247
P value .04 Not significant
(67.8%) (12.0%) (18.1%) (2.1%) (5.4%) (17.6%) (58.0%)
Not significant !.01 !.01 Not significant
* Data are given as mean G SD.
co-infected with both HBV and HCV; however, 73% of HCV co-infected women (16/22 women) had evidence of past HBV infection. The Table summarizes the demographic characteristics of our co-infected population compared with our patients who were not co-infected. There were no differences in racial background or history of sexually transmitted diseases between the groups. However, patients who were co-infected with either of the hepatitis viruses and HIV were older (P Z .04), and were more likely to abuse alcohol and intravenous drugs (P ! .01 for both). The HBV co-infected pregnant women were compared with the HCV co-infected patients. There was a significant difference in immune status between the groups, as shown by a lower median CD4 cell count in those patients with HBV (310 cells/mm3 vs 453 cells/mm3; P Z .02). Drug use was also significantly more common in the HCV co-infected cohort (63.6% vs 14.3%; P Z .03). There were no differences, however, in age, rates of alcohol abuse or history of sexually transmitted diseases. Women who were asymptomatic HBV carriers and those who had serologic evidence of previous infection and natural immunity were also compared with each other. The women who were chronic carriers of HBV had lower median CD4 counts than those who had cleared previous HBV infection (310 cells/mm3 vs 466 cells/mm3; P Z .03). Injection drug use was identified as a risk factor for HCV co-infection (odds ratio, 3.8; 95% CI, 1.3-10.9). Alcohol abuse was identified as a risk factor for HCV co-infection (odds ratio, 7.4; 95% CI, 2.5-22.1) and any HBV co-infection (odds ratio, 5.8; 95% CI, 2.2-15.4).
Comment Prevalence of HBV in the general US population is 0.4%. HCV is present in approximately 1.8% of the United States. Because of shared routes of transmission,
co-infection with either HBV or HCV is common among HIV-infected patients, and the prevalence of both is higher than in the general population. The prevalence of HBV and HCV in the US female HIV-infected cohort is 4.6% and 7.7% to 9.7%, respectively.12,13 Overall, co-infection with HBV or HCV appears to be lower in our cohort of pregnant patients than reported elsewhere in HIV-infected women in the United States. The prevalence of HBV in our HIV-infected pregnant patients is 1.5% and that of HCV is 4.9%. This is most likely due to differences in risk factors between the groups, unlike in highly endemic areas, where the prevalence of HBV or HCV is unchanged in the presence of HIV coinfection. The lower prevalence of both HBV and HCV can be explained by the young age of our cohort. It can also be explained by differences in indications for medical care (prenatal care vs acute or ambulatory care). In this cohort in which local endemic rates of HBV and HCV are low, risk factors in the acquisition of HBV and HCV assume more importance than in highly endemic areas.5-9 This effect is illustrated in the study by Choy et al14 in which increasing age and HIV infection are risk factors that are associated significantly with HCV infection. As expected, injection drug use is an efficient mode of HCV transmission. This is not apparent for HBV co-infection in this population. Alcohol abuse is a strong independent risk factor, but it is likely that heterosexual transmission is most efficient for HIV and HBV infection in this cohort. We found a lower median CD4 count in patients who were carriers of HBV infection as compared with those patients with serologic evidence of resolution of past HBV infection. This difference in CD4 count suggests immune-mediated differences between HBV carriers and those patients who were able to recover successfully from HBV infection. This attenuation of T-cell response in chronic HBV carriers has been described.15,16 All of the aforementioned factors underline the importance of the routine identification of hepatitis coinfection in HIV-infected patients. It is unclear whether chronic HBV or HCV infection increases HIV disease
Santiago-Munoz et al progression, but they may increase the risk of hepatotoxicity of anti–retroviral therapy.17 Appropriate counseling, therapy, and lifestyle changes may have an opportunity to decrease the occurrence and morbidity of co-infection at an earlier age. Likewise, routine testing for viral hepatitis during pregnancy provides the opportunity to assess the potential for vertical transmission, which allows the obstetrician and pediatrician to act jointly with interventions that decrease the incidence of HIV, HBV, and potentially HCV transmission to the newborn infant. Similarly, the patient herself may benefit from the knowledge of her co-infected status because therapy is available to modify disease status.
