Hepatitis E virus (HEV) infection is known to cause severe liver disease in pregnant women. It is unclear whether obstetric and fetal outcomes are worse in pregnant women with HEV infection than in women with other forms of viral hepatitis.
To compare maternal, obstetric, and fetal outcomes in pregnant women with acute viral hepatitis caused by HEV and other hepatitis viruses.
Tertiary care hospital, New Delhi, India.
220 consecutive pregnant women presenting with jaundice caused by acute viral hepatitis.
Maternal mortality and medical complications, obstetric complications, deliveries, and fetal outcomes.
Infection with HEV caused acute viral hepatitis in 60% of included women. Fulminant hepatic failure was more common (relative risk, 2.7 [95% CI, 1.7 to 4.2]; P = 0.001) and maternal mortality was greater (relative risk, 6.0 [CI, 2.7 to 13.3]; P < 0.001) in HEV-infected women than in non-HEV-infected women. Women with HEV infection were more likely than those with other forms of viral hepatitis to have obstetric complications (relative risk, 4.1 [CI, 1.7 to 10.2] for antepartum hemorrhage and 1.9 [CI, 1.3 to 2.7] for intrauterine fetal death; P < 0.001 for both) and poor fetal outcomes (relative risk, 1.2 [CI, 1.0 to 1.4] for preterm delivery [P = 0.005] and 1.8 [CI, 1.2 to 2.5] for stillbirth [P = 0.026]).
The findings may not apply to community settings, to women who are asymptomatic or have only minor symptoms, or in the setting of an HEV epidemic.
Pregnant women with jaundice and acute viral hepatitis caused by HEV infection had a higher maternal mortality rate and worse obstetric and fetal outcomes than did pregnant women with jaundice and acute viral hepatitis caused by other types of viral hepatitis.
"Among pregnant women with acute HEV infection, Beniwal et al. found that 54.3% presented with acute viral hepatitis whereas 21/46 (45.7%) presented with fulminant hepatic failure. In another study, 55% females developed fulminant hepatic failure while 45% developed acute viral hepatitis. "
[Show abstract][Hide abstract] ABSTRACT: Background: Pregnant women are at increased risk of complications in hepatitis E virus (HEV) infection, with the risk increasing as the pregnancy progresses, often leading to fulminant hepatic failure and adverse fetal outcome. Aims: The primary objective of the following study is to evaluate the maternal and fetal complications of this infection and secondary aim is to compare the clinical features of hepatitis E in pregnant women to those in non-pregnant women. Subjects and Methods: This was a hospital based case-controls study, carried out from July 2008 to June 2010. Over a period of 2 years, cases were serologically confirmed pregnant women with hepatitis E, selected by screening in antenatal clinic. Controls were serologically confirmed non-pregnant women with hepatitis E, selected by screening in Medicine Outpatient Department. We studied 96 women with HEV infection, of which 52 were pregnant and 44 were non-pregnant. Clinical and laboratory profile of patients in both groups were studied. Patients were treated as per protocol and the outcome was studied in both groups. Pregnant women were followed-up for fetal and maternal outcome. We used t-test and z-test to compare normally distributed data and non-normally distributed data, respectively. Chi-square test was used to compare discrete values between groups. Results: Mean (standard deviation [SD]) age in pregnant patients was 24.1 (3.3) years while 32.6 (10.5) years in non-pregnant patients. 71.1% (37/52) of the patients were primigravida and 28.8% (15/52) patients were multigravida, by natural occurrence. Mean (SD) gestational age when infection occurred was 27.5 (7.2) weeks. Among pregnant women, 63.4% (33/52) were in 3 rd trimester. Jaundice 1-5 days before presentation was seen in 51.9% (27/52) pregnant and 44.2% (23/44) non-pregnant women. Myalgia/arthralgia, fever, nausea/vomiting, right upper quadrant pain, jaundice, dark urine, light-colored stools, pruritus, diarrhea, altered sensorium and hematemesis/melena were presenting features. In pregnant group, 46.1% (24/52) patients developed encephalopathy while in non-pregnant group 34% (15/44) developed this complication. Among pregnant cases, 67.3% (35/52) survived and 32% (17/52) cases died. In non-pregnant group, nearly 90% (40/44) patients survived and only 9% (4/44) patients died. This difference was statistically significant (P < 0.01). Adverse fetal outcome was seen in 71.1% (37/52) pregnant women with acute hepatitis E, including pre-term delivery in 23% (12/52), stillbirth in 23% (12/52), abortion in 3.8% (2/52) and intra-uterine fetal death in 21.1% (11/52) patients. Conclusions: There is significantly higher occurrence of hepatitis E infection in pregnant women than in non-pregnant women, which increases with gestation, with associated fulminant hepatic failure, maternal mortality and worse fetal outcome.
