By Ozele, KC; Ozele, N (2022).

Greener Journal of Medical Sciences

Vol. 12(1), pp. 25-40, 2022

ISSN: 2276-7797

Copyright 2022, the copyright of this article is retained by the author(s)

https://gjournals.org/GJMS

 

 

 

 

 

Mother -To -Child Transmission of Hepatitis B in Jos Metropolis

 

 

Ozele, Kingsley Chukwuka (MBBS, FMCOG); Ozele Nonyelim (BSC, FMLSCN)

 

 

Consultant Special Grade 1 (Obstetrics and Gynaecology) and Head Medicine and Health Services Department, National Institute for Policy and Strategic Studies Kuru Jos Plateau State, (NVRI) Vom.1

Chief Medical Laboratory Scientist Biochemistry Division National Vertinary Research Institute (NVRI) Vom.2

 

 

ARTICLE INFO

ABSTRACT

 

Article No.: 020122011

Type: Research

Full Text: PDF, HTML, EPUB, PHP

 

Background: Hepatitis B virus infection is a major public health issue worldwide and more seriously in Africa and Asia3. In Jos, like in the most parts of Nigeria, information on mother to child transmission of HBV is scarce. This study was undertaken to determine the mother- to- child transmission of hepatitis B markers at delivery.

Objectives: To determine the prevalence of HB s Ag in maternal blood and that of cord blood at delivery at JUTH .To determine the proportion of HB s Ag positive to HB e Ag positive on maternal and also proportion of the same markers in the cord blood.

Method: Descriptive cross sectional study

Result: The results of the study showed that the prevalence of HB S Ag among women at delivery in Jos metropolis is 12.77%. It also revealed that the prevalence of HB S Ag on cord blood is 2.2%, which is an issue of concern. Also, the proportion of HB S Ag to HB E Ag in women at delivery is 23:3. That is, 13.04% of those that are HB S Ag positive were infectious. Association was statistically significant. There was no HB E Ag positivity in all the 4 cord blood that was HB S Ag positive.

Conclusion: Jos is an area of high endemicity for hepatitis B virus infection. In line with WHO recommendation of routine antenatal screening for HB'sAg. for pregnant women at booking,2, routine screening for HB S Ag on all pregnant women should be introduced at the booking clinic.

 

Accepted: 05/02/2022

Published: 17/02/2022

 

*Corresponding Author

Dr Ozele KC MBBS FMCOG

E-mail: kingsleyozele9@ gmail.com

 

Keywords: Mother - To Child; transmission; Hepatitis-B; Jos.

 

 

 

 

 

 


INTRODUCTION

 

Hepatitis B virus (HBV) is a double stranded DNA virus belonging to Hepadnaviridae family. Whose incubation period is between 6 weeks and 6 months 1 .HBV infection affects over 350 million people worldwide and about 2 million die annually of HBV- related chronic hepatic disease2,3. Liver cirrhosis and hepatocellular carcinoma lead to death in these patients2.

The prevalence of HBV infection according to the geographical area, may be high (≥8%), intermediate (2-7%), or low (≤2%)3. Nigeria is classified among the countries that are highly endemic for viral hepatitis4. The prevalence of HB s Ag in normal population in Nigeria ranges from 2.7% to 13.3%5, 6

Generally, pregnant women have depressed immunity, thus infection of HBV is of clinical importance. Acute Viral hepatitis is one of the medical disorders in pregnancy known to be associated with to high morbidities and sometimes mortalities because it could lead to fulminant hepatitis which, though rare (1-2%), is associated with a dramatically high mortality (63-93%) 7.

Hepatitis B e antigen (HBeAg) is a soluble non-particulate antigen that is found only when HBsAg is present1. Pregnant women who are HB e Ag positive in the third trimester frequently transmit this infection to the offspring in up to 90% of cases in the absence of immunoprophylaxis, whereas those who are negative rarely infect their offspring1, 8. Amongst those infected, 90% will develop chronic infection and 25% will die due to complication of liver disease 7, 10.

HBV is transmitted primarily through parenteral and sexual exposure to HB s Ag positive blood or other body fluid from those who are chronic HBV carriers or who have acute hepatitis B 3.

HBV is also transmitted prenatally, with the possibility of vertical transmission8. Since a large number of these transmitted cases progress to chronicity, infected infants can initiate new cycle of both horizontal and vertical infection. Infection acquired during the perinatal period has the highest risk of chronicity 7, 8 47, 48. Prevention of perinatal transmission is thus important to prevent chronic carrier state. Recent studies have shown a higher incidence of low birth weight among infants born to mothers with acute infection during pregnancy9. However, knowledge about mother to child transmission of hepatitis B in Jos, which is the researchers area of study is scarce, hence the need for the study.

 

Statement of the Problem

 

Nigeria is classified among the countries that are highly endemic for viral hepatitis4. The prevalence of the viral infection amongst pregnant population is as high as 8.3%63 in Zaria and value as high as 13.3%5 has also been reported. Perinatal transmission is an important route for neonatal infection, because infection acquired during the perinatal period has the highest risk of chronicity, thereby perpetuating the vicious cycle47, 48. Prevention of perinatal transmission is thus important to prevent chronic carrier state. This would only be possible if the prevalence of mother to child transmission of hepatitis B virus is identified. There is scarcity of knowledge in this area of study, so that the problem on ground in relation to the study is identifying and examining the rate and extent of mother-to-child transmission of hepatitis B in Jos metropolis.

 

Study Hypothesis

 

This study hypothesizes that the prevalence of hepatitis B virus infection in pregnancy is comparable to that in the general population and mother to child transmission do occur at birth.

 

Justification of the Study

 

The prevalence of HB s Ag in normal population is high and it is said to be between 2.7% to 13.3% 5, 6.

Hepatitis B infection in pregnancy is an important health issue because infected mothers can transmit same to their offspring with such consequences as low birth weight babies, chronic hepatitis, liver cirrhosis and possible hepatocellular carcinoma7.

Ninety percent of perinatal infection can be prevented if HB s Ag positive mothers are identified and their newborn treated promptly with hepatitis B immunoglobulin and HBV vaccine 10. Transmission of HBV will add to a large number of carriers in the community and becomes a public health problem. This study which is aimed at ascertaining the rate of mother -to- child transmission of hepatitis B markers at delivery, will help to inform policy formulation and programming in health planning for women and children in Jos metropolis in particular, and Nigeria (including the outside world) in general. It is for this reason that this dissertation mother- to- child transmission of Hepatitis B in Jos metropolis was conducted.

 

 

Aim

 

General: The aim of the study is to determine if the transmission of hepatitis B virus from mother to child in Jos metropolis occurs. It is further to identify the extent to which this occurrence or otherwise is evident, and to proffer solutions as applicable.

 

 

 

Specific Objectives Are:

 

1.      The study is designed to determine the prevalence of HB s Ag among women at delivery at Jos

2.      It is to determine the prevalence of HB s Ag on cord blood after delivery at Jos

3.      In addition to the above, it is also to determine the proportion of HB s Ag positive women that are HB e Ag positive

4.      It is also to determine the proportion of HB s Ag positive cord blood that are HB e Ag positive

5.      Finally, based on the above, to see if it is rational to recommend the inclusion of routine hepatitis B screening test for pregnant women

 

LITERATURE REVIEW

 

Hepatitis B Virus

 

HBV is a small (42-nm) DNA virus that contains partially double-stranded DNA within its core12. Using its own DNA polymerase for replication, the virus is able to reproduce within a host's infected hepatocytes, drawing from the cell's pool of nucleotide precursors12.

