|
|
| Year : 2007 | Volume
: 4
| Issue : 1 | Page : 12-23 |
|
| Hepatitis B virus and pregnancy |
|
|
Silvia Sookoian
Laboratory of Clinical and Molecular Hepatology, Molecular Genetics and Biology of Complex Diseases Department, Institute of Medical Research. A. Lanari, University of Buenos Aires, CONICET, Ciudad Autonoma de Buenos Aires, Argentina
Click here for correspondence address and email
|
|
 |
|
 Abstract | | |
Hepatitis B virus (HBV) infection is very common, with over 350 million chronically infected people worldwide. This review plans to answer some key questions regarding hepatitis B infection during pregnancy, in order to provide healthcare professionals with updated information on the current knowledge in this field. The focus is on the following topics: the main risk factors associated with vertical transmission of HBV in pregnant women who are chronically infected, the influence of pregnancy on HBV viral load, and the effect of pregnancy on the clinical course of chronic hepatitis B. Some recommendations have also been made that may be effective in decreasing the vertical transmission rates of chronic viral hepatitis. Keywords: Acute liver disease, chronic liver disease, hepatitis B, pregnancy, viral hepatitis
How to cite this article:
Sookoian S. Hepatitis B virus and pregnancy. Hep B Annual 2007;4:12-23 |
| Acute Hepatitis B during Pregnancy | |  |
Acute viral hepatitis is the most common cause of jaundice in pregnancy. [1],[2] The course of most viral hepatitis infections (e.g., hepatitis A, B, C, and D) is unaffected by pregnancy; however, a more severe course of viral hepatitis in pregnancy has been observed in patients with hepatitis E. [1] Hepatitis B virus (HBV) has a high rate of vertical transmission, causing fetal and neonatal hepatitis. Additionally, mother-to-child transmission of HBV infection predisposes to carriage, liver cirrhosis, and hepatocellular carcinoma in young adults. Thus, acute hepatitis B in pregnancy presents risks not only for the mother but also for the newborn.
Some special characteristics of HBV need to be considered in order to understand the behavior of acute hepatitis B. HBV is a double-stranded DNA virus of the Hepadnaviridae family. Its incubation period, from time of exposure to onset of symptoms, is 6 weeks to 6 months. HBV is found in highest concentrations in the blood, with lower concentrations in semen, vaginal secretions, and wound exudates. Perinatal transmission of HBV occurs if the mother has had acute HBV infection during late pregnancy or in the first months postpartum or if the mother is a chronic HBsAg carrier. Sixty percent of pregnant women who acquire acute HBV infections at or near delivery will transmit the HBV to their offspring. [3] Furthermore, intrauterine HBV infection has been suggested to be caused by transplacental transmission, which cannot be blocked by hepatitis B vaccine. A case-control study that included 402 newborn infants from 402 HBsAg-positive pregnant women showed that there is a significant association between intrauterine HBV transmission and HBV infection in villous capillary endothelial cells in the placenta (OR = 18.46, P = 0.0002). [4] In fact, the authors state that the main risk factors for intrauterine HBV infection are maternal serum HBeAg positivity, history of threatened preterm labor, and HBV in the placenta (especially the villous capillary endothelial cells).
