HBV Burden on Population, a Comparative Study between Two Districts Mardan and Charsadda of KPK, Pakistan

2018 ◽  
Vol 9 (09) ◽  
pp. 20269-20274 ◽  
Author(s):  
Iftikhar Ali Shah ◽  
Faheem Anwar ◽  
Ihtesham Ul Haq ◽  
Yasir Anwar ◽  
Faizan Ullah ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Hepatitis B Virus ◽  
Chronic Infection ◽  
Prevalence Ratio ◽  
Health Condition ◽  
The Other ◽  
Spread Rate ◽  
Blood Samples ◽  
B Virus ◽  
The World

The purpose of this study is to check out the spread rate of Hepatitis B Virus in the districts of Mardan and Charsadda, KPK Pakistan. As we know that Hepatitis results in damaging liver tissues, so it is one of the serious threats to the human health across the world. Hepatitis can give rise to acute and chronic infection which give rise to Liver cancer or Liver cirrhosis. It may be transfer from one person to another. Its transmission routs are oral, fecal and parental. The purpose of this paper is to check and judge health condition. Blood serum was collected from Mardan Medical Complex, Mardan and District Head Quarter, Charsadda. The paper was design to calculate anti-HBV antibody positive patients with ICT(immune-chromatography technique)based detection among various patients in MMC Mardan and DHQ hospital Charsada and from various regions of Mardan and Charsadda, KPK Pakistan.  Total of 10852 patients of HBV in Charsadda and 14168 patients of HBV in Mardan. The blood samples were collected from Oct 2017 to May 2018 from both districts of KPK. The method for testing blood sample was ICT (immune chromatography technique). Our study about 10852 patients in district Charsadda who were at the risk of HBV infection, 103 were screened positive with the prevalence ratio of 0.949%. On the other hand, 14168 patients`s samples were collected in district Mardan, among them 149 were detected positive and ratio of prevalence is 1.051%. According to the above study the ratio of prevalence is lower in Charsadda as compare to Mardan

scholarly journals Innumerable cerebral microbleeds in hepatitis B virus-related decompensated liver cirrhosis: a case report

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chi Hyuk Oh ◽  
Jin San Lee
Keyword(s):  
Liver Cirrhosis ◽  
Hepatic Encephalopathy ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Brain Mri ◽  
Cerebral Microbleeds ◽  
Amyloid Angiopathy ◽  
Decompensated Liver Cirrhosis ◽  
B Virus ◽  
The Brain

Abstract Background Cerebral microbleeds (CMBs) are small, rounded, dark-signal lesions on brain MRI that represent cerebral hemosiderin deposits resulting from prior microhemorrhages and are neuroimaging biomarkers of cerebral amyloid angiopathy (CAA). Here, we report a case of innumerable CMBs in a patient with hepatic encephalopathy underlying decompensated liver cirrhosis. Case presentation An 83-year-old woman diagnosed with hepatitis B virus-related liver cirrhosis 40 years before was referred to our neurology clinic for progressive disorientation of time and place, personality changes, and confusion with somnolence over 2 weeks. Based on the laboratory, neuroimaging, and electrophysiological findings, we diagnosed the patient with hepatic encephalopathy, and her symptoms recovered within 12 h after proper medical management. Brain MRI showed innumerable CMBs in the bilateral frontal, parietal, temporal, and occipital lobes. Since the distribution of CMBs in the patient was mainly corticosubcortical and predominantly in the posterior cortical regions, and the apolipoprotein E genotype was ε4/ε4, we speculated that CAA and hepatic encephalopathy coexisted in this patient. Conclusions We suggest that severe liver dysfunction associated with long-term decompensated liver cirrhosis may be related to an increased number of CMBs in the brain. Our findings indicate that decompensated liver cirrhosis may be a risk factor for the development of CMBs and corroborate a link between the liver and the brain.

The association between hepatitis B virus mutations and the risk of liver disease and hepatocellular carcinoma

2021 ◽  
Vol 21 ◽  
Author(s):  
Hassan Akrami ◽  
Mohammad Rafiee Monjezi ◽  
Shahrzad Ilbeigi ◽  
Farshid Amiri ◽  
Mohammad Reza Fattahi
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Immune Escape ◽  
Vaccine Failure ◽  
Occult Hbv Infection ◽  
Occult Hbv ◽  
B Virus ◽  
The World

: Hepatitis B virus [HBV], the best-described hepadnavirus, distributed all around the world and may lead to chronic and acute liver disease, cirrhosis, and hepatocellular carcinoma. Despite the advancement in treatment against HBV, an error-prone reverse transcriptase which is require for HBV replication as well as host immune pressure lead to constant evolution and emergence of genotypes, sub-genotypes and mutant viruses; so, HBV will be remained as a major healthcare problem around the world. This review article mainly focuses on the HBV mutations which correlated to occult HBV infection, Immune scape, vaccine failure and eventually liver cirrhosis and HCC. Current study indicated that preS/S region mutations are related to vaccine failure, immune escape, occult HBV infection and the occurrence of HCC. Whereas, P region Mutations may lead to drug resistance to NA antivirals. PreC/C region mutations are associated to HBeAg negativity, immune escape, and persistent hepatitis. Moreover, X region Mutations play an important role in HCC development.

