Sunday, September 19, 2021

Hepatitis A During Pregnancy Case File

Posted By: Medical Group - 9/19/2021 Post Author : Medical Group Post Date : Sunday, September 19, 2021 Post Time : 9/19/2021
Hepatitis A During Pregnancy Case File
Eugene C. Toy, MD, Edward Yeomans, MD, Linda Fonseca, MD, Joseph M. Ernest, MD

Case 13
A 22-year-old G2P1 woman is seen in the office at 18 weeks’ gestation after noting a week of anorexia, nausea, vomiting, and dark-colored urine. She also feels her skin and sclera have become jaundiced. She has noted mild pruritus, but no right upper quadrant (RUQ) pain or pharyngitis. She has been your patient for a number of years and has no history of prescription medications, drug or alcohol abuse, blood transfusions, or sexually transmitted infections (STIs). She knows no one with a similar illness and is monogamous with her husband. She works as a scrub tech in your hospital and has received the full hepatitis B immunization series. She cannot remember the last time she was stuck by a needle in the operating room (OR), but was recently exposed to blood of a liver transplant patient when it soaked through the cuff of her surgical gown.

She denies travel other than a week’s trip to the beach 1 month ago where she ate both fried shrimp and raw oysters. Her 2-year-old daughter attends day care and neither her daughter nor her husband has been noted to be sick recently.

➤ What is the most likely diagnosis?
➤ What is your next step?
➤ What are the potential complications of the patient’s disorder?

Hepatitis A During Pregnancy

Summary: This 22-year-old patient became jaundiced with nausea, vomiting, and pruritus after ingesting raw shellfish within the previous month and may have contracted hepatitis A by the fecal-oral route. Alternatively, this patient may have contracted hepatitis A from contact with her asymptomatic daughter who possibly became infected at the day care center (epidemics possible in day cares where a portion of the children require diaper changes; the majority of infected children are either asymptomatic or have subclinical infection).

Most likely diagnosis: Hepatitis A.
Next step: Obtain hepatitis serologies and liver function tests in order to make an exact diagnosis and other laboratory studies in order to determine severity of illness and whether hospitalization is required.
Potential complications: Care for acute viral hepatitis in pregnancy is entirely supportive. Fulminant hepatitic failure in pregnancy is rare, but patients with a prolonged prothrombin time (PT) and other evidence of acute hepatitic failure should be hospitalized. Patients should be educated on preventive measures and behaviors that will prevent transmission of hepatitis infection to others.

  1. Be able to advise patients about hepatitis risk after various exposures.
  2. Understand the evaluation of the pregnant patient with evidence of liver disease.
  3. Be able to counsel a hepatitis-positive patient about means to reduce vertical or postpartum transmission.
  4. Understand recommendations for prophylaxis against various forms of hepatitis.

This 22-year-old, G2P1 presented at 18 weeks’ gestation with signs and symptoms of acute hepatitis including anorexia, nausea, vomiting, dark urine, jaundice, and mild pruritus. She had received the full hepatitis B vaccination series, which generates immunity to hepatitis B in over 90% of recipients. Immunity to hepatitis B infection (HBV) also prevents acquisition of hepatitis D (HDV) infection. She had no history of recent needlesticks or blood transfusions, intravenous drug abuse, sexually transmitted diseases, and is in a monogamous relationship, thus making her at low risk for contracting hepatitis C (HCV). Her only stated possible risk factor for HCV was her recent exposure to blood via exposure to a liver transplant patient’s blood which soaked through her cuff (in the United States, liver failure due to chronic HCV is the most common indication for liver transplantation). However, she would have to have had a break in her skin for this blood-soaked cuff to place her at risk for contracting HCV. This patient denied travel to foreign countries where hepatitis E (HEV) is endemic, thus making HEV highly unlikely. She does have a risk factor for HAV by virtue of her history of having eaten raw oysters (or other raw or undercooked shellfish); the fried shrimp should have posed no risk since they were well-cooked unless they happened to be handled by a restaurant worker actively infected with HAV who had used substandard hygienic measures (inadequate hand-washing after using the bathroom) after the shrimp were prepared. In this circumstance, any food (not just shellfish) may be a vector for infection if handled by an infectious food service worker after it has been prepared. HAV is transmitted via fecal-oral route. Alternatively, a less obvious risk factor for HAV infection may have been the fact that her 2-year-old daughter is in day care; outbreaks of HAV in day care centers have been well documented, though they are decreasing as adoption of the Advisory Committee on Immunization Practices (ACIP) recommendation for routine infant vaccination for HAV is becoming more common. The majority of HAV infections in children are asymptomatic or are subclinical. This patient may have contracted HAV after fecal-oral contamination from her daughter after changing a diaper. In a study of adults who did not have an identifiable source, 52% lived in a household with a child younger than 6 years of age. Since this patient is not taking any prescription medications, a drug-induced hepatitis is excluded. Because this patient is in the mid-second trimester of pregnancy, pregnancy complications such as acute fatty liver of pregnancy and HELLP syndrome which may cause gastrointestinal signs and symptoms are not part of the differential diagnosis.