Acute hepatitis B in pregnancy is not associated with increased abortion rate, stillbirth, or congenital malformation. However, prematurity seems to be increased if hepatitis is acquired in the last trimester. [5] Finally, HBV infection does not appear to be teratogenic. However, there appears to be a higher incidence of low birth weight among infants born to mothers with acute HBV infection during pregnancy. [6],[7]
| Prevention and Vaccination | | |
Several aspects should be considered while making universal recommendations for acute viral hepatitis B in pregnancy. First of all, testing for the HBV is generally a standard, routine test performed in all pregnant women at or before their first antenatal visit, (usually before 12 to 14 weeks of pregnancy). [8] Second, pregnant women who think they may have been exposed to hepatitis B should be given an injection of hepatitis B immunoglobulin (HBIG) against the virus (ideally within 72 h of exposure) as well as hepatitis B vaccine (within 7 days of exposure). A second hepatitis B vaccination needs to be given about 1 month later, with a third injection at around 6 months after the first vaccination (or 5 months after the second vaccination). Besides, pregnant women who are identified as being at risk for HBV infection during pregnancy (e.g., those who have had more than one sex partner during the previous 6 months, been evaluated or treated for a sexually transmitted disease, have a history of recent or current injection-drug use, or have had an HBsAg-positive sex partner) should be vaccinated. [9]
At present, it is thought that administering the hepatitis B vaccine to pregnant women is relatively safe, even though sufficient research evidence is not available to completely confirm its safety for the unborn baby. However, the risks of a woman becoming infected with HBV, and possibly infecting her baby, are thought to outweigh the small risks from the vaccination. [3] Besides, limited data indicate no apparent risk of adverse effects to developing fetuses when hepatitis B vaccine is administered to pregnant women. Additionally, the current vaccines contain noninfectious HBsAg and should cause no risk to the fetus. [10] Pregnant women at risk for HBV infection during pregnancy should be counseled regarding the other methods for prevention of HBV infection. [10]
| Breastfeeding Recommendations | | |
Mothers who carry the HBV are encouraged to breastfeed their babies. [11] It is recommended that the baby breastfeeds after the administration of the HBIG but not necessarily before the first hepatitis B vaccination. The hepatitis B vaccination can be delayed by more than 24 h after the baby's birth but definitely needs to be given before the baby is 7 days old. [12] Caution is however advised, since transmission of HBV through breast milk has been reported in some studies. [13],[14]
| Chronic Hepatitis B during Pregnancy | | |
Women with chronic viral hepatitis generally do quite well during pregnancy, provided that they have not progressed to decompensated cirrhosis. As a general rule, a stable liver is associated with a safe pregnancy. However, there is concern about how preexisting chronic liver disease may affect the pregnancy and the unborn baby.
| Vertical Transmission of Hepatitis B in Pregnant Women with Chronic Hepatitis | | |
Vertical transmission of HBV is the main cause of chronic HBV infection in endemic areas. When the mother is a chronic HBsAg carrier (with serum positive for viral DNA), the risk of the neonate becoming a chronic carrier is close to 80-90%. [15] On the contrary, if the mother's serum is negative for viral DNA, the transmission rate is about 10-30% only. [16] There are three possible routes of transmission of hepatitis virus from infected mothers to infants: transplacental transmission in the uterus (antenatal transmission), transmission during delivery, and postnatal transmission from mothers to infants during child care or through breastfeeding. [17] The baby usually first encounters the hepatitis virus upon entering the birth canal. However, several reports demonstrate that in the case of HBV infection uterine infection too plays an important role. [18] Besides, most researchers believe that the mechanism of intrauterine HBV infection is transplacental infection. In fact, it has been suggested that transplacental leakage of HBeAg-positive maternal blood, which is induced by uterine contractions during pregnancy and the disruption of placental barriers, is the most likely mechanism responsible for intrauterine HBV infection. [19] In addition, it has been shown that the main risk factors for intrauterine HBV infection are maternal serum HBeAg positivity, history of threatened preterm labor, and the presence of HBV in the placenta (especially in the villous capillary endothelial cells). [4] The presence of HBsAg in cord blood may indicate intrauterine infection. Unfortunately, intrauterine transmission of HBV can be a possible cause of vaccination failure and spread of HBV.