Hepatitis B surface antigen (HBsAg) is the HBV serum marker that has come to be used most commonly in clinical situations and screening protocols. Discovered by Blumberg and co-workers in 196513, it initially was not known to be a virus-associated marker. The antigen, first isolated in the serum of an Australian aborigine during a study of serum protein polymorphisms (hence it being labeled the Australia antigen) 14, was found incidentally to cross-react with the serum of patients who have had multiple blood transfusion. It was later found to be present in the serum of institutionalized patients and, it was believed to be possibly associated with Down syndrome.15

Subsequent work by Blumberg's group and others established a link between the newly identified antigen and acute hepatitis B, an association confirmed by electron microscopy identification of particles dense with the antigen in the serum of patients who were acutely ill with hepatitis.16 Those particles are now known to represent incomplete portions of the viral envelope, synthesized in great excess during the process of viral replication12, 16. In addition, intact viral particles bear the surface antigen on their outer envelope16. The presence of HBsAg in serum indicates infectivity16, although such presence alone cannot distinguish acute from chronic infection, an often confusing exercise that requires a more complete elaboration of HBV-related serologies. Although HBsAg is the first antigen detectable in the course of HBV infections, predating even the appearance of symptoms in those patients who become clinically ill, it is the predictable appearance and disappearance of other HBV-associated antigens and antibodies over time that allows patterns compatible with either acute or chronic infection to be described.

The complete hepatitis B viral particle, also known as the Dane particle, after Dane and co-workers who described it in 197017, consists of the viral core surrounded by its HBsAg-rich envelope. If the envelope is removed by the use of detergents in vitro, a viral core antigen (HBcAg) can be identified. Unlike HBsAg, HBcAg does not circulate freely in serum and is found in blood only as an integral component of the internal viral nucleocapsid17. A third antigen, the e antigen (HBeAg), is serologically distinct from both HBsAg and HBcAg. HBeAg is associated primarily with the core antigen in the virus' internal structure, but unlike HBcAg, it can be found circulating in serum, frequently in complexes with immunoglobulin.18 All three serologically unique antigens stimulate the production of equally distinct antibodies (HBsAb, HBcAb, and HBeAb) in the course of non chronic host infection.

The presence of HBeAg has been closely correlated with both the infectivity of a particular patient's serum and the microscopic detection in serum of the HBV virus itself 19, 20, and an increased risk for chronic liver disease21, 22. Seropositivity for HBeAg is taken as a marker of active viral replication and the most infectious phase of the disease, either in acute or in chronic illness. Practically, however, HBsAg is used in screening protocols because of the high concentrations of this antigen produced in response to viral presence and replication. More vigorous HBV serologic testing is performed, along with liver function evaluation, in HBsAg-positive individuals, both symptomatic and asymptomatic, to characterize the nature and extent of their disease. The appearance of HBsAb in the serum of patients occurs in the setting of resolution of acute infection; it is this antibody that appears to confer protective immunity. However, both HBcAb and HBeAb have been shown experimentally to be protective against reinfection 23,24,25,26.

 

 

Prevalence

 

The prevalence of HBV infection, according to the geographical area, may be high (≥8%), intermediate (2-7%), or low (≤2%) 3. Nigeria is classified among the countries highly endemic for viral hepatitis4. The prevalence of HB s Ag in normal population in Nigeria ranges from 2.7% to 13.3%5, 6

Viral hepatitis infection remains a public health problem in developing countries. A 12.3% overall prevalence for HBsAg in pregnant women attending antenatal clinic at General Hospital Minna has been reported66. This was a descriptive cross-sectional study using 261 pregnant women to determine social characteristics and seroprevalence of hepatitis B virus. This also corroborates the World Health Organization (WHO, 1990) report for Nigeria as a highly endemic area with prevalence greater than 8%. In related studies in different parts of Nigeria, higher prevalence rates of 11.6% were reported among pregnant women in including 2.19 % in Benin City 64, 4.3% in Port Harcourt in 2005 and 2.89% in 200665.

There is a relatively higher hepatitis B virus infection rate in patients co-infected with HIV. Agbaji et al67 carried a cross sectional study in Jos amongst 1042 HIV positive patients and reported that hepatitis B co- infection was found to be 14.2% amongst females and 19.4% amongst male in the study. Sirisena et al68 quoted a higher co infection rate of 28.7% in an earlier study

 

Manifestation of Hepatitis B Infection in the Host

 

This can be either an acute infection (which invariably occurs during pregnancy in a previously otherwise normal person), or a chronic infection (which is usually preexistent in either overt or latent form and with pregnancy occurring later)


Acute Hepatitis:

 

Hepatitis B infection does not have any special predilection for pregnancy12, 13. In a study of acute viral hepatitis in pregnancy from North India, HBV infection was observed in 19% and 18% of the pregnant and nonpregnant females respectively13. Moreover, acute HBV infection is not more severe in pregnant women than in non pregnant individuals12, 14. The presentation, as a rule, does not differ from that in non pregnant women. Persons with overt acute viral hepatitis initially have non-specific complaints including fatigue, malaise, anorexia, nausea, headache, myalgia and low grade fever. The nausea and vomiting of prodromal stage may be confused with the symptoms present in pregnancy without hepatitis. If the illness resolves before there is sufficient liver cell injury and consequent secondary dysfunction to cause jaundice, these prodromal symptoms are passed off as a flu-like viral syndrome or even for the normal physiological effects of pregnancy itself. Otherwise, jaundice develops within 2 to 10 days of the prodrome. These patients may also complain of right upper quadrant discomfort and examination may reveal tender hepatomegaly14. Splenomegaly is noticed in about 10% of cases14, 15. In the later stages of pregnancy, the abdominal examination for hepatosplenomegaly may be difficult. Most often, jaundice and symptoms of liver disease resolve in 6 weeks14. Some of them have a violent course resulting in fulminant hepatic failure with features of cerebral edema, coagulopathy, multiple organ system failure and a few others have a persistent course beyond 6 months to result in chronic hepatitis14, 15.

Acute hepatitis, particularly late in pregnancy, may induce premature labour, but this seems to have little adverse effect on the foetus.13 Heiber et al14 have also noticed an increase in the incidence of prematurity (31.6%) over that seen in the general delivery population (10-11%). Apart from this, there are possibilities of intrapartum or postpartum hemorrhage, especially if the prothrombin time is prolonged as in fulminant hepatic failure13. The usual hematologic examinations are unremarkable. The aminotransferases are high even if the bilirubin is normal (as in anicteric hepatitis) 13. The viral markers like HBsAg and IgM Anti-HBc are helpful in diagnosing acute hepatitis due to HBV13.