Since this patient’s history is most consistent with an acute viral hepatitis, serologies should be done to make a specific diagnosis, including hepatitis B surface antigen (HBsAg), IgM antibody to hepatitis B core antigen (IgM anti- HBc), IgM antibody to hepatitis A (IgM anti-HAV), and antibody to hepatitis C (anti-HCV). Anti-HCV should be repeated if serologies fail to establish a diagnosis and no other cause can be found, since anti-HCV may not be present until 6 to 10 weeks after the onset of symptoms. In this patient, only the IgM anti-HAV would return positive, establishing a diagnosis of acute hepatitis A infection.

Other laboratories that should be drawn in this patient include serum aminotransferases (AST and ALT), fractionated bilirubin levels, complete blood cell count and differential, and a prothrombin time. An elevated PT signifies more extensive liver damage and confers a worse prognosis, and the degree of liver damage does not always correlate with the size of elevations in serum aminotransferase levels.

In this patient who presented with signs and symptoms of acute HAV infection, immunoprophylaxis with immunoglobulin (Ig) or hepatitis A vaccine would not be helpful or necessary; she will develop a natural lifelong immunity as her infection resolves. However, close family contacts such as her husband and child are at risk for acute infection and should receive immunoprophylaxis (if they are not already vaccinated or do not already have natural immunity).

Because this patient is experiencing an acute HAV infection at 18 weeks’ gestation, she is likely to resolve her infection within 2 months and should not be infectious at the time of her expected delivery. However, even if a patient acquired acute HAV later in gestation and was still infectious at the time of delivery, cesarean delivery should be reserved for the usual obstetric indications. Mothers with acute infection may breast-feed safely by observing strict hygienic measures that would prevent fecal-oral transmission to her child.

Hepatitis A During Pregnancy
There are five major viral causes of hepatitis: hepatitis A, B, C, D, and E. All produce clinically indistinguishable illness which can vary from asymptomatic to symptomatic but resolving, to fulminate hepatic failure and death. Acute infection with hepatitis B, C, and D sometimes may lead to chronic infection and chronic liver disease with resultant risks of progression to cirrhosis, progressive hepatic failure, and hepatocellular carcinoma. Infection with hepatitis A and E viruses never produces a chronic infectious carrier state. Thus, infection with these viruses does not convey a risk for progression to cirrhosis and hepatocellular cancer. Hepatitis E is the only one of these viral infections whose course seems to be unfavorably altered by pregnancy; the case fatality ratio in the gravid population is approximately 10% to 20% compared to 1% to 2% in a nonpregnant adult population.

Since there are no acceptable specific therapies for any of the acute viral hepatitides in pregnancy and because there are no acceptable treatment regimens for chronic hepatitis during pregnancy, the obstetrician/gynecologist’s most effective means of impacting maternal and fetal/neonatal outcome is through primary prevention of maternal disease acquisition. Prevention can be via education of patients in avoidance of high-risk behaviors that increase the risk for acquisition of viral hepatitis and via appropriate vaccinations. Additionally, prevention by timely administration of immunoprophylaxis when an exposure has occurred or may occur in the future (travel to an endemic area) may prevent occurrence of a viral hepatitis episode.