References 1. McQuillan GM, Coleman PJ, Kruszon-Moran D, Moyer LA, Lambert SB, Margolis HS. Prevalence of hepatitis B virus infection in the United States: the National Health and Nutrition Examination Surveys, 1976 through 1994. Am J Public Health 1999;89:14-8. 2. Alter M, Kruszon-Moran D, Nainan OV, McQuillan GM, Gao F, Moyer LA, et al. The prevalence of hepatitis C virus infection in the United States, 1988 through 1994. N Engl J Med 1999;341: 556-62. 3. American College of Obstetricians and Gynecologists. Viral hepatitis in pregnancy: ACOG educational bulletin no. 248. Washington (DC): The College; 1998. 4. Centers for Disease Control and Prevention. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR Recomm Rep 1998;47:1-39. 5. Ahmed SD, Cuevas LE, Brabin BJ, Kazembe P, Broadhead R, Verhoeff FH, et al. Seroprevalence of hepatitis B and C and HIV in Malawian pregnant women. J Infect 1998;37:248-51. 6. Sobeslavsky O. Prevalence of markers of hepatitis B virus infection in various countries: a WHO collaborative study. Bull WHO 1980;58:621-8.
1273 7. Oshitani H, Kasolo FC, Mpabalwani M, Mizuta K, Luo NP, Suzuki H, et al. Prevalence of hepatitis B antigens in human immunodeficiency virus type in seropositive and seronegative women in Zambia. Trans R Soc Trop Med Hyg 1996;90:235-6. 8. Kowo MP, Goubau P, Ndam EN, Njoya O, Sasaki S, Seghers V, et al. Prevalence of hepatitis C virus and other blood-borne viruses in Pygmies and neighbouring Bantus in southern Cameroon. Trans R Soc Tro Med Hyg 1995;89:484-6. 9. Darwish MA, Faris R, Clemens JD, Rao MR, Edelman R. High seroprevalence of hepatitis A, B, C and E viruses in residents in an Egyptian village in the Nile Delta: a pilot study. Am J Trop Med Hyg 1996;54:554-8. 10. Soriano V, Puoti M, Bonacini M, Brook G, Cargnel A, Rockstroh J, et al. Care of patients with chronic Hepatitis B and HIV co-infection: recommendations from an HIV-HBV International Panel. AIDS 2005;19:221-40. 11. Immunodeficiency virus type 1 (HIV-1) Fluorognost HIV-1 IFA, Product Insert. Vienna, Austria; Sanochemia Pharmazeutika AG; 1996. 12. Sherman KE, Rouster DS, Chung RT, Rajicic N. Hepatitis C virus prevalence among patients infected with human immunodeficiency virus: a cross sectional analysis of the US Adult AIDS Clinical Trials group. HIV/AIDS CID 2002;34:831-7. 13. Kellerman SE, Hanson DL, McHaghten AD, Fleming PL. Prevalence of chronic hepatitis B and incidence of acute hepatitis B infection in human immunodeficiency virus-infected subjects. J Infect Dis 2003;188:571-7. 14. Choy Y, Gittens-Williams L, Apuzzio J, Skurnick J, Zollicoffer C, McGovern PG. Risk factors for hepatitis C infection among sexually transmitted disease-infected, inner city obstetric patients. Infect Dis Obstet Gynecol 2003;11:191-8. 15. Ganem D, Prince AM. Hepatitis B virus infection: natural history and clinical consequences. N Engl J Med 2004;350:1118-29. 16. Chisari FV, Ferrari C. Hepatitis B virus immunopathogenesis. Annu Rev Immunol 1995;13:29-60. 17. Department of Health and Human Services (DHHS). Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents, April 7, 2005. Last accessed: June 5, 2005. Available at: http://aidsinfo.nih.gov/guidelines/adult/AA_040705.pdf
www.ajog.org
Prevalence of hepatitis B and C in pregnant women who are infected with human immunodeficiency virus Patricia Santiago-Munoz, MD,* Scott Roberts, MD, MS, Jeanne Sheffield, MD, Barbara McElwee, BSN, RNC, WHCNP, George D. Wendel Jr, MD Department of Obstetrics and Gynecology, The University of Texas Southwestern Medical Center, Dallas, TX Received for publication March 1, 2005; revised June 1, 2005; accepted June 30, 2005
KEY WORDS Hepatitis B virus Hepatitis C virus Human immunodeficiency virus Pregnancy Co-infection
Objective: The purpose of this study was to evaluate the prevalence of hepatitis B and hepatitis C virus co-infection among pregnant women who are infected by human immunodeficiency virus and who attend an obstetric complications prenatal clinic. Study design: A de-identified research obstetric human immunodeficiency virus database was reviewed regarding patient demographic characteristics, risk factors for infection, history of sexually transmitted diseases, and initial CD4 count. Results: Four hundred fifty-five women who are infected with human immunodeficiency virus with 572 pregnancies were delivered over 11 years. The overall prevalence of human immunodeficiency virus and hepatitis B or C virus co-infection in our population was 6.3%. More specifically, 