An interesting finding is the fact that some of the fetuses that have contact with HBV antigens early in embryonic development may became immunologically tolerant to HBV antigens. [20]
Finally, in chronic HBV infection, high maternal viremia and intrapartum exposure to virus-contaminated maternal blood increases the risk of virus transmission during vaginal deliveries. The main risk factor for vertical transmission of HBV seems to be the mother's viral load. Accordingly, maternal HBV-DNA seems to be a stronger independent predictor of persistent infection than HBeAg status. In effect, vertical transmission was most frequently seen in HBeAg-positive mothers who had very high levels of viremia. [21] Additionally, it was reported that among HBeAg-negative mothers, the odds ratio for having a persistently infected infant was 19.2 (95% confidence interval, 2.3 to 176.6) in mothers with high vs low levels of serum HBV-DNA. [22] Thus, perinatal exposure to high levels of maternal HBV-DNA is the most important determinant of infection outcome in the infant. However, at the same time it has been suggested that the outcome of HBV infection in newborns depends not only on the host's immunocompetence and on the viremia level in maternal blood, but also on the heterogeneity of HBV. Transmission of mixed HBV populations appears to be associated with an early immunoelimination of the virus, while infection with wild-type HBV alone contributes to the induction of chronicity. [23] Specific allelic mutations in maternal HBV and the level of maternal viremia are potential predictors of vertical breakthrough infection. [24]
However, there is a paucity of information on how pregnancy influences viremia levels in women with chronic HBV infection. In a retrospective study that analyzed the changes in HBV-DNA levels during and after 55 pregnancies in HBsAg-positive women, it was shown that although the majority of HBeAg-negative women had low and relatively stable HBV-DNA during pregnancy, viremia was also relatively high in some HBeAg-negative mothers, and both viremia and ALT increased significantly late in pregnancy or shortly after delivery. [21] The authors also found that HBV-DNA increased by a mean of 0.4 log late in pregnancy or in the early postpartum period and that HBV-DNA ranged from 1010 copies/ml in HBeAg-positive, to undetectable (< 100 copies/ml) in HBeAg-negative mothers. With regard to chronic HBV infection during pregnancy, it was shown that both viral load and ALT increase significantly late in pregnancy or shortly after delivery. [21] However, it is important to note that ALT levels have low sensitivity as a surrogate marker for high HBV-DNA levels; it has been reported that there is no correlation between ALT and HBV-DNA levels. [25]
Although cesarean delivery has been proposed as a means of reducing mother-to-child transmission of HBV, [26] the mode of delivery does not appear to have a significant effect on the interruption of this form of HBV transmission. [27] In fact, delivery by cesarean for the purpose of reducing vertical transmission of HBV is presently not recommended by the CDC (Center for Disease Control), [28] the American Academy of Pediatrics, or the American College of Obstetricians and Gynecologists. [28],[29]
| Recommendations to Decrease Vertical Transmission Rates of Chronic Viral Hepatitis | | |
1. HBsAg screening
Testing for the HBV (HBsAg) is generally a standard, routine test performed on all pregnant women at or before her first antenatal visit (usually before about 12 to 14 weeks of the pregnancy). [10],[17]
2. Management of infants born to women who are HBsAg positive
An unvaccinated baby whose mother is a hepatitis B carrier has an up to 40% chance of becoming infected with the virus during the first 18 months of life; 90% of such babies can become long-term carriers and be infectious to others, besides being at risk of developing chronic liver disease and liver cancer in later life. Therefore, all infants born to HBsAg-positive women should receive both hepatitis B vaccine and hepatitis B immunoglobulin (HBIG) (0.5 ml) within 12 h of birth; the two should be administered at different injection sites. [12],[30] Administered in standard doses, HBIG provides passively acquired anti-HBs and temporary protection (i.e., for 3-6 months). The vaccine series should be completed according to the recommended schedule for infants born to HBsAg-positive mothers. The final dose in the vaccine series should not be administered before the age of 24 weeks (164 days). [15] For preterm infants weighing < 2000 gm, the initial vaccine dose (birth dose) should not be counted as part of the vaccine series because of the potentially reduced immunogenicity of hepatitis B vaccine in these infants; three additional doses of vaccine (i.e., a total of four doses) should be administered, beginning when the infant reaches the age of 1 month. [10]
The hepatitis B vaccination can be delayed by more than 24 h after the baby's birth but it should definitely be administered before the baby is 7 days old. Although not indicated in the manufacturer's package labeling, HBsAg containing combination vaccines may be used for infants aged ≥6 weeks, born to HBsAg positive mothers, to complete the vaccine series after receipt of a birth dose of single-antigen hepatitis B vaccine and HBIG. [8] A recent meta-analysis that evaluated the effects of hepatitis B vaccine and immunoglobulin in newborn infants of mothers positive for HBsAg showed that there was no significant difference between recombinant vaccine and plasma-derived vaccine on hepatitis B infections (relative risk 1.00; 95% CI 0.70 to 1.42). [15] However, more infants who received recombinant vaccine achieved antibody levels to hepatitis surface antigen > 10 IU/l.