Hepatitis Risk Factors and Prophylaxis
The risk factors for various hepatitis viruses vary and are not identical. There are no immunoprophylactic treatments available for hepatitis C and E; immunoprophylaxis is available for HAV, HBV, and HDV infection (by virtue of HBV immunoprophylaxis).

Infection with HAV is almost always via the fecal-oral route. Both sporadic and epidemic infections are described; epidemics are facilitated by conditions of overcrowding and poor personal hygiene. Outbreaks may occur at restaurants anytime an infected cook or waitstaff mishandles food and transmits virus onto that food after substandard hand-washing techniques (fecal-oral contamination). Specific food sources that are at higher risk of harboring HAV virus include raw or undercooked shellfish and uncooked produce such as green onions and strawberries. Persons at increased risk for HAV infection include those traveling to or moving from countries with intermediate or high endemicity of HAV infection and users of illicit drugs (whether injectable or not). HAV may also be contracted by ingestion of contaminated well water or other infected water supplies.

Primary prevention of HAV infection is by vaccination and/or administration of Ig. The vaccine is inactivated, carries no risk of causing disease, and is safe for administration during pregnancy. There are two different hepatitis A vaccine preparations available in the United States with a third vaccine being a combination of hepatitis A and hepatitis B vaccine. Travelers to endemic areas are considered protected if they have received the initial HAV vaccine dose four or more weeks prior to travel. If travel to endemic areas is necessary before 4 weeks has elapsed, Ig (0.02 mL/kg) should be given at a different injection site (usually contralateral anatomic site).

HBV is most efficiently transferred as a blood-borne illness. Other important modes of transmission include perinatal (most common source of HBV infection worldwide) and via intimate sexual contact. Thus, any exposure to infected blood products via intravenous drug use (needle-sharing), needlesticks, etc. places an individual at risk for acquisition of acute HBV infection. Exposure to infected blood through mucous membranes or broken skin also may result in infection. Other risk factors for HBV infection include individuals with multiple sexual partners, individuals who use intravenous drugs, and individuals who have sexual partners that engage in high-risk behaviors. Epidemiologic studies suggest that the majority of perinatal infections occur either intrapartum or postpartum, although up to 10% of these infections may be hematogenously spread in utero. These in utero infections may thus only be prevented by primary prevention of maternal infection. There is some limited literature to suggest that maternal administration of lamivudine or maternal administration of HBIG may decrease the risk for in utero (transplacental) hepatitis B infection. However, such treatment is not currently generally recommended in the United States. Perinatal transmission is relatively uncommon in America and western Europe, but is a very frequent mode of

transmission in Asia and many developing nations where the seroprevalence of HBsAg positivity and incidence of the chronic carrier state are high. Prevention of perinatal HBV infection is important since 90% of infected neonates will develop chronic HBV infection and 25% will ultimately die from either cirrhosis or hepatocellular carcinoma. Semen and saliva, while not as efficient as blood, are other possible sources of infection. Individuals who are sexually intimate with infected people are at substantial risk of acquiring hepatitis B if they have not been actively or passively immunized. In developed nations where neonates will be given HBIG and hepatitis B vaccine, breastfeeding by HBsAg-positive mothers is not contraindicated.