 

Chronic Hepatitis and Cirrhosis

 

In most affected individuals, chronic viral hepatitis is asymptomatic either indefinitely or until there is sufficient liver damage for the patient to develop manifestations of end-stage liver disease16. Many cases of chronic viral hepatitis are therefore diagnosed after serum transaminase levels are incidentally noted to be abnormal16. This commonly occurs, when an apparently healthy young woman becomes pregnant and consults an obstetrician. Apart from the abnormal transaminase, the other investigations are usually normal unless the liver disease is severe16. Patients with severe chronic hepatitis are usually aware of the liver problem before deciding about conception. In cirrhosis, the situation is slightly different; fertility is decreased probably due to amenorrhea and non-ovulating cycles, and hence pregnancy is less often seen in them.

Physical examination may be normal or the patient may have subtle physical findings consistent with early cirrhosis, including palmer erythema, splenomegaly, and a small liver (sometimes with enlargement of the left lobe). Palmer erythema, if present, may be confused with that of pregnancy (physiological). Examination of the abdomen is difficult and may be ambiguous in the later stages of pregnancy, when the liver and spleen are not palpable. In a minority of patients with end-stage liver disease, clinical features of liver failure gradually becomes apparent and may be mistaken for a hepatic complication of pregnancy16.

Chronic HBV carriers usually have normal pregnancies, unless there is severe chronic hepatitis or secondary cirrhosis and associated complications.16 Infeld et al had reported pregnancies in at least 28 of mild chronic hepatitis patients without any harmful maternal effects17. In cirrhotics, the main maternal risk is related to the degree of portal hypertension and the likelihood of esophageal variceal haemorrhage18,19. The onset of labour increases the intraabdominal pressure thereby increasing the chances of variceal bleeding. Besides this, the deterioration of hepatic function also occurs. Liver and renal failures are the other causes of maternal mortality 16

 

Management of Acute Viral Hepatitis

 

The management is similar to that for non pregnant state. The management, like in a non- pregnant state consists of supportive measures like high calorie diet, bed rest and vitamins15. If marked anorexia or vomiting is present hospitalization may be required for intravenous fluid administration15. There is no recommended antiviral therapy for acute viral hepatitis because most adults clear the infection spontaneously15. Early antiviral treatment may only be required in the 1-2% of patients with fulminant hepatitis and those who are immunocompromised15.

 

Management of Chronic Liver Disease and Cirrhosis

 

Treatment of chronic infection may be necessary to reduce the risk of cirrhosis and liver cancer17,18. Supportive management of liver disease is similar to that in the non pregnant state. There are no dietary restrictions unless cirrhosis with complications has set in17. Management of esophageal varices needs special attention by way of prophylactic banding17. Use of pharmacoprophylaxis for bleeding requires very careful monitoring of the haemodynamic status18. Coagulopathy should be managed with administration of fresh frozen plasma.

Antiviral therapy is considered as applicable to non pregnant state. Of the three recommended available drugs for chronic hepatitis B, interferon alpha is not used possibly due to lack of adequate controlled studies even though reports of its use in HCV infection does not show significant interferon related fetal malformation 20,21. The safety of Adefovir, Dipivoxil in pregnancy has not been clearly established22. Only Lamivudine which is used in an oral dose of 100mg daily has been found to be safe and has been advocated for use in pregnancy23.

 

Vertical Transmission and Effect on the Fetus

 

The significance of HBV infection during pregnancy derives in major part from its potential to be transmitted vertically 24. Ten percent of infants born to women with acute HBV infection during the first trimester of pregnancy are HBsAg positive at birth25 and 80 to 90% of neonates become HBsAg positive without prophylactic therapy if acute maternal infection develops during the third trimester of pregnancy14,26. This variable rate of vertical transmission from mothers with acute disease is explained by the fact that the placenta is a reasonably effective barrier to the spread of HBV infection27,28. According to Okada et al27, 85% of neonatal HBV infections are caused by intrapartum exposure to infectious blood and vaginal secretion, and the remaining 15% by haematogenous transplacental viral spread. However, Zhang28 in 2004 showed by measuring concentration of HBsAg & HBcAg in maternal decidual cells, trophoblastic cells, villous mesenchymal cells and villous capillary endothelial cells, that the main route of HBV transmission from mother to fetus is transplacental, from the mother's side of the placenta, to the fetal side. He also detected HBV DNA in amniotic fluid samples and vaginal secretion samples - emphasizing transmission of infection by these during parturition.

Okada et al24, examined the newborn infants of 139 asymptomatic carriers and did not find HBsAg positivity in the cord blood at any of them. However, on follow up for more than seven months, eight of the 11 mother-child pairs tested showed antigenemia, the earliest appearing 5 days after delivery. The sub-type of HBsAg was identical for each mother-child pair. In the true sense, this could be an instance of horizontal transmission from the mother during the immediate post natal period. Subsequently Okada et al27 showed that all babies born to e antigen positive mothers developed surface antigenemia. In contrast, all of the babies born to e antibody negative mothers escaped surface antigenemia. From this it is quite clear that e antigen positivity in the mother is a reliable marker to predict transmission of infection from mother to child. In the absence of appropriate prophylaxis, 40% of the neonates of HB e antigen negative mothers and 90% of the neonates of HB e antigen positive mothers will develop HBV infection.27, 30 However Sinatra et al29 reported that three infants born to anti-HB e positive mothers developed acute icteric hepatitis B within 3 months of birth. Liu et al31 have demonstrated that HLA-DR3 is positively correlated with chronic HBV carriage and highly replicative status in pregnant women. HLA-DR13 shows negative correlation with chronic HBV carriage in pregnant women.

The strong possibility of vertical transmission lends importance to diagnosing acute or chronic HBV infection in pregnant women and justifies mandatory ante partum serum HBsAg screening32. By doing so, previously unsuspected chronic HBV infection is diagnosed in otherwise healthy individuals. This has the added benefit of making it possible to refer them for appropriate antiviral therapy before development of significant liver damage and associated functional insufficiency.

The infants of potentially infectious mothers are treated with HBV Human Hyper globulin (HBIG) at delivery and simultaneously active immunoprophylaxis is initiated32. This approach is effective in preventing chronic HBV in approximately 85% neonates33; it is ineffective in cases of haematogenous transplacental infection (15%)34.

Different measures have to be adopted to modify (interrupt) the vertical transmission of HBV Infection.

 

HBIG HBIG can be administered a dose of 200 IU i.m. every week from 28th week of gestation reduces the intrauterine infection to 16.1% against 32.7% (in controls).34

 

Lamivudine - Lamivudine has been used with good safety and efficacy in the last four weeks of pregnancy to decrease the risks of vertical transmission35. Li et al34 showed that the intrauterine infection was reduced to 16.3% against 32.7% (controls) with its use from 28th week of gestation in a dose of 100mg/day. This is also substantiated by other studies23. However, there is a report of failure of vertical transmission of hepatitis B virus despite antenatal Lamivudine therapy36. Of course, in this case, the authors detected precore mutant in both the mother and the child and this is to be interpreted appropriately without undermining the vertical transmission lowering effect of Lamivudine.

 

Caesarean-section does not show any extra reduction in the incidence of vertical transmission in comparison to vaginal delivery37. Apart from vertical transmission, the maternal HBV infection does not have any effect on the fetal outcome37. Although there was an increase in incidence of prematurity, it had no effect on congenital malformations, stillbirths, abortions or intrauterine malnutrition in comparison to the controls14.

