ObjectiveVertical transmission of the hepatitis B virus (HBV) is the commonest mode of infection and can be prevented with immunoprophylaxis of the infant and antiviral therapy in the mother. Our aim was to review a cohort of subjects with HBV in pregnancy to determine the prevalence of active disease or high HBV-DNA levels that required treatment to prevent transmission, and to review the management of mothers and infants.MethodsA retrospective case-note review was conducted of all the HBV-infected pregnant women and their infants who attended the Newcastle obstetric services from 2007 to 2011.ResultsThere were 113 pregnancies in 81 women (median age 28 years; 15% hepatitis B e antigen (HBeAg) positive) during 2007–11. 71% of mothers were first diagnosed with HBV during pregnancy. The mothers were born in 28 different countries. 69% of mothers had an HBV-DNA level less than 2000 IU/mL and 13% had HBV-DNA levels greater than 1.0×107 IU/mL so would be eligible for antiviral therapy to prevent transmission to the infant. 9% had active eAg-positive HBV and 3% had active eAg-negative HBV requiring treatment. All infants born to HBeAg-positive mothers received hepatitis B immunoglobulin (HBIG) appropriately and 76% of infants received a full HBV vaccination course. One infant born to an HBeAg-negative mother was hepatitis B surface antigen positive 1 year post-delivery.ConclusionsOne in six women had active HBV requiring treatment or high HBV-DNA levels that would benefit from antiviral treatment to reduce the transmission risk. HBIG was administered appropriately but completion of the vaccination course was suboptimal.
renal failure requiring short-term dialysis post transplantation. Long-term complications included biliary anastomotic stricture in 6 (31%) patients and vascular complications in 3 (2 hepatic artery thrombus, 1 hepatic vein stenting). One patient acquired hepatitis B from the transplanted liver. Reasons for re-transplantation were hepatic artery thrombosis (2), recurrent cirrhosis with portal hypertension (1) and primary non-function of the graft (1). Seven (35%) transplants had cirrhosis confirmed on biopsy (5) or clinically (ascites (1) or oesophageal varices (1)) at a mean time of 25.6 months post transplant (range 12e48 months). Five-year mortality in the cohort was 25%. Conclusion Hepatitis C accounted for <10% of OLT episodes in Northern Ireland during the study period. This demand may increase in the future as the chronic complications of previously undiagnosed hepatitis C are seen. One third of this small cohort developed cirrhosis within a few years of OLT.
):A1-A306 A93 BSG abstracts inflammation, inclusions, siderosis and neoplastic changes were scored semi-quantitatively. Results Median age was 54 and the majority (70%) were male. All patients had a long history of alcohol excess but reported abstinence for at least 6 months by transplantation. The aetiology was ALD (n = 80) and mixed ALD/HCV (n = 4). The majority (n = 83) had a mixed or macronodular cirrhosis with evidence of re-modelling in a significant number; one had pre-septal cirrhosis. Alpha-1 antitrypsin inclusion bodies were seen in 9 (10.7%); only 4 of these had serum A1AT levels below normal. Parenchymal siderosis was present in 39 (46.4%); in 19 (22.6%) this was grade 3-4. Amongst these, only single mutations of the HFE gene were identified. Induced cell change was seen in 67 (79.8%) and 47 (56%) had the "abstinent cell" phenotype. While 46 (54.8%) had Mallory-denk bodies (MDB), 22 (26.1% of total) patients had both "abstinent cells" and MDB. Ballooning (n = 45, 53.6%) and steatosis (n = 31, 36.9%) were also seen. HCC was present in 14 (16.7%), with dysplastic nodules in 15 (17.9%), small-cell change in 20 (23.8%) and large-cell change 50 (59.5%). Phlebosclerosis and parenchymal extinction were universal findings. Conclusion We describe a wide spectrum of histological features in a large cohort transplanted for end-stage ALD. We demonstrate that despite abstinence, over half have residual MDB and ballooning. Conversely, over half had the recently described "abstinent cell" phenotype. Therefore, the presence of MDB should not be used as evidence of continued alcohol consumption; the presence of induced or abstinent cells correlates more strongly with reported abstinence.
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