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1.
J Viral Hepat ; 20 Suppl 2: 1-20, 2013 Aug.
Article in English | MEDLINE | ID: mdl-23827008

ABSTRACT

The burden of disease due to chronic viral hepatitis constitutes a global threat. In many Balkan and Mediterranean countries, the disease burden due to viral hepatitis remains largely unrecognized, including in high-risk groups and migrants, because of a lack of reliable epidemiological data, suggesting the need for better and targeted surveillance for public health gains. In many countries, the burden of chronic liver disease due to hepatitis B and C is increasing due to ageing of unvaccinated populations and migration, and a probable increase in drug injecting. Targeted vaccination strategies for hepatitis B virus (HBV) among risk groups and harm reduction interventions at adequate scale and coverage for injecting drug users are needed. Transmission of HBV and hepatitis C virus (HCV) in healthcare settings and a higher prevalence of HBV and HCV among recipients of blood and blood products in the Balkan and North African countries highlight the need to implement and monitor universal precautions in these settings and use voluntary, nonremunerated, repeat donors. Progress in drug discovery has improved outcomes of treatment for both HBV and HCV, although access is limited by the high costs of these drugs and resources available for health care. Egypt, with the highest burden of hepatitis C in the world, provides treatment through its National Control Strategy. Addressing the burden of viral hepatitis in the Balkan and Mediterranean regions will require national commitments in the form of strategic plans, financial and human resources, normative guidance and technical support from regional agencies and research.


Subject(s)
Carcinoma, Hepatocellular/epidemiology , Hepatitis B, Chronic/epidemiology , Hepatitis C, Chronic/epidemiology , Liver Neoplasms/epidemiology , Antiviral Agents/economics , Antiviral Agents/therapeutic use , Balkan Peninsula/epidemiology , Carcinoma, Hepatocellular/etiology , Cross Infection/epidemiology , Cross Infection/prevention & control , Cross Infection/transmission , Disease Transmission, Infectious/prevention & control , Epidemiological Monitoring , Hepatitis B Vaccines/administration & dosage , Hepatitis B, Chronic/complications , Hepatitis B, Chronic/diagnosis , Hepatitis B, Chronic/prevention & control , Hepatitis C, Chronic/complications , Hepatitis C, Chronic/diagnosis , Hepatitis C, Chronic/prevention & control , Humans , Liver Neoplasms/etiology , Mediterranean Region/epidemiology , Treatment Outcome , Vaccination/statistics & numerical data
2.
Clin Genet ; 69(5): 404-9, 2006 May.
Article in English | MEDLINE | ID: mdl-16650078

ABSTRACT

Familial adenomatous polyposis (FAP) is one of the two commonest familial syndromes that predispose to colorectal cancer. FAP is caused by mutations in the adenomatous polyposis coli (APC) tumour suppressor gene that has a high penetrance. The disease is characterized by the occurrence of hundreds to thousands of colorectal polyps, which if left untreated give rise to colorectal cancer. In Cyprus, there are no molecular data available as yet on families with FAP. This work presents the results of APC analysis in our population for the first time. The APC gene was analyzed in 33 DNA samples from 20 individuals belonging to four FAP families and 13 patients with sporadic polyposis. We identified three truncating mutations, four missense mutations and 11 polymorphisms. It is of interest that two of the three truncating mutations, 2307delA and Q1242X, are novel, which supports the existence of a unique genetic pool in the Cypriot population. This ethnic molecular study in addition to highlighting population heterogeneity also contributes to phenotype-genotype associations that are essential for the clinical management of FAP families in Cyprus.


Subject(s)
Adenomatous Polyposis Coli/genetics , Genes, APC , Germ-Line Mutation , Adenomatous Polyposis Coli/diagnosis , Adolescent , Adult , Cyprus/ethnology , DNA Mutational Analysis , Female , Humans , Male , Middle Aged , Polymorphism, Genetic
3.
Dig Dis Sci ; 32(3): 332, 1987 Mar.
Article in English | MEDLINE | ID: mdl-3816487
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