"HEV infection is commonly transmitted from mother to child via the intrauterine and perinatal routes, and in fetuses and neonates it causes severe liver disease with high rates of mortality.55,74,98–100 The clinical course in vertically transmitted HEV infection in survivor neonates is self-limiting with short lasting viremia.74 "
[Show abstract][Hide abstract] ABSTRACT: Hepatitis E virus (HEV) infection is an important public health concern in many developing countries, causing waterborne outbreaks as well as sporadic autochthonous hepatitis. HEV is mainly transmitted by the fecal-oral route in endemic areas through drinking of contaminated water. However, zoonotic transmission from animal reservoirs to humans has also been suggested. Three additional routes of HEV transmission have been proposed to occur: blood borne, human to human, and vertical transmission from mother to child. Acute HEV infection is usually diagnosed by detecting specific anti-HEV antibodies. However, the performance of the available assays in different settings is not optimal. Analysis of HEV ribonucleic acid in biologic specimens such as stools, serum, and liver biopsy by using nucleic acid amplification techniques is also employed. Nonetheless, additional consensus regarding the best technologies suitable for serosurveys and diagnosis of acute HEV infection is also needed. This review article summarizes the current status of HEV infection end epidemiology with particular emphasis in transmission, diagnosis, and clinical management.
Hepatic Medicine: Evidence and Research 06/2014; 6:45-59. DOI:10.2147/HMER.S63417
"One remarkable example of the threat to public health posed by such viruses is the severe acute respiratory syndrome-coronavirus (SARS-CoV) 2003 outbreak in Asia (Tsang et al., 2003). Zoonotic strains of HEV have the potential to cause serious disease and mortality (Aggarwal, 2011; Mizuo et al., 2005; Patra et al., 2007) in infected patients or change into phenotypes that may become more transmissible among humans (Krawczynski et al., 2000; Purdy et al., 2012a). The need to assess the risk of HEV outbreaks calls for genetic surveillance of the emerging zoonotic strains in their reservoir hosts. "
[Show abstract][Hide abstract] ABSTRACT: Hepatitis E virus (HEV) causes epidemic and sporadic cases of hepatitis worldwide. HEV genotypes 3 (HEV3) and 4 (HEV4) infect humans and animals, with swine being the primary reservoir. The relevance of HEV genetic diversity to host adaptation is poorly understood. We employed a Bayesian network (BN) analysis of HEV3 and HEV4 to detect epistatic connectivity among protein sites and its association with the host specificity in each genotype. The data imply coevolution among ∼70% of polymorphic sites from all HEV proteins and association of numerous coevolving sites with adaptation to swine or humans. BN models for individual proteins and domains of the nonstructural polyprotein detected the host origin of HEV strains with accuracy of 74%-93% and 63%-87%, respectively. These findings, taken together with lack of phylogenetic association to host, suggest that the HEV host specificity is a heritable and convergent phenotypic trait achievable through variety of genetic pathways (abundance), and explain a broad host range for HEV3 and HEV4.
Infection, genetics and evolution: journal of molecular epidemiology and evolutionary genetics in infectious diseases 06/2014; 24. DOI:10.1016/j.meegid.2014.03.011 · 3.02 Impact Factor
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