Unfortunately, failure of postnatal immunoprophylaxis for hepatitis B has been reported and specific allelic mutations in maternal HBV and level of maternal viremia were potential predictors of vertical breakthrough infection. [24] Actually, it seems that S variants emerge or are selected under the immune pressure generated by the host or by administration of HBIG and hepatitis B vaccination. [31]
Mothers who carry the HBV are encouraged to breastfeed their babies. However, it is recommended that the baby breastfeeds after the administration of HBIG but not necessarily before the first hepatitis B vaccination (HBV). [11],[30]
As HBV transmission through breast milk has been reported in some studies, [13],[14] several groups do not recommend breastfeeding on the basis of the published data. [32],[33] Finally, keeping in mind that HBV is commonly transmitted by blood-to-blood routes, it is recommended that mothers should be told that when breastfeeding they should take good care of their nipples, ensuring proper latch-on and allowing the nipples to dry before covering to avoid cracking or bleeding.
| Use of Antiviral Therapy in the Mother to Prevent Vertical Transmission of HBV | | |
The fact that vertical transmission of HBV may occasionally occur despite vaccination of the child has prompted physicians to treat viremic patients with nucleoside analogues to prevent mother-to-child transmission. In this regard, some authors have observed that in highly viremic HBsAg-positive mothers, reduction of viremia by lamivudine therapy in the last month of pregnancy could be an effective and safe measure to reduce the risk of child vaccination breakthrough. [34],[35] Moreover, no side effects were observed ,either in the mother or in the babies, an observation that had already been made earlier while studying the safety, pharmacokinetics, and antiretroviral activity of lamivudine alone and in combination with zidovudine in pregnant women infected with human HIV-1. [36] Nonetheless, in spite of the reported encouraging results in controlling vertical transmission with optimum maternal therapy and neonatal vaccination, some authors have reported that lamivudine therapy might not prevent perinatal transmission. [37] Finally, it is necessary to keep in mind that lamivudine or any other nucleoside should be used with caution during the first trimester of pregnancy in view of the possible lethal effects during embryogenesis. [38]
As a general rule, there is no reason for the occurrence of adverse pregnancy outcomes in compensated chronic HBV carriers. However, there have been a few case reports and studies indicating an increased incidence of maternal and neonatal morbidity in HBV infection, for instance, premature delivery before 34 weeks and raised incidence of antepartum hemorrhage, [39] fetal distress, and meconium peritonitis. [5],[13],[34] Additionally, it has been suggested that there exists an association between the HBsAg carrier state in mothers and chromosomal abnormalities in their newborns, [40] an observation that has not been replicated. One interesting finding is the association between gestational diabetes mellitus and HBsAg carrier status observed by Lao et al. [41] and Tse et al. [39] both studies were in Chinese women. The authors hypothesize that this phenomenon may be explained by the increased level of proinflammatory cytokines induced by chronic HBV infection, in particular by the effect of the tumor necrosis factor-α.
