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1.
Panminerva Med ; 54(1): 1-9, 2012 Mar.
Article in English | MEDLINE | ID: mdl-22278112

ABSTRACT

Hepatitis C virus (HCV) is the most common infectious cause of chronic liver disease in Europe. With the introduction of interferon based therapy in combination with ribavirin treatment of chronic HCV has become feasible. This therapy has become the standard of care for patients with HCV and depending on the HCV genotype treatment is successful in 40-70% of patients. In the recent years a new class of drugs have emerged that changed the landscape of HCV treatment. These direct antiviral agents inhibit the NS3/N4A serine protease of HCV. Prototypes are telaprevir and boceprevir and they specifically exert antiviral activity against genotype 1 HCV. A series of landmark trials has paved the way for introduction of these agents, and they have documented a great improvement in the care of genotype 1 HCV patients. Telaprevir and boceprevir are given in combination with pegylated interferon and ribavirin and are useful for treatment naive as well as treatment experienced patients. The clinician should be aware of these developments as they have implications for side effect management, and drug-drug interactions. Finally, strategic use of these agents comes with stopping rules and require close monitoring of the HCV viral load.


Subject(s)
Antiviral Agents/therapeutic use , Hepatitis C/drug therapy , Antiviral Agents/adverse effects , Drug Therapy, Combination , Hepatitis C/diagnosis , Hepatitis C/epidemiology , Humans , Patient Selection , Practice Guidelines as Topic , Risk Assessment , Risk Factors , Treatment Outcome , Viral Load
2.
Neth J Med ; 69(9): 367-71, 2011 Sep.
Article in English | MEDLINE | ID: mdl-21978978

ABSTRACT

Autosomal dominant polycystic kidney disease (ADPKD) is a multisystem disorder. It is the most common genetic cause of end-stage renal disease. One frequent extra-renal manifestation is hepatic cyst formation. The majority of ADPKD patients develop complications as a result of renal cyst formation; however, a small proportion develop extensive hepatic disease with minor renal features. Both phenotypes seem to represent the spectrum of ADPKD. This review discusses the current understanding of the pathogenesis of the disease, its manifestations and the mechanisms of cyst formation. Furthermore, it focuses on monitoring the disease and the treatment options currently available.


Subject(s)
Kidney Failure, Chronic/etiology , Liver Diseases/etiology , Polycystic Kidney, Autosomal Dominant/complications , Humans , Hypertension/etiology , Liver Diseases/therapy , Polycystic Kidney, Autosomal Dominant/diagnosis , Polycystic Kidney, Autosomal Dominant/genetics , Polycystic Kidney, Autosomal Dominant/therapy
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