 

Breastfeeding

Breast feeding is an important outcome of pregnancy and successful delivery. So, once the HBV infected mother, with all possible precautions delivers a baby without any evidence of infection at birth, the next question that comes to mind is: whether breast feeding can be done safely? Even though, breast milk of infected mother contains HBV DNA, with appropriate immunoprophylaxis, including hepatitis B immunoglobulin and hepatitis B vaccine, breast feeding of infants of chronic HBV carriers (irrespective of replicative status) poses no additional risk for the transmission of the hepatitis B virus38.

 

Prevention

 

Mothers positive for both HBsAg and HBeAg are at highest risk for transmitting the virus; 85% to 100% of their offspring become infected, with 70% to 90% becoming chronic carriers37. Mothers who are HBsAg-positive but HBeAg-negative, presumably indicating lower levels of replicating virus, do have a lower risk of transmitting the virus, but up to 35% of their children still will become carriers in the absence of neonatal therapy.39,40,41,42. In addition to the long-term risks of HBV-related sequelae in chronic carriers, such as cirrhosis and hepatocellular carcinoma, both fulminant fetal neonatal hepatitis 43, 44, 45, and childhood-onset hepatic carcinoma46 have been described in children born to HBsAg-positive mothers.

Early attempts at interrupting the perinatal transmission cycle used HBIG alone, administered in the neonatal period. Globulin alone had a protective efficacy against the carrier state of 70% to 75%, even though the protection was not permanent, and many children eventually became infected after the passively acquired antibody was cleared, undoubtedly through household contact46. With the advent of the hepatitis B vaccine, trials were established to test its efficacy when administered in the newborn period, both alone and in conjunction with HBIG41. A combination of HBIG and vaccine in the newborn period conferred significantly greater protection against perinatally transmitted HBV than even the vaccine alone, increasing efficacy from a range of 75% to 85% up to 90% to 95%,42,47,48,49,50,51,52,53,54,55. A small but identifiable percentage of babies, who become infected despite even combined HBV therapy at birth, is believed to represent intrauterine infection55, 56.

HBV DNA has been identified in abortus tissue extracted from an HBsAg-positive mother 57, and other reports show evidence of intrauterine infection in clinical situations, increasing risks for transplacental leakage, such as preterm labour associated with placental abruption55,56. Still, combination HBV-specific immunotherapy provides the best opportunity to prevent the chronic carrier state in the offspring of HBsAg-positive mothers37. In the United States alone, approximately 16,500 births occur in HBsAg-positive women each year, approximately 4300 of whom are also HBeAg-positive58. Infants born to these women should receive HBIG (0.5 ml) intramuscularly (IM), ideally within 12 hours of birth59. HBV vaccine should be administered concurrently at a different site (0.5 ml IM) or can be administered up to 7 days after birth if it is not immediately available59. The timing of HBIG appears to be more critical than that of vaccine in achieving maximal effectiveness of passiveactive therapy. Subsequent vaccination is performed, also 0.5 ml IM, at ages 1 month and 6 months59. Follow-up for these infants is crucial, because one recent study confirms the concern that in the United States, groups at highest risk for HBV infection are also least likely to be compliant with follow-up care. It is the recommendation of the American College of Obstetricians and Gynecologists that HBsAg screening be performed as part of routine prenatal testing in all pregnant women32.

 

 

MATERIAL AND METHOD

 

Study Area.

 

This study was carried out in the maternity unit of the Department of Obstetrics and Gynaecology, Jos University Teaching Hospital (JUTH) Jos. Jos University Teaching Hospital (JUTH) is a tertiary health institution situated in Jos. It is one of the two teaching hospitals in the north-central geopolitical zone of Nigeria, although there are Federal Medical Centres (FMCs) in the other states within the geo-political zone. Jos is the capital city of Plateau State, which has over 30 different ethnic groups 11.

The 2006 Nigerian census puts the population of Plateau State at 2,959,588 with 1,031,662 being female11.

Plateau State lies between latitude 70 and 110 North and Longitude 700 and 2500 east11. The capital city is a pear-shaped upland known as Jos Plateau. This upland stretches for approximately 104km from north to south, and 80km from east to west, covering an area of about 8,600 sq km11. It has a height of 1,200m above sea level11. Jos University Teaching Hospital has recently re-located to its permanent site at Laminga, Jos North Local Government Area of the State capital, in North central Nigeria. The hospital has a well established Obstetrics and Gynaecology Department.

 

Study Population

 

The study population were women who present in labour at the labour ward of Jos University Teaching Hospital, North Central, Nigeria

 

 

Study Design

 

The study is a descriptive cross-sectional study and hospital based. It was conducted between 1st March, 2011 and 31st August ,2011. The parturients who give an informed consent were recruited to the study during the last 5 weeks of pregnancy and the prestructured questionnaires were administered. As the women came in labour, blood samples were taken from the ante-cubital vein. Cord blood was also collected at delivery of the baby after cutting the umbilical cord

 

Inclusion Criteria

 

1.                Pregnant women who gave informed consent and who presented in Labour at the labour ward of JUTH for delivery and met the criteria.

 

Exclusion Criteria

 

1.                Women who were not pregnant

2.                Pregnant women who have had hepatitis B immunization

3.                Pregnant women who were HIV positive

4.                Pregnant women who declined to participate in the study.

 

Ethical Consideration

 

This proposal was presented to the research and ethical committee of Jos University Teaching Hospital for approval. Informed consents were obtained from the subjects before enlistment into the study.

 

Estimate of Sample Size

 

The sample size was calculated using the formula60

N=z2 pq/d2

 

Where,

N= desired sample size

Z=standard normal deviate 1.96 which correspond to 95% confidence interval.

P= prevalence expressed as 100% that is, 13.3%5

q=complimentary proportion 1-p

d=degree of accuracy desired=0.05

 

N=(1.96)2 x 0.133 x 0.867

(0.05)2

 

=177.2

 

A minimum of 180 pregnant women were recruited for the study.

 

 

Data Collection

 

Collection Of Blood Sample /Serum Preparation

 

Blood samples were collected aseptically by venepuncture using 5 ml sterile disposable hypodermic syringes and needles from the ante-cubital vein of pregnant women who presented in labour in the labour ward of Jos University Teaching Hospital. The blood samples collected were dispensed into pre-labeled specimen bottles. The samples were allowed to clot and centrifuged at 3,000 rpm for 5mins to separate the serum. The sera were extracted using micropipette and testing carried out as explained below

 

Procedure for Detecting HB s Ag

 

Hepatitis B surface antigen (HBsAg) detection was done using the in vitro diagnostic kit manufactured by ACON Laboratories, Inc. ,4108 Sorrento Valley Blvd., San Diego, CA 92121, USA. The test kit (dipsticks) is a rapid immunochromatographic assay designed for qualitative determination of HBsAg in human serum or plasma. Assays were carried out at room temperature. The test strips were removed from their foil pouches and immersed into serum samples with arrows pointing towards the samples. The strips were taken out after about 10secs and placed on a clean, dry, non-absorbent surface. This was to allow time for the reaction to take place. The specimen was absorbed into the test strips and moved by capillary action upward towards the control line. Results were read after 10mins post immersion. Positive samples generated a colour band in the test region of the strips and another in the control region while negative samples had a colour band in the control regions only.