Adult prophylaxis for HBV infection consists of three IM injections (deltoid, not gluteal) at 0, 1, and 6 months. Five years after vaccination, 80% to 90% of healthy vaccines have protective anti-HBs levels. Even after anti- HBs levels become undetectable, some protection appears to persist (those individuals should have Ig administered for new situations in which postexposure prophylaxis would be indicated). Because the incidence of new HBV infection in the United States continued to rise after the introduction of the vaccine and targeting of “high-risk” groups, universal childhood HBV vaccination has now been recommended. If an unvaccinated individual has an exposure to HBV, postexposure prophylaxis consists of a combination of HBIG (0.06 mL/kg) and a full HBV vaccination series. When HBIG and HBV vaccine are administered at the same time they should be given at different anatomic sites. Immunoprophylaxis should be given as soon as possible after the exposure and is not recommended if more than 14 days have elapsed since the occurrence of an at-risk sexual encounter. For newborns born to HBsAg-negative mothers, routine vaccination with the three shot hepatitis B vaccine is recommended. The first dose should be given prior to hospital discharge followed by doses at 1 to 2 months and 6 to 18 months, respectively. For newborns born to HBsAg-positive mothers or to mothers whose HBsAg status is unknown, the recommendation is to give HBIG and the first dose of hepatitis vaccine within 12 hours of delivery at different anatomic sites followed by the 1 to 2 month and 6 to 18 month doses.

HCV is primarily contracted by intravenous exposure to infected blood. High-risk groups are similar to those of HBV, intravenous drug users, hemophiliacs, and patients who attend sexually transmitted disease clinics. Persons who are recommended for HCV screening include ever users of injectable illicit drugs, persons who received a blood product transfusion before 1987 or from a known HCV positive donor, persons who received an organ transplant before 1992, hemodialysis patients, and persons requiring care for an STI including HIV. The incidence of transfusion-associated hepatitis C (then called non-A non-B hepatitis) began falling in the late 1980s with the introduction of anti-HBc and ALT screening and has now fallen to trivial levels (1/1,000,000) with the use of the newer anti-HCV assays. As a result, sharing of infected needles has become a much more important source of hepatitis C infection. Although many individuals with hepatitis C infection have no identifiable risk factor, sexual and perinatal transmission are not thought to be important contributors, unless there is coinfection with HIV. Factors associated with increased risk for perinatal transmission include high maternal HCV viral loads, coinfection with HIV (HAART therapy appears to decrease this risk by reducing HCV viral load) intravenous drug use, and placement of a fetal scalp electrode. Duration of rupture of membranes for greater than 6 hours has been less convincingly shown to be a risk factor. Gestational age at delivery, mode of delivery, and the presence of chorioamnionitis have not been shown to be risk factors for vertical transmission. High-risk groups should be considered for HCV screening but universal screening is currently not recommended in either the gravid or nonpregnant population. There are no vaccines or well-established prophylactic treatments for postexposure prophylaxis for adults or newborns at risk for HCV infection.

HDV infection only occurs as coinfection or superinfection with HBV. In the United States, HDV infection most often occurs in intravenous drug users, hemophiliacs, and other individuals frequently exposed to infected blood. Individuals who have moved from endemic areas and are HBsAg positive should also be considered for HDV testing, especially if they have symptoms of hepatitis. Hepatitis D may be effectively prevented by prevention of hepatitis B infection. 

Hepatitis E infection occurs primarily in the developing areas of Asia, India, Central America, and Africa and is acquired via fecal-oral infection. Infection occurs most commonly after fecal contamination of water supplies caused by natural disasters such as floods, monsoons, and typhoons. HEV differs from HAV in that person-to-person transmission of infection is very rare, even to close contacts. HEV is not often encountered in the United States outside of recent immigrants or recent travelers from endemic areas. No vaccines or postexposure prophylactic treatments are available to prevent HEV infection.

Clinical Considerations
Therapies for chronic HBV and HCV infection are not offered to pregnant patients due to concerns for possible teratogenicity of ribavirin. These patients, however, should receive counseling and inform sexual, household, and needle-sharing contacts of their infectious status and refrain from behaviors such as sharing of toothbrushes, razors, and needles which could have blood on them and serve as vectors for infection. Additionally, infected patients should be educated that hepatitis viruses can remain stable and infectious even after long periods in the outside environment such as on countertops, even when blood is not visible on the infected surface. Thus, blood and infected secretions should be meticulously cleaned with a 1:100 dilution of household bleach in tap water. Patients with chronic HBV, HCV, or HDV should be followed by a physician experienced in the evaluation and management of liver disease and should be referred for postpartum evaluation if they do not have such a physician involved in their care. There is inadequate data available to quantify the risk for vertical transmission with various intrapartum management maneuvers such as artificial rupture of membranes, fetal scalp electrode placement, or operative vaginal delivery. However, a 2002 NIH Consensus Statement recommended against the use of fetal scalp electrodes and many academic institutions avoid procedures that may potentially expose the neonate’s bloodstream to infection from maternal blood or body secretions, especially for chronic HCV patients whose neonates do not have any known effective prophylactic treatments available to them.

