Epidemiological study of viral hepatitis types A, B, C, D and E among Inuits in West Greenland

Langer, Barbara; Frösner, Gert; Brunn, Albrecht von

doi:10.1046/j.1365-2893.1997.00063.x

Cited by 42 publications

(42 citation statements)

References 27 publications

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“…However, other circumpolar regions outside of Canada had much lower prevalence rates. In Greenland, seropositivty for HCV was 0% to 1.5% and Alaska Native individuals had a seroprevalence of 0.8% [134][135][136].…”

Section: Discussionmentioning

confidence: 99%

Serological and molecular epidemiological outcomes after two decades of universal infant hepatitis B virus (HBV) vaccination in Nunavut, Canada

Huynh¹,

Minuk

Uhanova

et al. 2017

Vaccine

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Section: Discussionmentioning

confidence: 99%

Serological and molecular epidemiological outcomes after two decades of universal infant hepatitis B virus (HBV) vaccination in Nunavut, Canada

Huynh¹,

Minuk

Uhanova

et al. 2017

Vaccine

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“…However, the risk of hepatocellular carcinoma was not increased among first-degree relatives. A possible association might be obscured, as the incidence of hepatocellular carcinoma in Greenland is low, despite a high prevalence of HBsAg carriers (2,37,38), indicating a limited influence of hepatitis B infection on the risk of hepatocellular carcinoma among Greenlanders. Likewise, an increased risk of EBV-associated Hodgkin's lymphoma could have been expected (4), but Hodgkin's lymphoma is a rare malignancy in the Inuit population (2).…”

Section: Discussionmentioning

confidence: 99%

Cancer Susceptibility in Nasopharyngeal Carcinoma Families—A Population-Based Cohort Study

et al. 2005

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Undifferentiated nasopharyngeal carcinoma is a result of environmental factors, in particular EBV infection, affecting genetically susceptible individuals. The familial risk of nasopharyngeal carcinoma is among the highest of any malignancy. Whether this susceptibility is restricted to nasopharyngeal carcinoma is unknown as information on the risk of other cancers in relatives is limited. We did a population-based study of the cancer incidence in nasopharyngeal carcinoma families in Greenland, a nasopharyngeal carcinoma-endemic area. Using population-based registers, a cohort of all persons born in Greenland was followed from 1973 to 2002. In this cohort, 134 individuals developed nasopharyngeal carcinoma and their relatives were identified through registers and interviews. Subsequently, the occurrence of cancer was determined by linkage to the populationbased cancer register and the risk of cancer in nasopharyngeal carcinoma relatives and nonrelatives compared by relative risks. Among 766 first-degree relatives, the relative risk of nasopharyngeal carcinoma following the family index case was 8.0 [95% confidence interval (95% CI), 4.1-14.0]. Sex and age of the relative or the index case had no modifying effect on the familial risk of nasopharyngeal carcinoma. The relative risks of carcinoma of the salivary glands, 8.4 (95% CI, 2.7-19.5), and uterine cervix, 2.2 (95% CI, 1.1-3.9), were also significantly increased. In families with multiple cases of nasopharyngeal carcinoma, the risk of other cancers than nasopharyngeal carcinoma was further increased. These results indicate that the increased risk of cancer in nasopharyngeal carcinoma families is not restricted to nasopharyngeal carcinoma, but extends to the virally associated cancers of the salivary glands and cervical uteri. (Cancer Res 2005; 65(18): 8567-72)

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“…17,[31][32][33][34][35] However, precore mutants have also been detected in Northern Europe, 22 United Kingdom, 36 and Canada. 37 In Asian countries, where both A and non-A genotypes exist, in addition to precore mutants, BCP mutants are found. 38 For example in a recent study from China, 38% of the HBeAg-negative patients harbored the precore stop codon, 42% possessed the double BCP mutation and 12% had both mutations.…”

Section: Prevalencementioning

confidence: 99%

Hepatitis B e antigen-negative chronic hepatitis B

2001

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Thirty years ago, the diagnosis of chronic hepatitis B (CHB) was thought to require the presence of hepatitis B e antigen (HBeAg), as a reliable and sensitive marker of hepatitis B virus (HBV) replication. 1 Individuals positive for hepatitis B surface antigen (HBsAg) but negative for HBeAg were considered to have nonreplicative HBV infection, and if their liver enzymes were normal or nearly normal they were referred to as asymptomatic or healthy HBsAg or HBV carriers. 2 If, on the other hand, they displayed elevated serum aminotransferases and liver histology indicative of chronic hepatitis, they were generally thought to be suffering from other superimposed or complicating conditions such as hepatitis D virus infection, alcohol-induced, metabolic, autoimmune, drug-induced, or other forms of chronic liver disease. 3 In the early 1980s it became apparent that HBV could replicate in the absence of HBeAg. [4][5][6] Patients from the Mediterranean area, although negative for HBeAg and positive for antibodies to HBeAg (anti-HBe), were reported to have CHB with replicating HBV. 7 The term anti-HBe-positive or HBeAgnegative CHB was then proposed 4 and subsequently became widely accepted. In 1989 the molecular basis of this form of CHB was discovered 8,9 with the identification of HBV mutations preventing HBeAg formation from an otherwise normally replicating HBV. 10,11 With time, it became apparent that HBeAg-negative CHB, initially viewed as an atypical and rare form of CHB mainly restricted in the Mediterranean area, had a much wider geographical distribution and that its frequency was increasing. 12 Its molecular virology and immunology were found to be more complex than initially thought, 13 whereas the selection of precore HBV mutants was shown to be largely determined by the HBV genotype. 14 Mutations abolishing or diminishing HBeAg formation were identified along with changes in other parts of the HBV genome. 14 More recently, the new nucleoside analog, lamivudine, has been used to treat a sizeable number of patients with HBeAg-negative CHB, and important information on its efficacy and the development of resistance has been collected. [15][16][17][18] DEFINITION AND NOMENCLATUREThe term HBeAg-negative CHB defines the condition as disease caused by strains of HBV that are not producing HBeAg. 12 It does not specify the mutations responsible for the lack of HBeAg, i.e., a precore stop-codon mutation, 10 a double basic core promoter (BCP) mutation, or other, 14 and it says nothing about the level of HBV replication. The alternative term "precore mutant CHB," used by some investigators, also does not specify the nature of the precore mutation. In clinical practice, the term HBeAg-negative CHB is appropriate for patients with chronic HBV infection who test negative for HBeAg, are usually positive for anti-HBe, have increased alanine aminotransferase (ALT) levels and display detectable HBV DNA in serum by classical hybridization techniques. 12 Despite the fact that the identification of the underlying mutations in ...

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Epidemiological study of viral hepatitis types A, B, C, D and E among Inuits in West Greenland

Cited by 42 publications

References 27 publications

Serological and molecular epidemiological outcomes after two decades of universal infant hepatitis B virus (HBV) vaccination in Nunavut, Canada

Serological and molecular epidemiological outcomes after two decades of universal infant hepatitis B virus (HBV) vaccination in Nunavut, Canada

Cancer Susceptibility in Nasopharyngeal Carcinoma Families—A Population-Based Cohort Study

Hepatitis B e antigen-negative chronic hepatitis B

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