High prevalence of hepatitis B virus infection and inferior vena cava obstruction among patients with liver cirrhosis or hepatocellular carcinoma in Nepal

Shrestha, Santosh Man; Shrestha, Ananta; Tsuda, Fumio; Endo, Kazuyuki; Takahashi, Masaharu; Okamoto, Hiroaki

doi:10.1111/j.1440-1746.2006.04611.x

Cited by 20 publications

(28 citation statements)

References 46 publications

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“…Interestingly, the further west, the more ‘CD2’ recombinant can be observed. Across the Himalayas, genotype D is the most prevalent HBV strain, followed by genotypes A and C in India and Nepal [27], [28], [29]. Our results demonstrate that the HBV C/D recombinant is restricted to a specific region in western China, mainly on the Qinghai-Tibet Plateau, which rises about 4000 meters above sea level.…”

Section: Discussionmentioning

confidence: 69%

Geographical and Ethnic Distribution of the HBV C/D Recombinant on the Qinghai-Tibet Plateau

et al. 2011

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Two forms of hepatitis B virus (HBV) C/D recombinant have been identified in western China, but little is known about their geographical and ethnic distributions, and particularly the clinical significance and specific mutations in the pre-core region. To address these questions, a total of 624 chronic HBV carriers from four ethnic populations representing five provinces in western China were enrolled in this study. Genotypes were firstly determined by restriction fragment length polymorphism, and then confirmed by full or partial genome nucleotide sequencing. The distribution of HBV genotypes was as follows: HBV/B: 40 (6.4%); HBV/C: 221 (35.4%); HBV/D: 39 (6.3%); HBV/CD: 324 (51.9%). In the 324 HBV C/D recombinant infections, 244 (75.3%) were infected with the “CD1” and 80 (24.7%) were infected with the “CD2.” The distribution of HBV genotypes exhibited distinct patterns in different regions and ethnic populations. Geographically, the C/D recombinant was the most prevalent HBV strain on the Qinghai-Tibet Plateau. Ethnically, the C/D recombinant had a higher prevalence in Tibetan patients than in other populations. Clinically, patients with HBV/CD1 showed significantly lower levels of serum total bilirubin than patients with HBV/C2. The prevalence of HBeAg was comparable between patients with HBV/CD1 and HBV/C2 (63.3% vs 50.0%, P = 0.118) whether patients were taken together or stratified by age into three groups (65.6% vs 58.8% in <30 years, P = 0.758; 61.9% vs 48.0% in 30–50 years, P = 0.244; 64.3% vs 33.3%, P = 0.336). Virologically HBV/CD1 had a significantly lower frequency of G1896A than HBV/C2. In conclusion, the HBV C/D recombinant is restricted to the Qinghai-Tibet Plateau in western China and is found predominantly in Tibetans. The predominance of the premature pre-core stop mutation G1896A in patients with the HBV C/D recombinant may account for the higher prevalence of HBeAg in these patients.

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Section: Discussionmentioning

confidence: 69%

Geographical and Ethnic Distribution of the HBV C/D Recombinant on the Qinghai-Tibet Plateau

et al. 2011

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“…It was confirmed by inferior vena cavography [10] in 31, hepatography or transhepatic venography [25] in 5, and liver biopsy in 34 patients. Patients were assessed for other risk factors for cirrhosis and HCC such as alcohol (alcohol consumption of C40 g of ethanol per day for C5 years was considered significant), hepatitis B (HBsAg, anti-HBc, and HBV DNA) and hepatitis C virus (HCV) infections (anti-HCV, HCV RNA) by methods described earlier [20].…”

Section: Methodsmentioning

confidence: 99%

“…The reported incidence (Table 1) of LC in the disease had varied from 71% to 100% [2,3,5] and that of HCC from 4.6% to 47% [2,3,5,7,9,11,12,18,19]. As HVD occurred in areas endemic for hepatitis B virus (HBV) infection [11,20], some considered HBV infection as the likely cause of LC/HCC in this disease [21]. Findings of equally high incidence of HCC in IVCO S. M. Shrestha (&) Liver Foundation Nepal, Sitapaela Height, P.O.…”