Amniocentesis in viremic patients may theoretically cause fetal infection by either maternal-fetal blood exchange via damaged fetal vessels in the placenta or by fetal swallowing of infected amniotic fluid after transplacental trauma from the amniocentesis needle. Though available information in the literature demonstrates that the risk for vertical transmission of HBV and HCV with amniocentesis appears to be low, the data are not conclusive. Currently, the available data appear to show a low risk for fetal infection in HBsAg-positive patients but perhaps a higher risk in the HBeAg-positive population. There is insufficient data to evaluate level of risk in patients undergoing chorionic villus sampling where the likelihood of maternal-fetal blood exchange is much higher than with non-transplacental amniocentesis. Given this limited data set and the potentially dire consequences of in utero HBV or HCV infection, it seems prudent to discuss and exhaust noninvasive screening options with these patients and avoid invasive diagnostic procedures unless there is a well-established risk that outweighs the risk of vertical transmission. In the rare cases where an invasive diagnostic procedure is deemed necessary in an HBsAg-positive patient, consider HBIG immunoprophylaxis (especially in the more infectious HBeAg patient), although data that would support or refute this recommendation is currently unavailable.

Unless there are fissures or abrasions on the breast that would increase neonatal exposure to maternal blood, breast-feeding with hepatitis is not contraindicated. Patients with HAV infections should use appropriate hygienic precautions that prevent fecal-oral spread of infection. As long as the neonate receives appropriate HBIG and HBV vaccination, breast-feeding has not been observed to increase the risk for vertical transmission of HBV. Current recommendations support no increase in vertical transmission in asymptomatic chronic HCV. However, there does appear to be an increased risk for vertical transmission of HCV in patients with high HCV viral loads (exact level considered high has not been established). Thus, in patients with typically high viral loads such as new acute HCV infections and symptomatic recurrent infections, breast-feeding should probably be proscribed. Even though there is no immunoprophylaxis for HCV and HEV, breast-feeding has not been shown to increase the risk for childhood HCV and HEV infection. In fact, in reported cases of HEV where infected local water supplies were the likely source of infection, breast-feeding would likely decrease the risk for the infant acquiring disease decreasing exposure to the infected water source.

Laboratory Evaluation
Serum aminotransferases (AST and ALT) typically rise to 400 to 4000 IU or more and precede increases in serum bilirubin levels. Increased serum bilirubin usually consists of both direct and indirect fractions; scleral icterus and jaundice are typically visible with bilirubin levels greater than or equal to 2.5 mg/dL. An initial lymphopenia and neutropenia is followed by an atypical lymphocytosis. A prothrombin time (PT) should always be checked since clotting factor administration may be necessary and severity of liver damage does not always correlate with elevations in serum transaminases. An elevated PT level signifies more extensive liver damage and a worse prognosis. A variety of nondiagnostic and nonspecific elevations in laboratory values also may occur with acute viral hepatitis including elevations in serum IgG and IgM, anti-smooth muscle antibodies, antinuclear antibody, heterophil antibodies, and elevations in rheumatoid factor. The presence of rheumatoid factorpositive arthritis can give rise to a false-positive serologic diagnosis of both acute hepatitis A and B, based on the laboratory findings of a false-positive IgM anti-HAV or IgM anti-HBc.