1.5% was co-infected with hepatitis B virus, and 4.9% was co-infected with hepatitis C virus. Patients with hepatitis virus were more likely to use intravenous drugs (52% vs 18%; P ! .01) and alcohol (38% vs 5%; P ! .01). Co-infected patients were older (28 vs 25.6 years; P Z .04), but there were no racial differences. Median baseline CD4 counts in hepatitis B virus co-infected patients were significantly lower (310 cells/mm3) than those in either hepatitis C virus co-infected patients (453 cells/mm3) or patients who were not co-infected with human immunodeficiency virus (414 cells/mm3). Conclusion: One of 16 pregnant women who were infected with human immunodeficiency virus was co-infected with hepatitis B or hepatitis C virus. Hepatitis B co-infections appear to be associated with more compromised immune status in our cohort. Ó 2005 Mosby, Inc. All rights reserved.
Estimates for the prevalence of hepatitis B virus (HBV) and hepatitis C virus (HCV) infections in the United States are 0.4% and 1.8%, respectively.1,2 Data are limited regarding the estimates of these prevalences Presented at the Twenty-Fifth Annual Meeting of the Society for Maternal Fetal Medicine, Reno, Nevada, February 7-12, 2005. * Reprint requests: Patricia Santiago-Munoz, MD, Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9032. E-mail: [email protected] 0002-9378/$ - see front matter Ó 2005 Mosby, Inc. All rights reserved. doi:10.1016/j.ajog.2005.07.002
in pregnancy: 0.5% to 1.5% for HBV and 1% for HCV.3,4 Absent from the obstetric literature is a description of HBV and HCV prevalence in pregnant women who are infected with human immunodeficiency virus (HIV) in the United States. The HIV-infected pregnant cohort represents a unique population. Risk factors that are associated with HIV infection are also associated with HBV and HCV infection. One study from sub-Saharan Malawi, Africa, described the prevalence of persistent HBV as
Santiago-Munoz et al 13% and HCV as 16.5% in HIV-infected pregnant women. In this region, HBV and HCV are highly endemic and are not associated with HIV co-infection.5 These prevalences were in agreement with other reports from highly endemic areas.6-9 The aim of this study was to describe the seroprevalence of HBV and HCV co-infections in HIV-infected pregnant women who attended an inner city obstetric complications clinic in the United States. Liver disease that is caused by chronic HBV and HCV is currently an important cause of morbidity and death among HIVinfected patients.10
Material and methods Study population Patients who were eligible for this study were drawn from an obstetric complications clinic that specializes in infectious diseases. Participation in this clinic includes all patients in the Parkland Health and Hospital System who were known to be HIV-infected before or during pregnancy. The prevalence of HIV infection in our general obstetric population is approximately 0.4% to 0.5%. Parkland Hospital, which is a county-supported tertiary care center in Dallas County, Tex, delivers approximately 15,000 to 16,000 women annually, and serves a predominantly young, indigent Hispanic population. Institutional Review Board approval was obtained before this study was performed. Our study cohort consisted of all HIV-infected pregnant women who were followed in this prenatal clinic over the course of 11 years. The study involved 455 individual patients consecutively who were seen from January 1, 1993, to December 31, 2003, some of whom had O1 delivery during this time period. Patients with HIV infection who were cared for in the infectious disease clinic followed an evidence-based treatment protocol. In addition to routine prenatal laboratory evaluations, pregnant HIV-infected patients were tested for HBV and HCV infection at the initial visit. At intake, CD4 cell count, HBV surface antigen (HBsAg), HBV anti-core antibodies (anti-HBc immunoglobulin G and M), and HCV antibodies were obtained. If hepatitis serologic test results returned positive, the appropriate confirmatory tests were ordered. HIV viral loads were not collected consistently until the latter part of this longitudinal study and were not included in our final analysis. Demographic information and details concerning risk factors for infection such as alcohol abuse, intravenous drug use, and history of sexually transmitted diseases were collected. All pregnant women who were found to be infected with HBV or HCV underwent appropriate counseling and treatment, if warranted.