| References | | |
| 1. | Mishra L, Seeff LB. Viral hepatitis, A through E, complicating pregnancy. Gastroenterol Clin North Am 1992;21:873-87.  [PUBMED] |
| 2. | Riely CA. Hepatic disease in pregnancy. Am J Med 1994;96:18S-22S. [PUBMED] |
| 3. | Levy M, Koren G. Hepatitis B vaccine in pregnancy: Maternal and fetal safety. Am J Perinatol 1991;8:227232. |
| 4. | Xu DZ, Yan YP, Choi BC, Xu JQ, Men K, Zhang JX, et al. Risk factors and mechanism of transplacental transmission of hepatitis B virus: A case-control study. J Med Virol 2002;67:20-6. [PUBMED] [FULLTEXT] |
| 5. | Hieber JP, Dalton D, Shorey J, Combes B. Hepatitis and pregnancy. J Pediatr 1977;91:545-9. [PUBMED] |
| 6. | Pavel A, Tirsia E, Maior E, Cristea A. Detrimental effects of hepatitis B virus infection on the development of the product of conception. Virologie 1983;34:35-40. |
| 7. | Smithwick EM, Pascual E, Go SC. Hepatitis-associated antigen: A possible relationship to premature delivery. J Pediatr 1972;81:537-40. [PUBMED] |
| 8. | Samuels P, Cohen AW. Pregnancies complicated by liver disease and liver dysfunction. Obstet Gynecol Clin North Am 1992;19:745-63. [PUBMED] |
| 9. | Mast EE, Hwang LY, Seto DS, Nolte FS, Nainan OV, Wurtzel H, et al. Risk factors for perinatal transmission of hepatitis C virus (HCV) and the natural history of HCV infection acquired in infancy. J Infect Dis 2005;192:1880-9. [PUBMED] [FULLTEXT] |
| 10. | Mast EE, Margolis HS, Fiore AE, Brink EW, Goldstein ST, Wang SA, et al. A comprehensive immunization strategy to eliminate transmission of hepatitis B virus infection in the United States: Recommendations of the Advisory Committee on Immunization Practices (ACIP) part 1: Immunization of infants, children and adolescents. MMWR Recomm Rep 2005;54:1-31. |
| 11. | Hill JB, Sheffield JS, Kim MJ, Alexander JM, Sercely B, Wendel GD. Risk of hepatitis B transmission in breast-fed infants of chronic hepatitis B carriers. Obstet Gynecol 2002;99:1049-52. [PUBMED] [FULLTEXT] |
| 12. | Atkinson WL, Pickering LK, Schwartz B, Weniger BG, Iskander JK, Watson JC. General recommendations on immunization: Recommendations of the Advisory Committee on Immunization Practices (ACIP) and the American Academy of Family Physicians (AAFP). MMWR Recomm Rep 2002;51:1-35. |
| 13. | Boxall EH, Flewett TH, Dane DS, Cameron CH, MacCallum FO, Lee TW. Letter: Hepatitis-B surface antigen in breast milk. Lancet 1974;2:1007-8. |
| 14. | Linnemann CC Jr, Goldberg S. Letter: HBAg in breast milk. Lancet 1974;2:155. |
| 15. | Lee C, Gong Y, Brok J, Boxall EH, Gluud C. Effect of hepatitis B immunisation in newborn infants of mothers positive for hepatitis B surface antigen: Systematic review and meta-analysis. BMJ 2006;332:328-36. [PUBMED] [FULLTEXT] |
| 16. | Schaefer E, Koeppen H, Wirth S. Low level virus replication in infants with vertically transmitted fulminant hepatitis and their anti-HBe positive mothers. Eur J Pediatr 1993;152:581-4. [PUBMED] |
| 17. | Ghendon Y. Perinatal transmission of hepatitis B virus in high-incidence countries. J Virol Methods 1987;17:69-79. [PUBMED] [FULLTEXT] |
| 18. | Vranckx R, Alisjahbana A, Meheus A. Hepatitis B virus vaccination and antenatal transmission of HBV markers to neonates. J Viral Hepat 1999;6:135-9. |