The serologic diagnosis of acute viral hepatitis can be made with four serologic tests which include HBsAg, IgM anti-HAV, IgM anti-HBc, and anti- HCV. Currently there are no good diagnostic serologies available outside the research setting for acute hepatitis D and E. A diagnostic algorithm can then be applied (Table 13–1). It should be noted that anti-HCV may never become detectable in 20% to 30% of acute hepatitis C infections and may disappear after recovery from acute infections. Because a false-positive anti-HCV ELISA serology can occur, a confirmatory recombinant immunoblot assay (RIBA) should be considered, especially in patients without an identifiable risk factor for hepatitis C. Viremias (acute or chronic) may be tested by measuring HAV RNA, HBV DNA, HCV RNA, and HDV RNA.

Testing of patients suspected of having chronic viral hepatitis should include HBsAg and anti-HCV. Though almost all textbooks recommend testing HBsAg-positive patients for HBeAg and anti-HBe to evaluate the degree of infectivity, this testing serves no practical value for the pregnant patient whose neonate should be given HBIG and HBV vaccination series regardless of these results and who themselves are not eligible for pegylated interferon or ribavirin therapy (FDA category X) for chronic HBV or HCV infection while they are pregnant. Testing for hepatitis D (anti-HDV) can be helpful in the clinical settings of acute fulminant hepatitis, severe chronic cases, acute exacerbations in patients with chronic HBV infection, and in areas of the world where HDV is endemic. Additionally, patient with frequent percutaneous exposures (intravenous drug users) should be tested for hepatitis D.

Hepatitis A During Pregnancy

Data from Fauci AS, Braunwald E, Kaspar DL, Hauser SL. Harrison's Principles of Internal Medicine.
17th ed. New York:McGraw-Hill, 2008.

Comprehension Questions

13.1 A 25-year-old woman G1P0 at 15 weeks’ gestation is noted to have an active hepatitis infection. She asks whether she can breast-feed. Which of the following statements is most accurate?
A. She may breast-feed if it is hepatitis A but she should not breastfeed if it is hepatitis B.
B. She may breast-feed if it is hepatitis C.
C. She may breast-feed in the case of hepatitis A and B, but should not breast-feed with hepatitis C.
D. She should not breast-feed with any of the viruses.
E. There is insufficient information to render an opinion.

13.2. A 36-year-old G2P1 woman at 15 weeks’ gestation is noted to have an increased risk of fetal aneuploidy. She is infected with hepatitis C. Which of the following statements regarding invasive diagnostic techniques such as CVS or amniocentesis in HBV and HCV infected patients on vertical transmission to the fetus is true?
A. There is no evidence of increased vertical transmission in these procedures.
B. This is some evidence of increased vertical transmission with both procedures.
C. The evidence indicates an increased risk of vertical transmission with HBV but not with HCV.
D. The evidence indicates that CVS carries a greater vertical transmission than amniocentesis.

13.3. The most effective method of improving neonatal outcomes with regards to hepatitis infections in pregnancy is which of the following?
A. Treatment of acute viral infection with antiviral agents such as lamivudine.
B. Separation of the baby from a mother with an acute hepatitis infection.
C. Patient education or avoidance of risk behaviors and appropriate vaccinations and postexposure prophylaxis to the neonate.
D. The use of passive immunization for the pregnant patient has been shown to improve neonatal outcome.


13.1 B. There is no contraindication with breast-feeding with any of the hepatitis virus infections.

13.2 B. The literature indicates that there may be an increased risk of vertical transmission with HBV and HCV with invasive prenatal testing.

13.3 C. Patient education, avoidance of risk behaviors, and appropriate vaccination to the neonate is the best strategy to improve neonatal outcome. Antiviral medication is not indicated solely for pregnancy, but may generally be used if indicated. The baby does not need to be separated from the infected mother. Immunization is not helpful once the patient has developed an infection.