1271
Laboratory tests Presence of anti-HIV antibodies was determined by enzyme-linked immunosorbent assay screen (Abbott Laboratories, Abbott Park, Ill). All positive tests were retested in duplicate and confirmed by indirect immunofluorescence assay (Fluorognost HIV-1; Sanochemia Pharmazeutika, Vienna, Austria). This test is an in vitro, qualitative assay for the detection of antibodies to HIV-1 in human serum or plasma and has been found to be highly concordant with the Western blot. It is O99.98% specific and O99.7% sensitive in the detection of anti– HIV-1. There is no stated false-positive rate for indirect immunofluorescence assay.11 HBV surface antigen and HBV core immunoglobulin G and immunoglobulin M antibodies were determined by enzyme-linked immunosorbent assay. HCV antibody was identified by enzymelinked immunosorbent assay. For the purpose of this study, we defined asymptomatic HBV carriage as having a reactive HBsAg, reactive anti-HBc immunoglobulin G, and non-reactive antiHBc immunoglobulin M. HBV natural immunity was defined as nonreactive HBsAg, and a reactive anti-HBc immunoglobulin G. Positive HCV status was defined as having a reactive anti-HCV result. No co-infection was defined by the absence of anti-HCV and anti-HBsAg.
Statistical analysis All data for the study, including both demographic characteristics and laboratory results, were abstracted from a de-identified research HIV database that was reviewed for the purpose of documenting the prevalence of HBV or HCV infection in this population of pregnant patients. A de-identified database is one in which a particular patient cannot be recognized because key identifying characteristics, such as name and medical record numbers have been removed. Continuous data were analyzed with the Student t and Wilcoxon rank sum tests. Discrete data were analyzed with chi-square tests. Risk factors for chronic HBV, HCV, and a history of HBV infection were analyzed with logistic regression.
Results Between January 1, 1993, and December 31, 2003, a total of 455 women with HIV infection were followed and were delivered of 572 pregnancies through the infectious disease complications clinic. All of these women were included in our study cohort. The overall prevalence of HIV and HBV or HCV co-infection among pregnant women tested in this population was 6.3% (29/455 women). More specifically, 1.5% (7/455 women) were co-infected with HBV, and 4.9% (22/455 women) were co-infected with HCV. No women were
1272 Table
Santiago-Munoz et al HBV or HCV co-infected cohort versus no hepatitis co-infected HIV cohort
Variable
HBV or HCV (n Z 29)
Age (y)* Race n (%) Black White Hispanic Other Median CD4 count (cells/mm3) Alcohol abuse n (%) Injection drug use n (%) Sexually transmitted diseases n (%)
28 G 6.0 20 (69.0%) 5 (17.2%) 4 (13.8%) 0 415 11 (37.9%) 15 (51.7%) 21 (72.4%)
No co-infection (n Z 426) 25.6 G 6.1 289 51 77 9 414 23 75 247
P value .04 Not significant
(67.8%) (12.0%) (18.1%) (2.1%) (5.4%) (17.6%) (58.0%)
Not significant !.01 !.01 Not significant
* Data are given as mean G SD.
