ABSTRACT
Combination therapy with pegylated interferon alfa (PEG-IFN alfa) and the nucleoside analogue ribavirin is the current standard of care in patients infected with hepatitis C virus (HCV). Patients with HCV genotype 1 have a much less favorable response to therapy and are treated for 12 months, compared with patients infected with genotypes 2 and 3, in whom a 6-month course of therapy is sufficient. If viremia is present after 6 months, additional therapy has a negligible benefit, and treatment should be stopped in all patients regardless of the viral genotype. With HIV coinfection, all patients with a response to therapy at the end of 6 months should receive an additional 6 months of combination therapy regardless of the genotype. Patients with acute HCV infection should be treated for 6 months. The addition of protease inhibitors to the combination of PEG-IFN alfa and ribavirin is becoming the new standard of care for the treatment of chronic HCV infection. Regimens that include a protease inhibitor significantly improve sustained virologic response rates in patients with genotype 1 HCV infection.
Subject(s)
Drug Therapy, Combination/methods , Hepacivirus/genetics , Hepatitis C/drug therapy , Interferon-alpha/therapeutic use , Polyethylene Glycols/therapeutic use , Protease Inhibitors/therapeutic use , Ribavirin/therapeutic use , Genotype , Hepatitis C/prevention & control , Humans , Interferon-alpha/adverse effects , Liver Transplantation/adverse effects , Oligopeptides , Polyethylene Glycols/adverse effects , Proline/analogs & derivatives , Recombinant Proteins/adverse effects , Recombinant Proteins/therapeutic use , Recurrence , Ribavirin/adverse effects , Sofosbuvir , Time Factors , Uridine Monophosphate/analogs & derivatives , Uridine Monophosphate/therapeutic useABSTRACT
Variceal bleeding is one of the dreaded complications of portal hypertension. Although its prognosis has improved over the last several decades, it still carries substantial mortality. Although most portal hypertensive bleeds result from the ruptured distal esophageal varices, bleeding from other sources such gastric varices, portal hypertensive gastropathy, and ectopic varices can lead to clinically significant bleeding. Variceal bleeding typically presents as massive gastrointestinal (GI) bleeding with hematemesis, melena or hematochezia. In general, the terapeutic aims of management are to initially correct hypovolemia, to control bleeding, to prevent complications of bleeding, such as infection and renal failure and to prevent early rebleeding. The treatment of bleeding esophageal varices differs substantially foom the treatment of other lesions of the upper gastrointestinal tract. Moreover, patients with esophageal varices typically have severe liver disease and thus are likely from poor nutrition, blood clotting disorders, and encephalopathy, all of which can adversaly affect morbidity and mortality.