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Epstein-Barr virus hepatitis can cause transient hepatopulmonary syndrome.

ABSTRACT:

Introduction

Hepatopulmonary syndrome is commonly seen in the patients with chronic liver disease. Acute liver diseases are rarely associated with HPS. We have reported here a case of Transient HPS caused by Epstein-Barr virus hepatitis.

Case report

The patient was a 31 years old man that came to hospital due to RUQ pain and yellowish skin. In examination the patient was tachypnic and O2 saturation was 71% with prominent JVP. ver enzyme and bilirubin were high. All viral hepatitis was negative except anti viral capsid antigen-antibody of EBV. In Blood gas PaO2 was 54?mmHg, O2 saturation 73% and alveolar-arterial gradient was 18?mmHg. Stress Echocardiography with saline injection reported pulmonary arterial pressure 32 cmHg with delayed opacification of left atrium.

Conclusion

transient HPS can be manifestation in the acute hepatitis caused by EBV infection.

SUBMITTER: Ghayumi SMA

PROVIDER: S-EPMC6010599 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Epstein-Barr virus hepatitis can cause transient hepatopulmonary syndrome.

Ghayumi Seiyed Mohammad Ali SMA Rohani Maryam M Hasanzadeh Sajad S Sadeghi Shahrokh S Roozbehi Amrollah A Jokar Saeid S

Respiratory medicine case reports 20180403

<h4>Introduction</h4>Hepatopulmonary syndrome is commonly seen in the patients with chronic liver disease. Acute liver diseases are rarely associated with HPS. We have reported here a case of Transient HPS caused by Epstein-Barr virus hepatitis.<h4>Case report</h4>The patient was a 31 years old man that came to hospital due to RUQ pain and yellowish skin. In examination the patient was tachypnic and O2 saturation was 71% with prominent JVP. ver enzyme and bilirubin were high. All viral hepatitis ...[more]

PMID: 29977758

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Project description:AIM:In recent years, studies have suggested that Epstein-Barr virus (EBV) is associated with HCC. The present study was to determine the prevalence of EBV in HCC patients, and whether EBV acted synergistically with hepatitis viruses in HCC carcinogenesis. METHODS:Liver tissue 115 HCC patients and 26 non-carcinoma patients were studied. Polymerase chain reaction (PCR) was performed to detect EBV BamHI W DNA, EBV LMP1 DNA, HBV X DNA, and HBV S DNA. Reverse transcription PCR (RT-PCR) was performed to detect HCV RNA and HDV RNA. Immunohistochemistry was performed to detect LMP1, HBsAg, HBcAg and HCV. The positive ratios were compared between HCC group and control group by chi2 test. RESULTS:Totally, 78 HCC samples whose beta-globulin DNA was positively detected by amplified PCR were selected. PCR was performed in all cases for EBV DNA and HBV DNA. RT-PCR was performed in 18 cases for HCV RNA and HDV RNA. EBV BamHI W and EBV LMP1 were positive in 18 and 6 cases, respectively. HBV X gene and HBV S gene were positive in 42 and 27 cases respectively. HCV was positive in one of the 18 cases, and none was positive for HDV. The positive rates were 28.2% (22 of 78) for EBV DNA (BamHI W and/or LMP1) and 56.4% (44 of 78) for HBV DNA (X gene and/or S gene) respectively. In addition, 12 cases were positive for both EBV DNA and HBV DNA. Among the 26 cases in the control group, 2 cases were positive for EBV BamHI W, 4 positive for HBV X gene and 3 positive for HBV S gene. The positive rates were 8.0% (2 of 26) and 23.1% (6 of 26), respectively, for EBV DNA and HBV DNA. The result of DNA sequencing of BamHI W was 100% homologous with the corresponding sequence of B95-8. There was significant difference in EBV infection rate between HCC patients and controls (chi2 = 4.622, P<0.05). The difference in HBV infection rate was also significant (chi2 = 8.681, P<0.05). However, there was no obvious correlation between HBV and EBV in HCC patients (chi2 = 0.835, P>0.05). LMP1, HBV (HBsAg, HBcAg) and HCV were detected positively in 25, 45 and 6 of 78 cases of HCC tissues respectively. In the 26 control cases, the corresponding positive cases were 2, 4 and 0. The difference in EBV infection rate between HCC patients and control cases was statistically significant (chi2 = 6.02, P<0.05). The difference in HBV infection rate was also statistically significant (chi2 = 10.03, P<0.05). In the 25 cases with positive LMP1 expression, 6 were in the nuclei of tumor cells, 9 in the cytoplasm of tumor cells and 10 in mesenchymal lymphocyte cytoplasm. CONCLUSION:The existence of EBV infection in HCC tissues suggests that EBV may be involved in the hepatocellular carcinogenesis in China. HBV infection may be a major cause of HCC. There is no correlation between EBV and HBV in the development of HCC. The prevalence of HCV infection is low in our area, and HDV appears not to play a direct role in hepatocellular carcinogenesis.

Dataset Information

Epstein-Barr virus hepatitis can cause transient hepatopulmonary syndrome.

Introduction

Case report

Conclusion

Publications

Epstein-Barr virus hepatitis can cause transient hepatopulmonary syndrome.

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