Section: Introductionmentioning

confidence: 99%

Liver cirrhosis and hepatocellular carcinoma in hepatic vena cava disease, a liver disease caused by obstruction of inferior vena cava

Shrestha¹

2009

Hepatol Int

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Purpose Hepatic vena cava disease (HVD), a form of Budd-Chiari syndrome, is caused by the obstruction of hepatic portion of the inferior vena cava. It is a chronic disease characterized by the development of liver cirrhosis (LC) and hepatocellular carcinoma (HCC). As HVD occurred in areas with high incidence of hepatitis B virus (HBV) infection and some patients tested HBsAg positive, it was thought to be the cause of LC and HCC. To assess the pathogenesis of LC or HCC in HVD, a long-term follow-up study was done. Method Fifty-six patients with HVD diagnosed by ultrasound (US) and confirmed by cavography in 31 and liver biopsy in 34 were followed up for an average of 14.8 ± 9 years. The occurrence of LC was diagnosed by US and/or liver biopsy and that of HCC by US, elevated level of a-fetoprotein, and liver biopsy or fine-needle aspiration cytology, or computed tomographic scan. Other risk factors for LC/HCC such as alcohol use and HBV and hepatitis C virus (HCV) infections were assayed. Results Forty-four (78.5%) and 6 (10.7%) patients developed cirrhosis and HCC, respectively. LC/HCC occurred more frequently among those who had severe or frequent acute exacerbations (P = 0.017), but it was not related to alcohol use or HBV and HCV infections. Conclusion HVD is independent risk factors for LC and HCC. Severe and/or recurrent loss of hepatocytes caused by hepatic venous outflow obstruction and/or thrombotic obstruction of small radicals of hepatic and portal veins that occurred during acute exacerbations was considered important in the pathogenesis of LC and HCC in HVD.

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“…According to Epstein, there is no connection between hepatic decompensation and disturbance in renal sodium handling leading to ascites (76). In developing countries, HVCS is a common comorbid condition in patients with LC and HCC related to chronic hepatitis B and C or alcohol (77). Development of ascites in LC patient may be due to severe AE of associated HVCS that responds to medical treatment.…”

Section: Differential Diagnosis Of Primary Diseases Of Hvoomentioning

confidence: 99%

Hepatic Venous Outflow Obstruction: Suggestion of a New Classification

Shrestha¹

2017

jrenhep

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Hepatic venous outflow obstruction (HVOO) is common in developing countries. It is a serious condition that clinically manifests with ascites from sinusoidal hypertension, and carries the risk of high mortality or development of liver cirrhosis. In the past, the eponym Budd-Chiari Syndrome (BCS) was used synonymously for HVOO. In the West, hepatic vein (HV) thrombosis caused by prothrombotic disorders is the main cause of HVOO. In the East, obliterative disease of hepatic portion of inferior vena cava induced by bacterial infection, now renamed hepatic vena cava syndrome, is the common cause of HVOO. These two diseases with different etiology, epidemiology, and natural history are at present grouped together under BCS causing much confusion. Sinusoidal obstruction syndrome, another important cause of HVOO at the level of the sinusoid and terminal HV, was left out in the classification of HVOO. In this article, the pathophysiology of sinusoidal hypertension is described, the term BCS is redefined, and a new classification of HVOO is suggested.

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High prevalence of hepatitis B virus infection and inferior vena cava obstruction among patients with liver cirrhosis or hepatocellular carcinoma in Nepal

Abstract: Hepatitis B virus alone (especially genotype A) or in concert with IVCO may be responsible for development of HCC in Nepal.

Cited by 20 publications

References 46 publications

Geographical and Ethnic Distribution of the HBV C/D Recombinant on the Qinghai-Tibet Plateau

Geographical and Ethnic Distribution of the HBV C/D Recombinant on the Qinghai-Tibet Plateau

Liver cirrhosis and hepatocellular carcinoma in hepatic vena cava disease, a liver disease caused by obstruction of inferior vena cava

Hepatic Venous Outflow Obstruction: Suggestion of a New Classification

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