 

Procedure for Detecting HB e Ag

 

Sample positive for hepatitis B surface antigen were tested for hepatitis B e antigen to determine infectivity using CTK ONSITE test kit manufactured by CTK Biotech, Inc. 6748 Nancy Ridge Drive, San Diego, CA 92121, USA. 2-3 drops of plasma were dropped in the test kit well using a small plastic dropper. Results were read after 15 minutes. There are C and T bands on the test kit. The test is positive if C and T bands show colour development and is negative if only C band shows colour development. Mothers who are positive for hepatitis B surface antigen shall have the cord blood of their babies also similarly tested.

Positive samples were stored at -200C and were later confirmed by using a commercially prepared recombinant antigen-based Enzyme Linked Immunosolvent Assay (ELISA) test. This was done at the Immunology Laboratory of the Jos University Teaching Hospital, Jos.

 

Statistical Methods for Data Analysis

 

The results are expressed as means, and standard deviation. Chi square was used to determine significance of association. The relationship between HB s Ag and other variables in the questionnaire were examined using P values. Significance was determined using P<0.05 at 95% confidence interval. All analysis were conducted using the SPSS version 15 software.

 

 

Limitation to the Study

 

1. One of the limitations was poor knowledge of the disease entity and the myth surrounding Hepatitis B virus infection which affected consent

2. Repeat testing of the positive infants at 3 months, 6 months and at 12 months would been necessary to ascertain the actual mother to child transmission. This would be the basis for future studies

3. Other hepatitis B markers like Anti HBc, Anti HBs and Anti HBe would have been done to enable proper classification of patients. However, cost of testing for all the markers is high and therefore, a serious challenge.

 

The Benefits of the Study

 

This study will benefit both patients and humanity

 

Patient

 

The opportunity to have serum hepatitis B surface antigen test done free of- charge for these patients by the researcher.

Arrangement was made for immunization of those mothers who are negative after weaning for them to be immunized and arrangement was also made for co-administration of hepatitis B immunoglobulin and passive hepatitis B immunization to those babies born to hepatitis B s antigen positive mothers. Another benefit to the patient is that those who participated in the study were provided with free haematinics for 6 weeks by the researcher.

 

 

Humanity

 

The result of the study will assist in policy formulation in assessing the current non -screening of women for hepatitis B surface antigen during ANC booking.

 

 

RESULTS

 

Tables 1, 2, 3, 4 and 5 show the age distribution, educational status of mother, occupation of mother, educational status of father and occupation of father. The analysis did not show any statistically significant association between the above socio-demographic variables and the seropositivity of HB ' sAg. P values >0.05

Table 6 shows the gravidity of the participants and serostatus. Also no statistically significant association was found between gravidity and HB ' s Ag. X2=2.266, P value=0.519

Table 7 shows history of blood transfusion and HB ' s Ag. Sero status of the 180 enrollee in the study, 8 had history of blood transfusion. One in the eight with history of blood transfusion was HB ' s Ag. positive. Again this was not statistically significant. X2= 0.209, P value= 0.648

Table 8 compares the mean gestational age at delivery between the seropositive and the seronegative participants. Their mean gestational age was not statistically significantly different. P value=0.621

Table 9 shows the prevalence of HB ' s Ag. in the 180 study participant of 12.77%.

Table 10 shows the prevalence of HB e Ag in the 180 study participant of 1.7%.

Table 11 shows the prevalence of HB ' s Ag. in the cord blood of babies of the 180 participant of 2.2%.

Table 12 shows the cross tabulation of the maternal HB ' s Ag. and cord HB ' s Ag. Association was statistically significant. X2= 12.346, P value= 0.000

Table 13 shows the cross tabulation of the maternal HB ' s Ag. and maternal HB e Ag. In the general study population of 180, 3 (1.67%) tested positive for HB e Ag. That is 3 in the 23 that tested positive for HB ' s Ag. That is proportion of 23:3 or 13.04%. Association was statistically significant, X2=13.346, P value=0.000

Table 14 shows the cord HB s Ag and cord HB e Ag of babies of participants. Of the 4 cord blood that tested positive for HB ' s Ag., none was positive for HB e Ag.

 

 

 


TABLE 1: Age Distribution and Elisa Hepatitis B Surface Antigen Status (Hb B 'sAg)

 

Serostatus

Hb B 's Ag. Positive

Hb B 'sAg. Negative

Total

Age

18-23 yrs

5

14

18

24-29 yrs

12

72

84

30-35 yrs

3

61

84

36-45 yrs

3

10

13

Total

23

157

180

 

X2=6.932, P Value=0.074

 

 

TABLE 2: Educational Status of the Mother and Elisa Hepatitis B Surface Antigen Status (Hb B 'sAg)

Status

 

Hb B 'sAg. Positive

Hb B 's Ag. Negative

Total

Education

Primary

3

6

9

Secondary

9

71

80

Tertiary

10

78

88

None

1

2

3

Total

23

157

180

 

X2=3.430, P value=0.329

 

 

TABLE 3: Occupation and Maternal Elisa Hepatitis B Surface Antigen Status (Hb B 'S' Ag)

 

Status

Hb B 'sAg. Positive

Hb B 'sAg. Negative

Total

Occupation

Civil / public servant

7

44

51

Business women

6

24

30

Artisan

2

13

15

Student & corpers

1

23

24

Farmer

0

24

24

Housewives

7

53

60

Total

23

157

180

X2=3.543, P Value=0.320

 

 

TABLE 4: Educational Status of the Father and Maternal Elisa Hepatitis B Surface Antigen Status (HB 'sAg)

 

 

Status

HB'sAg. Positive

HB'sAg. Negative

Total

Education

Primary

3

6

9

Secondary

8

56

64

Tertiary

12

93

105

None

0

2

2

Total

23

157

180

X2=2.523, P value=0.471

 

 

TABLE 5: Occupation of the Father and Maternal Elisa Hepatitis B Surface Antigen Status (HB'sAg)

 

Status

HB'sAg. Positive

HB'sAg. Negative

Total

Occupation

Civil / public servant

11

80

91

Business man

8

52

60

Artisan

4

15

19

Student & corpers

0

3

3

Farmer

0

6

6

Unemployed

0

1

1

Total

23

157

180

X2=2.186, P Value=0.823

 

 

TABLE 6: Gravidity and Elisa Hepatitis B Surface Antigen Status (HB 's' Ag)

STATUS

HB'sAg. Positive

HB'sAg. Negative

Total

GRAVIDITY

Primigravidae

8

52

60

Secundigravidae

8

40

48

Multigravidae

7

47

54

Grandmultigravidae

0

18

18

Total

23

157

180

 

X2=2.266, P value=0.519

 

 

TABLE 7: History of Blood Transfusion and Elisa Hepatitis B Surface Antigen Status (HB'sAg)

STATUS

HB ' Ag. Positive

HB'sAg. Negative

Total

BLOOD TRANSFUSION

YES

1

7

8

NO

22

150

172

TOTAL

23

157

180

X2=0.209, P Value=0.648

 

 

TABLE 8: Elisa Hepatitis B Surface Antigen Status (HB's'Ag) and Mean Gestational Age at Delivery (days).

 

 

Number

Mean gestational age

Stand. Dev.