co-infected with both HBV and HCV; however, 73% of HCV co-infected women (16/22 women) had evidence of past HBV infection. The Table summarizes the demographic characteristics of our co-infected population compared with our patients who were not co-infected. There were no differences in racial background or history of sexually transmitted diseases between the groups. However, patients who were co-infected with either of the hepatitis viruses and HIV were older (P Z .04), and were more likely to abuse alcohol and intravenous drugs (P ! .01 for both). The HBV co-infected pregnant women were compared with the HCV co-infected patients. There was a significant difference in immune status between the groups, as shown by a lower median CD4 cell count in those patients with HBV (310 cells/mm3 vs 453 cells/mm3; P Z .02). Drug use was also significantly more common in the HCV co-infected cohort (63.6% vs 14.3%; P Z .03). There were no differences, however, in age, rates of alcohol abuse or history of sexually transmitted diseases. Women who were asymptomatic HBV carriers and those who had serologic evidence of previous infection and natural immunity were also compared with each other. The women who were chronic carriers of HBV had lower median CD4 counts than those who had cleared previous HBV infection (310 cells/mm3 vs 466 cells/mm3; P Z .03). Injection drug use was identified as a risk factor for HCV co-infection (odds ratio, 3.8; 95% CI, 1.3-10.9). Alcohol abuse was identified as a risk factor for HCV co-infection (odds ratio, 7.4; 95% CI, 2.5-22.1) and any HBV co-infection (odds ratio, 5.8; 95% CI, 2.2-15.4).
Comment Prevalence of HBV in the general US population is 0.4%. HCV is present in approximately 1.8% of the United States. Because of shared routes of transmission,
co-infection with either HBV or HCV is common among HIV-infected patients, and the prevalence of both is higher than in the general population. The prevalence of HBV and HCV in the US female HIV-infected cohort is 4.6% and 7.7% to 9.7%, respectively.12,13 Overall, co-infection with HBV or HCV appears to be lower in our cohort of pregnant patients than reported elsewhere in HIV-infected women in the United States. The prevalence of HBV in our HIV-infected pregnant patients is 1.5% and that of HCV is 4.9%. This is most likely due to differences in risk factors between the groups, unlike in highly endemic areas, where the prevalence of HBV or HCV is unchanged in the presence of HIV coinfection. The lower prevalence of both HBV and HCV can be explained by the young age of our cohort. It can also be explained by differences in indications for medical care (prenatal care vs acute or ambulatory care). In this cohort in which local endemic rates of HBV and HCV are low, risk factors in the acquisition of HBV and HCV assume more importance than in highly endemic areas.5-9 This effect is illustrated in the study by Choy et al14 in which increasing age and HIV infection are risk factors that are associated significantly with HCV infection. As expected, injection drug use is an efficient mode of HCV transmission. This is not apparent for HBV co-infection in this population. Alcohol abuse is a strong independent risk factor, but it is likely that heterosexual transmission is most efficient for HIV and HBV infection in this cohort. We found a lower median CD4 count in patients who were carriers of HBV infection as compared with those patients with serologic evidence of resolution of past HBV infection. This difference in CD4 count suggests immune-mediated differences between HBV carriers and those patients who were able to recover successfully from HBV infection. This attenuation of T-cell response in chronic HBV carriers has been described.15,16 All of the aforementioned factors underline the importance of the routine identification of hepatitis coinfection in HIV-infected patients. It is unclear whether chronic HBV or HCV infection increases HIV disease
Santiago-Munoz et al progression, but they may increase the risk of hepatotoxicity of anti–retroviral therapy.17 Appropriate counseling, therapy, and lifestyle changes may have an opportunity to decrease the occurrence and morbidity of co-infection at an earlier age. Likewise, routine testing for viral hepatitis during pregnancy provides the opportunity to assess the potential for vertical transmission, which allows the obstetrician and pediatrician to act jointly with interventions that decrease the incidence of HIV, HBV, and potentially HCV transmission to the newborn infant. Similarly, the patient herself may benefit from the knowledge of her co-infected status because therapy is available to modify disease status.