Clinical Pearls

See US Preventive Services Task Force Study Quality levels of evidence in Case 1
➤ Clinical course of hepatitis is unaltered by pregnancy except in cases of hepatitis E, where there is a 10- to 20-fold increased risk for fulminant hepatitis leading to death (Level II-2).
➤ Breast-feeding is acceptable with all types of acute viral hepatitis with precautions that normally minimize risk of transmission (Level II-2).
➤ Only supportive care is available for acute viral hepatitis and there are no specific treatments currently available for acute hepatitis in pregnancy (Level III).
➤ Vaccines for hepatitis A and B are safe in pregnancy, hepatitis B vaccine reduces the risk of hepatitis D, and there are currently no vaccines available for hepatitis C and hepatitis E (Level III).
➤ HBV infection acquired perinatally results in an 85% to 95% chance of chronic infection in the neonate with a 25% to 30% lifetime risk of serious or fatal liver disease (Level II-2).
➤ HBIG and hepatitis B vaccinations series reduces the neonatal transmission rate by 85% to 95% (Level I).
➤ High HCV viral titers, preterm premature rupture of the membranes, and internal fetal monitoring are risk factors for neonatal acquisition for HCV infection, although there are no well-established preventive measures for neonatal HCV infection, and routine HCV screen is not recommended (Level III).
➤ Patients at high risk for HCV infections such as HIV-positive patients, intravenous drug users, and patients with multiple sexual partners should be considered for HCV testing (Level III).
➤ For hepatitis C, there is no proven decreased risk of neonatal infection conferred by cesarean delivery as opposed to vaginal delivery (Level II-2).


1. Airoldi J, Berghella V. Hepatitis C in pregnancy. Obstet and Gynecol Surv. 2006;61(10):666-672. 

2. Alexander JM, Ramus R, Jackson G, Sercely B, Wendel GD Jr. Risk of hepatitis B transmission after amniocentesis in chronic hepatitis B carriers. Infect Dis Obstet Gynecol. 1999;7:283-286. 

3. Centers of Disease Control and Prevention. 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 I. Immunization of infants, children, and adolescents. MMWR. 2005;54(No. RR-16):1-34. 

4. Centers for Disease Control and Prevention. 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 II: Immunization of Adults. MMWR. 2006;55(No. RR-16):1-33. 

5. Centers for Disease Control and Prevention. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR. 1998;47(no. RR-19):1-39. 

6. Delamare C, Carbonne B, Heim N, et al. Detection of hepatitis C virus RNA (HCV RNA) in amniotic fluid: a prospective study. J Hepatol. 1993;31:416-420. (Level II-2) 

7. Ferrero S, Lungaro P, Bruzzone BM, Gotta C, Bentivoglio G, Ragni N. Prospective study of mother-to-infant transmission of hepatitis C virus: a 10-year study. Acta Obstet Gynecol Scand. 2003;82:229-234. (Level II-2) 

8. Hussaini SH, Skidmore SJ, Richardson P, Sherratt LM, Cooper BT, O’Grady JG. Severe hepatitis E infection during pregnancy. J Viral Hepat. 1997;4:51-54. (Level III) 

9. Ko TM, Tseng LH, Chang MH, et al. Amniocentesis in mothers who are hepatitis B virus carriers does not expose the infant to an increased risk of hepatitis B virus infection. Arch Gynecol Obstet. 1994;225:25-30. 

10. Kumar R, Shahul F. Role of breast-feeding in transmission of hepatitis C virus to infants of HCV-infected mothers. J Hepatol. 1998;29:191-197. 

11. Li SM, Shi MF, Yang YB, et al. Effects of hepatitis B immunoglobulin on interruption of HBV intrauterine infection. World J Gastroenterol. 2004;10:3215-3217. (Level I) 

12. Prevention of Hepatitis A through active or passive immunization. Recommendations of the Advisory Committee of Immunization Practices (ACIP). MMWR. 2006;55 (No.RR-7):1-23. 

13. Updated US Public Health Service Guidelines for the management of occupation exposures to HBV, HCV, HIV and recommendations for post-exposure prophylaxis. MMWR. 2001;50(RR-11):1-42. 

14. van Zonneveld M, van Nuren AB, Niesters HG, et al. Lamivudine treatment during pregnancy to prevent perinatal transmission of hepatitis B virus infection. J Viral Hepat. 2003;10:294-297. 

15. Viral Hepatitis in Pregnancy. ACOG Practice Bulletin No. 86. American College of Obstetricians and Gynecologists. Obstet Gynecol. 2007;110:941-955.


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