S.E of Mean

Status

Positive

23

271.2500

8.948

2.237

Negative

157

272.4381

8.926

0.871

P=0.621

 

 

TABLE 9: Elisa Maternal Hepatitis B Surface Antigen Status (HB'sAg)

 

Frequency

Percent

Valid Percent

Cumulative Percent

 

Status

Positive

23

12.77

12.77

12.77

 

Negative

157

87.23

87.23

100.0

 

Total

18O

100.0

100.0

 

Bar Chart 1: Showing Maternal Hepatitis B Surface Antigen Serostatus (HB 's' Ag) - Prevalence

 

 

 

TABLE 10: Maternal Elisa Hepatitis B ' Antigen Status (HB 'eAg)- Prevalence

 

Frequency

Percent

Valid Percent

Cumulative Percent

Sero status

Positive

3

1.7

1.7

1.7

Negative

177

98.3

98.3

100.0

Total

180

100.0

100.0

 

 

BAR CHART 2: Showing Maternal Elisa Hepatitis B 'E Antigen Status (HB 'e' Ag) - Prevalence

 

 

TABLE 11: Cord Elisa Hepatitis B Surface Antigen Status (HB 'sAg) - Prevalence.

 

Frequency

Percent

Valid Percent

Cumulative Percent

Sero-status

Positive

4

2.2

2.2

2.2

Negative

176

97.8

97.8

100.0

Total

180

100.0

100.0

 

Bar Chart 3: Showing Elisa Cord Hepatitis B Surface Antigen Status (HbB 's' Ag)

 

 

 

 

TABLE 12: Elisa Maternal Hepatitis B Surface Antigen Status (HB 's' Ag) and Cord Hepatitis B ' Antigen (HB 's' Ag)

CORD HB 's' .Ag

POSITIVE, (%)

NEGATIVE, (%)

TOTAL

MATERNAL HB 's' .Ag

POSITIVE

4, (17.39%)

19, (82.61)

23

NEGATIVE

0, (0%)

157, (100%)

157

TOTAL

4, (2.22%)

176, (97.78%)

180

X2=12.346, P value= 0.000

 

 

TABLE 13: Elisa Maternal Hepatitis B Surface Antigen Status (HB 's' Ag) and Hepatitis B ' Antigen (HB 'eAg)

H B 'e' .Ag

POSITIVE, (%)

NEGATIVE, (%)

TOTAL

HB 's' .Ag

POSITIVE

3, (13.04%)

20, (86.96%)

23

NEGATIVE

0, (0%)

157, (100%)

157

TOTAL

3, (1.67%)

177, (98.33%)

180

X2=13.346, P value= 0.000

 

 

TABLE 14: Cord Hepatitis B Surface Antigen Serostatus (HBs Ag) and Hepatitis B ' Antigen (HB 'eAg)

HB 'e'. Ag

POSITIVE

NEGATIVE

TOTAL

HB 's' .Ag

POSITIVE

0

4

4

NEGATIVE

0

176

176

TOTAL

0

180

180

 

 


DISCUSSION

 

This study was undertaken to find out the prevalence of HB ' sAg. among women at delivery and to assay the above marker in the respective cord bloods of their babies. Secondly, it is find the proportion of HB ' sAg Positive women that are HB 'e' Ag positive and also, to document same proportion in the cord bloods of their babies. Hepatitis B, a viral liver infection remains a public health problem in developing countries with high endemicity.

A prevalence rate of 12.77% for HB'sAg was found in this study. This finding makes Jos an area of high endemicity3 for hepatitis B virus. This prevalence rate compares to a rate of 12.6% by Jombo et al (2005) in prevalence study of hepatitis B virus infection in a rural settlement in Northern Nigeria69. Also in the same north central Nigeria, Mbaawuaga et al, (2008) find a prevalence of 11% in a study in Markudi, Nigeria involving 300 pregnant women70. Similar prevalence rates have been reported, 11.6% in Maiduguri, north eastern Nigeria61 and 13.8% in Lagos, south-western Nigeria. But lower prevalence rates have been reported from studies in the southern part of the Nigeria, 2.19% in Benin City64, and 4.3% in Port Harcourt65. Agbaji et al (2008) in a cross sectional study in Jos, Nigeria among 1042 HIV positive patients report a prevalence of HB ' sAg of 14.2% among the female and 19.4% among the males in the study67. Also in a similar study Sirisena et al (2002) quoted a higher co- infection prevalence rate of 28.7%68. But these were studies among HIV positive participants and studies have shown that prevalence of HB ' sAg is higher amongst HIV positive patients67, 68. In this study, the researcher excluded HIV positive women.

Prevalence rate of cord HB'sAg of 2.2% was found in this study. Of the 23 women that tested positive to HB'sAg, 4 (17.4%) had their respective cord blood also positive for HB'sAg. Though studies assessing the cord blood seropositivity for HB ' sAg at delivery in this part of the world is scarce, intrauterine infection though said to be rare is known to occur27, 28. Rates as low as 2.5% for mother-to- child transmission of hepatitis B infection prenatally, has been70. At delivery, cord blood of babies from HB ' Ag positive mothers have been found to be positive in up to 50% of cases7. This is however higher than the 17.4% that was found in this particular study. Ameer et al, (2007) found out that of the 300 women that enrolled in their study, 37 were positive for HB ' Ag (12.33%). Cord blood was positive for HB ' sAg in 4 out of the 37 HB ' s Ag positive women (that is 10.8%). Differences in the conduct of labour and delivery, and differences in transplacental transfer of infection, possibility of delayed sero-conversion could account for the variance. Whatever the reason for the difference, it is however shown that intrauterine or rather prenatal transmission making the cord blood to become positive do occur. Zuberi et al, (1989) reported a similar low vertical transmission72.

The study also revealed that of the 23 women that were HB ' s Ag positive, 3 were HB 'e Ag positive. Thus giving a proportion of 23:3 or 13.04%, the prevalence rate for HB 'e Ag in the study population of 1.7%. HB 'eAg is the marker for infectivity. Being HB 'sAg positive has a highly statistically significant association with being HB 'eAg positive. X2= 13.346, P value= 0.000. Ameer et al, (2007) found that HB e Ag was positive in 40.54% of patient that were HB s Ag positive71. This does not compare to the 13.04% found in this study.

This study showed that of the 4 babies whose cord bloods were positive for HB S Ag, none tested positive to HB 'eAg. Ameer et al (2007) find that 75% of cord bloods that were HB s Ag positive were also HB e Ag positive71. The difference could be due to the natural history of the disease.

 

 

CONCLUSION

 

The results of the study showed that the prevalence of HB s Ag among women at delivery in Jos metropolis is 12.77%. It also revealed that the prevalence of HB s Ag on cord blood is 2.2% which is an issue of concern. It also revealed that the Proportion of HB s Ag to HB e Ag in women at delivery is 23:3. This means that 13.04% of those that were HB s Ag positive were infectious. Association was statistically significant. There was no HB e Ag positivity in all the 4 cord blood that was HB s Ag positive.

 

 

Recommendations

 

Following this study, it is recommended that:

In line with WHO recommendation of routine antenatal screening for HB'sAg. For pregnant women at booking2, it recommended based on the finding of this study that routine screening for HB S Ag on all pregnant women be introduced at the booking clinic. This will help identify those that are positive. In this particular group further measures or interventions to protect the unborn babies can be taken

Also government and non-governmental agencies should intensify efforts to enlighten the public in general and those within the reproductive age group in particular of the public health importance of the disease

A larger multicentre study design to follow up babies born to mothers that are HB S Ag for 6 and 12 months is also recommended so as to ascertain both horizontal and vertical transmission of hepatitis B virus.