| 19. | Lin HH, Lee TY, Chen DS, Sung JL, Ohto H, Etoh T, et al. Transplacental leakage of HBeAg-positive maternal blood as the most likely route in causing intrauterine infection with hepatitis B virus. J Pediatr 1987;111:877-81. [PUBMED] |
| 20. | Tang JR, Hsu HY, Lin HH, Ni YH, Chang MH. Hepatitis B surface antigenemia at birth: A long-term follow-up study. J Pediatr 1998;133:374-7. [PUBMED] [FULLTEXT] |
| 21. | Soderstrom A, Norkrans G, Lindh M. Hepatitis B virus DNA during pregnancy and post partum: Aspects on vertical transmission. Scand J Infect Dis 2003;35:814-9. |
| 22. | Burk RD, Hwang LY, Ho GY, Shafritz DA, Beasley RP. Outcome of perinatal hepatitis B virus exposure is dependent on maternal virus load. J Infect Dis 1994;170:1418-23. [PUBMED] |
| 23. | Raimondo G, Tanzi E, Brancatelli S, Campo S, Sardo MA, Rodino G, et al. Is the course of perinatal hepatitis B virus infection influenced by genetic heterogeneity of the virus? J Med Virol 1993;40:87-90. |
| 24. | Ngui SL, Andrews NJ, Underhill GS, Heptonstall J, Teo CG. Failed postnatal immunoprophylaxis for hepatitis B: Characteristics of maternal hepatitis B virus as risk factors. Clin Infect Dis 1998;27:100-6. [PUBMED] |
| 25. | Sangfelt P, Von SM, Uhnoo I, Weiland O, Lindh G, Fischler B, et al. Serum ALT levels as a surrogate marker for serum HBV DNA levels in HBeAg-negative pregnant women. Scand J Infect Dis 2004;36:182-5. |
| 26. | Lee SD, Lo KJ, Tsai YT, Wu JC, Wu TC, Yang ZL, et al. Role of caesarean section in prevention of mother-infant transmission of hepatitis B virus. Lancet 1988;2:833-4. |
| 27. | Wang J, Zhu Q, Zhang X. Effect of delivery mode on maternal-infant transmission of hepatitis B virus by immunoprophylaxis. Chin Med J (Engl) 2002;115:1510-2. [PUBMED] [FULLTEXT] |
| 28. | Sexually transmitted diseases treatment guidelines 2002. Centers for Disease Control and Prevention. MMWR Recomm Rep 2002;51:1-78. |
| 29. | Davies G, Wilson RD, Desilets V, Reid GJ, Shaw D, Summers A, et al. Amniocentesis and women with hepatitis B, hepatitis C or human immunodeficiency virus. J Obstet Gynaecol Can 2003;25:145-52. |
| 30. | Wang JS, Zhu QR, Wang XH. Breastfeeding does not pose any additional risk of immunoprophylaxis failure on infants of HBV carrier mothers. Int J Clin Pract 2003;57:100-2. [PUBMED] [FULLTEXT] |
| 31. | Hsu HY, Chang MH, Ni YH, Lin HH, Wang SM, Chen DS. Surface gene mutants of hepatitis B virus in infants who develop acute or chronic infections despite immunoprophylaxis. Hepatology 1997;26:786-91. [PUBMED] [FULLTEXT] |
| 32. | Chen DS, Hsu NH, Sung JL, Hsu TC, Hsu ST, Kuo YT, et al. A mass vaccination program in Taiwan against hepatitis B virus infection in infants of hepatitis B surface antigen-carrier mothers. JAMA 1987;257:2597-603. [PUBMED] |
| 33. | Woo D, Cummins M, Davies PA, Harvey DR, Hurley R, Waterson AP. Vertical transmission of hepatitis B surface antigen in carrier mothers in two west London hospitals. Arch Dis Child 1979;54:670-5. [PUBMED] [FULLTEXT] |
| 34. | Su GG, Pan KH, Zhao NF, Fang SH, Yang DH, Zhou Y. Efficacy and safety of lamivudine treatment for chronic hepatitis B in pregnancy. World J Gastroenterol 2004;10:910-2. [PUBMED] [FULLTEXT] |
