Journal of Pharmacy Practice

Chronic hepatitis B is a global health concern in many resource-limited settings due to perinatal or pediatric hepatitis B virus transmission. In the United States, pediatric infection has been virtually eliminated due to maternal screening during pregnancy and the availability of an effective vaccine. However, young adults remain an at-risk group for hepatitis B virus infection due to sexual transmission and injection drug use. The frequency of progression from acute hepatitis B virus infection to chronic hepatitis B infection depends on multiple factors, including host immune function and age at time of hepatitis B virus infection. Fortunately, there are 7 currently approved therapies for chronic hepatitis B infection, and several emerging therapies that show promise. Despite the availability of these agents, many clinical questions still surround chronic hepatitis B therapy including when to start therapy, which agent is ideal for first and second line therapy, the appropriate duration of therapy, and the role of combination antiviral therapy. This review focuses on agents available for chronic hepatitis B management, including pharmacology, safety and efficacy data, monitoring parameters, and the role for each in chronic hepatitis B therapy in adult patients.

Chronic liver diseases are a significant cause of death worldwide. Cirrhosis is most frequently caused by hepatitis C or alcohol abuse, but other nonviral etiologies are now recognized as important contributors to the development of hepatitis. Nonalcoholic fatty liver disease, caused by abnormal accumulation of lipids in hepatocytes, can progress from simple steatosis to necroimflammation and cirrhosis. It is estimated to occur in up to 40% of the general population, and its pathophysiology is closely linked to features of metabolic syndrome. There is currently no proven treatment for nonalcoholic fatty liver disease. Management strategies largely address identification and treatment of associated risk factors and include drug therapy for obesity, insulin resistance (eg, metformin, thiazolidinediones), and dyslipidemia (eg, fibrates, HMG-CoA reductase inhibitors). Autoimmune hepatitis is characterized by necroinflammation mediated by autoantibody attack against liver antigens in genetically predisposed patients. It is considered a rare form of chronic liver disease but can progress to cirrhosis if unrecognized and untreated. Autoimmune hepatitis usually responds well to long-established immunosuppressive regimens with prednisone and azathioprine; however, new approaches are required for those patients who do not achieve or sustain desired outcomes or are intolerant to standard therapy.

Despite reductions in the incidence of new hepatitis C virus infections, infections from previous decades continue to place a substantial burden on our health care system. Although the course of the disease is highly variable, approximately 20% to 30% of patients develop cirrhosis, end-stage liver disease, or hepatocellular carcinoma. Fortunately, treatment with our current standard of care, peginterferon a and ribavirin, can reduce the complications of chronic liver disease. However, these drugs are associated with significant adverse effects, many patients are ineligible for treatment, and only 50% are cured. Thus, there is a tremendous need to improve our current therapies and develop new compounds for this disease. This review highlights the transmission, pathophysiology, and course of illness; the pharmacokinetics, proposed mechanisms of action, adverse events, and potential drug interactions with peginterferon a and ribavirin; current treatment trends; the role of the pharmacist in the treatment of this disease; and investigational drugs in later stages of clinical development. Despite the initial hope that these new drugs would replace our current standard of care, it has become clear that ribavirin and peginterferon a will continue to play an important role in the treatment of chronic hepatitis C virus in the years to come.

The authors present a case of nightmares induced by the 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) reductase inhibitors simvastatin and fluvastatin. A 79-year-old Caucasian male initially treated with simvastatin 10 mg every evening developed nightmares after the dose was increased to 40 mg. No relief was provided with a dose reduction to 20 mg, and simvastatin was held. Simvastatin was restarted 7 weeks later at 10 mg, with no complaints of nightmares until the dose was escalated to 20 mg. Simvastatin therapy was subsequently stopped. One month later, fluvastatin 80 mg was initiated and nightmares returned within 3 months, necessitating discontinuation of fluvastatin. The patient was rechallenged with fluvastatin 80 mg, and the nightmares returned 1 month later. Statin therapy was discontinued, and the patient was started on ezetimibe 10 mg. Lipophilic statins such as atorvastatin, lovastatin, and simvastatin have been associated with sleep disturbances. However, lipophilicity may not predict the likelihood of these adverse effects among the statins. Patients prescribed a statin should be counseled on sleep disturbances as potential adverse effects and should be encouraged to notify their providers if these disturbances develop.

Retraction

Erratum