 

Conflict of interest: There was no conflict of interest

 

Funding: There was no funding

 

 

REFERENCES

 

 

1. Guberman C et al .Renal, urinary tract, gastrointestinal and dermatologic disorders in pregnancy. In: Decherney AL et al (Eds.) Current Diagnosis and treatment Obstetric and Gynaecology 10th edition. McGraw-Hill Medical Publishing Division.2007; 382-385.

2. World Health Organization (WHO). Advanced Immunization Management (AIM). Hepatitis B(cited 2005 August.); available from www.who.int/mediacentre/factsheet/FS204/en/WHO. Assessed 15th August 2010

3. Maddrey WC. Hepatitis B: an important public health issue. J med virol. 2000; 61(3): 362-6.

4. Sirisena ND, Njoku MO, Idoko JA. HBsAg in patients with human immunodeficiency Virus1 (HIV-1) infection in Jos, Nigeria. Nigerian Medical Practitioner 2002; 41:18-20

5. Kulkarimi S, Alowola FO, Wayo GG. Prevalence of hepatitis B surface antigen in Northern Nigerian blood donors. Vox Sangunis 1996; 50: 151-153.

6. Muula AS. Tackling HIV/AIDS in Africa-another perspective. African Health 2000; 23 (1): 5-6

7. Sylvie RR, Francis D. Hepatitis B mother to child transmission. Expert Rev. Anti-infective ther. 2004; 2(1): 133-145

8. Sriprakash I, Anil TP. Routine prenatal screening of Indian women for HBsAg: benefits derived versus cost. Tropical Doctor 1997; 102: 10-15

9. Shepard TH. Catalog of teratogenic agents 9th ed. Baltimore, MD: John Hopkins University press; 1998.

10. Caruana SR, Keily HA, De silva SL, Chea l, Noun S, Saykav P. Knowledge about Hepatitis viruses in immigrant and refugees from the Mekong Region, Aust NZ. J Public Health 2005; 29: 64-68.

11. Daniel, Jos and Plateau State diff missen 2002. Available at http://www.widernet.org/josproject/josplateauintml. Assessed 15th August 2010.

12. Khuroo MS, Kamili S. Aetiology, clinical course and outcome of sporadic acute viral hepatitis in pregnancy. J Viral Hepat 2003; 10: 61-9.

13. Jaiswal SP, Jain AK, Naik G, et al. Viral Hepatitis during pregnancy. Int J Gynaecol Obstet 2001; 72: 103-8.

14. Hieber JP, Dalton D, Shorey J, et al. Hepatitis and pregnancy. J Pediatr 1977; 91: 545-9.

15. Adams RH, Combes B. Viral hepatitis during pregnancy. JAMA 1965; 192: 195-8.

16. Schweitzer IL, Peters RL. Pregnancy in Hepatitis B antigen positive cirrhosis. Obstet Gynecol 1976; 48 (suppl I): 53S-56S.

17. Infeld DS, Borkowf HI, Varma RR. Chronic persistent hepatitis and pregnancy. Gastroenterology 1979; 77: 524-7.

18. Cheng YS. Pregnancy in liver cirrhosis and/or portal hypertension. Am J Obstet Gynecol 1977; 128: 812-22.

19. Russell MA, Craigo SD. Cirrhosis and portal hypertension in pregnancy. Semin Perinatol 1998; 22: 156-65.

20. Hiratsuka M, Minakami H, Koshizuka S, et al. Adminstration of interferon-alpha during pregnancy: effects on fetus. J Perinat Med 2000; 28: 372-6.

21. Ozaslan E, Yilmaz R, Simsek H, et al. Interferon therapy for acute hepatitis C during pregnancy. Ann Pharmacother 2002; 36: 1715-8.

22. Dando T, Plosker G. Adefovir Dipivoxil: A review of its use in chronic hepatitis B. Drugs 2003; 63: 2215-34.

23. Su GG, Pan KH, Zhao NF, et al. Efficacy and safety of lamivudine treatment for chronic hepatitis B in pregnancy. World J Gastroenterol 2004; 10: 910-1.

24. Okada K, Yamada T, Miyakawa Y, et al. Hepatitis B surface antigen in the serum of infants after deliver from asymptomatic carrier mothers. J Pediatr 1975; 87: 360-3.

25. Sweet RL. Hepatitis B infection in pregnancy. Obstet Gynecol Report 1990; 2: 128.

26. Reinus J, Leikin E. Viral hepatitis in pregnancy. Clin Liver Dis 1999; 3: 115-30.

27. Okada K, Kamiyama I, Inomata M, et al. e antigen and anti-e in the serum of asymptomatic carrier mothers as indicators of positive and negative transmission of hepatitis B virus to their infants. N Engl J Med 1976; 294: 746-9.

28. Zhang SL, Yue YF, Bai GQ, et al. Mechanism of intrauterine infection of Hepatitis B virus. World J Gasroenterol 2004; 10: 437-8.

29. Sinatra FR, Shah P, Weissman JY, et al. Perinatal transmitted acute icteric Hepatitis B in infants born to Hepatitis B surface antigen-positive anti-Hepatitis B e positive carrier mothers. Pediatrics 1982; 70: 557-9.

30. McMahon BJ, Alward WL, Hall DB, et al. Acute Hepatitis B virus infection: relation of age to the clinical expression of disease and subsequent development of the carrier state. J Infect Dis 1985; 151: 599-603.

31. Liu HY, Kong BH, Luo X, et al. Study on the association between maternal-infantile vertical transmission of hepatitis B virus and human leukocyte antigen DR gene domain. Zhonghua Fu Chan Ke Za Zhi (Chinese) 2003; 38: 599-603.

32. ACOG Technical bulletin. Hepatitis in pregnancy. 174 November 1992.

33. Stevens CE, Taylor PE, Tong MJ, et al. Yeast-recombinant Hepatitis B vaccine - efficacy with hepatitis B immune globulin in prevention of perinatal Hepatitis B virus transmission. JAMA 1987; 257: 2612-6.

34. Li XM, Yang YB, Hou HY, et al. Interruption of HBV intrauterine transmission: a clinical study. World J Gastroenterol 2003; 9: 1501-3.

35. Van Zonneveld M, van Nunen AB, Neisters HG, et al. Lamivudine treatment during pregnancy to prevent perinatal transmission of hepatitis B virus infection. J Viral Hepat 2003; 10: 294-7.

36. Kazim SN, Wakil SM, Khan LA, et al. Vertical transmission of hepatitis B virus despite maternal lamivudine therapy. Lancet 2002; 359: 1488-9.

37. 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.

38. Hill JB, Sheffield JS, Kim MJ, et al. Risk of hepatitis B transmission in breast-fed infants of chronic hepatitis B carriers. Obstet Gynecol 2002; 99: 1049-52

39. Okada K, Kamiyama I ,Inomata M et al:The e antigen and Anti-e in the serum of asymptomatic carrier mothers as indicators of positive and negative transmission of hepatitis B virus to their infants .N Engl J Med 1976 ;294:746.