| 35. | van Zonneveld M, van Nunen AB, Niesters HG, de Man RA, Schalm SW, Janssen HL. Lamivudine treatment during pregnancy to prevent perinatal transmission of hepatitis B virus infection. J Viral Hepat 2003;10:294-7. [PUBMED] [FULLTEXT] |
| 36. | Moodley J, Moodley D, Pillay K, Coovadia H, Saba J, van Leeuwen R, et al. Pharmacokinetics and antiretroviral activity of lamivudine alone or when coadministered with zidovudine in human immunodeficiency virus type 1-infected pregnant women and their offspring. J Infect Dis 1998;178:1327-33. [PUBMED] [FULLTEXT] |
| 37. | Kazim SN, Wakil SM, Khan LA, Hasnain SE, Sarin SK. Vertical transmission of hepatitis B virus despite maternal lamivudine therapy. Lancet 2002;359:1488-9. [PUBMED] [FULLTEXT] |
| 38. | Divi RL, Leonard SL, Kuo MM, Walker BL, Orozco CC, St Claire MC, et al. Cardiac mitochondrial compromise in 1-yr-old Erythrocebus patas monkeys perinatally-exposed to nucleoside reverse transcriptase inhibitors. Cardiovasc Toxicol 2005;5:333-46. [PUBMED] |
| 39. | Tse KY, Ho LF, Lao T. The impact of maternal HBsAg carrier status on pregnancy outcomes: A case-control study. J Hepatol 2005;43:771-5. [PUBMED] [FULLTEXT] |
| 40. | Jhaveri RC, Verma RS, Rosenfeld W, Salazar DJ, Dosik H, Evans HE. Chromosomal abnormality in the newborns of hepatitis B surface antigen (HBsAg) carrier mothers. Clin Pediatr (Phila) 1980;19:66-8. [PUBMED] |
| 41. | Lao TT, Tse KY, Chan LY, Tam KF, Ho LF. HBsAg carrier status and the association between gestational diabetes with increased serum ferritin concentration in Chinese women. Diabetes Care 2003;26:3011-6. [PUBMED] [FULLTEXT] |
Correspondence Address:
Silvia Sookoian
Laboratory of Clinical and Molecular Hepatology, Molecular Genetics and Biology of Complex Diseases, Department. Institute of Medical Research, A. Lanari, University of Buenos Aires-CONICET, Combatiente de Malvinas 3150, 1427 - Ciudad Autónoma de Buenos Airesm
Argentina
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0972-9747.45086
|
|
| This article has been cited by | | 1 |
Frequency of Acute Viral Hepatitis A, B, C, and E in Pregnant Women Presenting to Hayatabad Medical Complex, Peshawar, Pakistan |
|
| Ahmad R. Khan, Salma Waqar, Zainab Rafiq, Rizwan Ullah, Muhammad Hayyan Wazir , Ayesha M Gul | | Cureus. 2022; | | [Pubmed] | [DOI] | | | 2 |
Sero-prevalence and risk factors of hepatitis B virus and human immunodeficiency virus infection among pregnant women in Bahir Dar city, Northwest Ethiopia: a cross sectional study |
|
| Yohannes Zenebe,Wondemagegn Mulu,Mulat Yimer,Bayeh Abera | | BMC Infectious Diseases. 2014; 14(1): 118 | | [Pubmed] | [DOI] | | | 3 |
Knowledge of hepatitis B virus infection, access to screening and vaccination among pregnant women in Ibadan, Nigeria |
|
| A. B. Adeyemi,O. O. Enabor,I. A. Ugwu,F. A. Bello,O. O. Olayemi | | Journal of Obstetrics & Gynaecology. 2013; 33(2): 155 | | [Pubmed] | [DOI] | |
|
|
|
|
|
|
|
|
|
|
|
|
| Article Access Statistics | | | Viewed | 9799 | | | Printed | 689 | | | Emailed | 7 | | | PDF Downloaded | 1367 | | | Comments | [Add] | | | Cited by others | 3 | | |
|
|