Proportion of Nonalcoholic Steatohepatitis in Patients with Chronic Liver Disease

2021 ◽  
Vol 15 (6) ◽  
pp. 1272-1274
Author(s):  
H.A. Abro ◽  
B. A. Shaikh ◽  
A. H. Mugheri ◽  
I. A. Ansari ◽  
Z. A. Shaikh ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Hepatitis C Virus ◽  
Liver Disease ◽  
Hepatitis C ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Nonalcoholic Steatohepatitis ◽  
Smoking Status ◽  
Virus Hepatitis ◽  
B Virus

Aim: To determine the frequency of nonalcoholic steatohepatitis in patients with liver cirrhosis. Study Design: Retrospective/observational Place and Duration of Study: Department of Medicine, Chandka Medical College Hospital, Larkana from 1st July 2020 to 31st March 2021. Methodology: One hundred and twenty patients of both genders presented with liver cirrhosis were enrolled in this study. Patient’s detailed demographics including age, sex, body mass index, smoking status, alcohol consumption and family history of liver disease were recorded after taking written informed consent. Laboratory examination was done to examine the proportion of hepatitis B virus, hepatitis C virus and nonalcoholic steatohepatitis. Results: There were 68 (56.67%) males and 52 (43.33%) were females with mean age 45.74±10.54 years. Among all the patients hepatitis C virus was found in 62 (51.67%) patients, 15 (12.5%) had hepatitis B virus, 17 (14.17%) had hepatitis B virus + hepatitis C virus and nonalcoholic steatohepatitis was found in 26 (21.67%) patients. Conclusion: Nonalcoholic steatohepatitis was the major cause of liver cirrhosis in Pakistani population. The proportion of NASH in liver cirrhosis patients was 21.67%. Keywords: Nonalcoholic steatohepatitis (NASH), Liver Cirrhosis, Hepatitis B virus, Hepatitis C virus

scholarly journals Hepatitis B: diagnosis, prevention, and treatment

1997 ◽  
Vol 43 (8) ◽  
pp. 1500-1506 ◽  
Author(s):  
Norman Gitlin
Keyword(s):  
Risk Factors ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Infection ◽  
Laboratory Tests ◽  
Chronic Viral Hepatitis ◽  
Hbv Infection ◽  
B Virus ◽  
The Us ◽  
Prevention And Treatment

Abstract Hepatitis B virus (HBV) infection occurs worldwide and is an important cause of acute and chronic viral hepatitis in the US. In this review, I describe the virus, risk factors for infection, clinical features of infection, results of laboratory tests during infection, and standard and emerging treatment for chronic infection. Although 95% of adult patients recover completely from HBV infection, 90% of children ≤4 years of age develop chronic infection. Active vaccination is highly efficacious.

scholarly journals Clinical characteristics of patients with hepatitis B virus related liver cirrhosis and primary liver cancer

2015 ◽  
Vol 23 (17) ◽  
pp. 2798
Author(s):  
Feng Lv ◽  
Yu-Feng Gao ◽  
Jian-Guo Rao ◽  
Wei Zhang ◽  
Gui-Zhou Zou ◽  
...  
Keyword(s):  
Liver Cirrhosis ◽  
Hepatitis B Virus ◽  
Liver Cancer ◽  
Hepatitis B ◽  
Clinical Characteristics ◽  
Primary Liver Cancer ◽  
B Virus

scholarly journals Estimation of hepatitis B virus cccDNA persistence in chronic infection using within-host evolutionary rates

2020 ◽  
Author(s):  
Katrina A. Lythgoe ◽  
Sheila F. Lumley ◽  
Jane A. McKeating ◽  
Philippa C. Matthews
Keyword(s):  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Chronic Infection ◽  
Standard Of Care ◽  
Evolutionary Rates ◽  
Mathematical Framework ◽  
Novel Approach ◽  
B Virus ◽  
Order Of Magnitude ◽  
Progressive Liver Disease

AbstractHepatitis B virus (HBV) infection is a major global health problem with over 240 million infected individuals at risk of developing progressive liver disease and hepatocellular carcinoma. HBV is an enveloped DNA virus that establishes its genome as an episomal, covalently closed circular DNA (cccDNA) in the nucleus of infected hepatocytes. Currently available standard-of-care treatments for chronic hepatitis B (CHB) include nucleos(t)ide analogues (NA) that suppress HBV replication but do not target the cccDNA and hence rarely cure infection. There is considerable interest in determining the lifespan of cccDNA molecules to design and evaluate new curative treatments. We took a novel approach to this problem by developing a new mathematical framework to model changes in evolutionary rates during infection which, combined with previously determined within-host evolutionary rates of HBV, we used to determine the lifespan of cccDNA. We estimate that during HBe-antigen positive (HBeAgPOS) infection the cccDNA lifespan is 61 (36-236) days, whereas during the HBeAgNEG phase of infection it is only 26 (16-81) days. We found that cccDNA replicative capacity declined by an order of magnitude between HBeAgPOS and HBeAgNEG phases of infection. Our estimated lifespan of cccDNA is too short to explain the long durations of chronic infection observed in patients on NA treatment, suggesting that either a sub-population of long-lived hepatocytes harbouring cccDNA molecules persists during therapy, or that NA therapy does not suppress all viral replication. These results provide a greater understanding of the biology of the cccDNA reservoir and can aid the development of new curative therapeutic strategies for treating CHB.

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