40. Beasley RP, Trepo C, Steven CE. Et al: The e antigen and vertical transmission of hepatitis B surface antigen .Am J Epidemiol 1977; 105:94.

41. Steven CE, Toy PT, Tong MJ et al: Perinatal hepatitis B virus transmission in the United States :Prevention by passive active immunization. JAMA 1985;253:1740.

42. Biswas SC, Gupta I, Gangul NK et al :Prevalence of Hepatitis B surface antigen in pregnant mothers and its perinatal transmission .Trans R Soc Trop Med Hyg.1989;83:698.

43. Dupuy JM, Frommel D,Alagille D:Severe viral hepatitis B in infancy.Lancet 1975;1:191.

44. Fawaz KA, Grady GF,Kaplan MM et al:Repetitive maternal-fetal transmission of fetal hepatitis B.N Engl J Med 1975;293:1357.

45. Delaplane D, Yoge VR, Crussi F et al :Fetal hepatitis B in early infancy:The importance of identifying HB s Ag positive pregnant women and providing immunoprophylaxis for their newborn .Paediatrics 1983;72:176

46. Chang MH, Chen DS, Hsu HC et al :Maternal transmission of hepatitis B virus in childhood hepatocellular carcinoma. Cancer 1989;64:237

47. Beasley RP, Hwang LY, Lin CC et al: Hepatitis B immune globulin (HBIG) efficacy in the interruption of perinatal transmission of hepatitis B virus carrier state: Initial report of a randomized double-blind placebo-controlled trial. Lancet 1981; 2:388.

48. Beasley RP, Hwang LY, Lee GC et al: Prevention of perinatally transmitted hepatitis B virus infections with hepatitis B immune globulin and hepatitis B vaccine. Lancet 1983;2:1099.

49. Tada H, Yanagida M, Mishina J et al: Combined passive and active immunization for preventing perinatal transmission of hepatitis B virus carrier state. Pediatrics 1982;70:613.

50. Wong VCW, Ip HMH, Reesink HW et al: Prevention of the HBsAg carrier state in newborn infants of mothers who are chronic carriers of HBsAg and HBeAg by administration of hepatitis-B vaccine and hepatitis-B immunoglobulin: Double-blind randomized placebo-controlled study. Lancet 1984; 2:921.

51. Pongpipat D, Suvatte V, Assateerawatts A: Efficacy of hepatitis-B immunoglobulin and hepatitis-B vaccine in prevention of the HBsAg carrier state in newborn infants of mothers who are chronic carriers of HBsAg and HBeAg. Asian Pac J Allergy Immunol 1986;4:33.

52. Schaln SW, Mazel JA, deGast GC et al: Prevention of hepatitis B infection in newborns through mass screening and delayed vaccination of all infants of mothers with hepatitis B surface antigen. Pediatrics 1989; 83:1041.

53. Poovorawan Y, Sanpavat S, Pongpunlert W et al: Protective efficacy of a recombinant DNA hepatitis B vaccine in neonates of HBe antigen-positive mothers. JAMA 1989; 269:3278.

54. Chen DS, Hsu HM, Sung JL et al: Immunization of newborns of HBsAg-positive mothers: Ag-positive mothers: A successful first step in control of hepatitis B virus in Taiwan. Hepatology 1989; 9:900.

55. London WT, O'Connell AP: Transplacental transmission of hepatitis B virus. Lancet 1:1037, 1986

56. Tang SX, Yu GL: Intrauterine infection with hepatitis B virus. Lancet 1990; 335:302.

57. Li L, Shen MH, Li YQ et al: A study of mother-infant transmission of hepatitis B virus. Shanghai, International Symposium on Liver Cancer and Hepatitis, 1986

58. Centers for Disease Control: Recommendations of the Immunization Practices Advisory Committee. Prevention of perinatal transmission of hepatitis B virus: Prenatal screening of all pregnant women for hepatitis B surface antigen MMWR Morb Mortal Wkly Rep 37:341, 1988

59. Jonas MM, Reddy RK, DeMedina M et al: Hepatitis B infection in a large municipal obstetrical population: Characterization and prevention of perinatal transmission. Am J Gastroenterol 1990; 85:277.

60. Araoye MO. Sample size determination.In :Araoye MO (ed) Research methodology with statistics for Health ans Social Sciences.Nathadex pub.,2003;6:115-121.

61. Harry TO., Bajani MD., Moses AE. Heaptitis B virus infection among blood donors and pregnant women in Maiduguri, Nigeria. East Africa Medical Journal1990; 70: 596-597.

62. Nasidi A, Harry, TO., Vyazor, SO., Numumbe, GMR., Azzan, BB., Ancinlev, VA. (1983). Prevalence of Hepatitis B infection marker in two different geographical areas of Nigeria. Proceedings of the first international conference, 12-15 December 1983, Lagos, Nigeria.

63. Luka, SA., Ibrahim, MB., Iliya, SN. Seroprevalence of hepatitis B surface antigen among pregnant women attending Ahmadu Bello University Teaching hospital, Zaria, Nigeria. Nigerian Journal of Parasitology 2008; 29(1): 38-41

64. Onakewhor, JUE., Offor, E., Okonofua, FE. Maternal and neonatal seroprevalence of Hepatitis B surface antigen (HBsAg) in Benin City. Journal of Obstetrics and Gynaecology 2001; 21(6): 583-586.

65. Akani, CI., Ojule, A C., Opurum, HC., Ejilemele, AA. Seroprevalence of HBsAg in pregnant women in Port Harcourt. Nigeria. Nigeria Postgraduate Medical Journal, 2005; 12(4): 266-270

66. Ndam IS.,Joshua IA., Luka SA.,Sadiq HO., Epidemiology of hepatitis B infection amongst pregnant women in Minna,Nigeria.Science World Journal .2008;3 :3

67. Agbaji OO,Ladep GN ,Agaba P, Badung BP, Danung ML, Imade G et al. Prevalence and characteristics of Hepatitis B Surface Antigenaemia amongst HIV infected Patient in Jos, Nigeria. Hungarian Medical Journal ,2008;2(1.9):77-82

68. Sirisena ND, Njoku M, Idoko JA . Hepatitis B Surface antigenaemia in patient with HIV 1 infection in Jos , Nigeria .Nigeria Medical Practitioner 2002;41:18-20.

69. Jombo GTA, Egah DZ, Banwat EB. Hepatitis B virus infection in a rural settlement in Northern Nigeria. Niger J med 2005; 4: 524-428.

70. Mbaawuga EM, Enenebeaku MNO, Okopi JA, Damen JG. Hepatitis B virus (HBV) infection among pregnant women in Markudi, Nigeria. Afr. J. Biomed. Res. 2000; 11: 155-159.

71. Ameer A, Abdul R, Ghulam QKK. Hepatitis B markers; its transmission in newborn from mothers. Professional med J 2007; 14(2): 307-311

72. Zuberi SJ, Lodi P. Pathern of HB s Ag/ HB e Ag antigenaemia in pregnant women. JAMA 1989; 39: 160.


 

 

Cite this Article: Ozele, KC; Ozele, N (2022). Mother -To -Child Transmission of Hepatitis B in Jos Metropolis. Greener Journal of Medical Sciences, 12(1): 25-40.