References 1. McQuillan GM, Coleman PJ, Kruszon-Moran D, Moyer LA, Lambert SB, Margolis HS. Prevalence of hepatitis B virus infection in the United States: the National Health and Nutrition Examination Surveys, 1976 through 1994. Am J Public Health 1999;89:14-8. 2. Alter M, Kruszon-Moran D, Nainan OV, McQuillan GM, Gao F, Moyer LA, et al. The prevalence of hepatitis C virus infection in the United States, 1988 through 1994. N Engl J Med 1999;341: 556-62. 3. American College of Obstetricians and Gynecologists. Viral hepatitis in pregnancy: ACOG educational bulletin no. 248. Washington (DC): The College; 1998. 4. Centers for Disease Control and Prevention. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR Recomm Rep 1998;47:1-39. 5. Ahmed SD, Cuevas LE, Brabin BJ, Kazembe P, Broadhead R, Verhoeff FH, et al. Seroprevalence of hepatitis B and C and HIV in Malawian pregnant women. J Infect 1998;37:248-51. 6. Sobeslavsky O. Prevalence of markers of hepatitis B virus infection in various countries: a WHO collaborative study. Bull WHO 1980;58:621-8.
1273 7. Oshitani H, Kasolo FC, Mpabalwani M, Mizuta K, Luo NP, Suzuki H, et al. Prevalence of hepatitis B antigens in human immunodeficiency virus type in seropositive and seronegative women in Zambia. Trans R Soc Trop Med Hyg 1996;90:235-6. 8. Kowo MP, Goubau P, Ndam EN, Njoya O, Sasaki S, Seghers V, et al. Prevalence of hepatitis C virus and other blood-borne viruses in Pygmies and neighbouring Bantus in southern Cameroon. Trans R Soc Tro Med Hyg 1995;89:484-6. 9. Darwish MA, Faris R, Clemens JD, Rao MR, Edelman R. High seroprevalence of hepatitis A, B, C and E viruses in residents in an Egyptian village in the Nile Delta: a pilot study. Am J Trop Med Hyg 1996;54:554-8. 10. Soriano V, Puoti M, Bonacini M, Brook G, Cargnel A, Rockstroh J, et al. Care of patients with chronic Hepatitis B and HIV co-infection: recommendations from an HIV-HBV International Panel. AIDS 2005;19:221-40. 11. Immunodeficiency virus type 1 (HIV-1) Fluorognost HIV-1 IFA, Product Insert. Vienna, Austria; Sanochemia Pharmazeutika AG; 1996. 12. Sherman KE, Rouster DS, Chung RT, Rajicic N. Hepatitis C virus prevalence among patients infected with human immunodeficiency virus: a cross sectional analysis of the US Adult AIDS Clinical Trials group. HIV/AIDS CID 2002;34:831-7. 13. Kellerman SE, Hanson DL, McHaghten AD, Fleming PL. Prevalence of chronic hepatitis B and incidence of acute hepatitis B infection in human immunodeficiency virus-infected subjects. J Infect Dis 2003;188:571-7. 14. Choy Y, Gittens-Williams L, Apuzzio J, Skurnick J, Zollicoffer C, McGovern PG. Risk factors for hepatitis C infection among sexually transmitted disease-infected, inner city obstetric patients. Infect Dis Obstet Gynecol 2003;11:191-8. 15. Ganem D, Prince AM. Hepatitis B virus infection: natural history and clinical consequences. N Engl J Med 2004;350:1118-29. 16. Chisari FV, Ferrari C. Hepatitis B virus immunopathogenesis. Annu Rev Immunol 1995;13:29-60. 17. Department of Health and Human Services (DHHS). Guidelines for the use of antiretroviral agents in HIV-1-infected adults and adolescents, April 7, 2005. Last accessed: June 5, 2005. Available at: http://aidsinfo.nih.gov/guidelines/adult/AA_040705.pdf