Community Pharmacy Supply for Hepatitis c pharmaceutical Care Information Pack



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Current HCV Medications


The primary goal of HCV therapy is to cure the infection, which leads to a reduction of patients developing the complications of the virus including cirrhosis and hepatocellular cancer (HCC)
In patients who achieve a SVR, antiviral agents shorten the clinical course of HCV, prevent complications, prevent latent and/or subsequent recurrences, decrease transmission, and eliminate established latency.

Peginterferon alfa-2b (ViraferonPeg®)


PEG-IFN alfa-2b consists of IFN alfa-2b attached to a single 12-kd PEG chain. It is excreted by the kidneys. The adult dose is 1.5 mcg/kg subcutaneous (SC).

Peginterferon alfa-2a (Pegasys®)


PEG-IFN alfa-2a consists of IFN alfa-2a attached to a 40-kd branched PEG molecule. The adult dosage is 180 mcg via SC injection once weekly in the thigh or abdomen.

Ribavirin (Rebetol®, Copegus®)


Ribavirin is an antiviral nucleoside analogue. Given alone, ribavirin has little effect on the course of hepatitis C. Given with IFN, it significantly augments the rate of sustained virologic response. Please refer to either the Copegus or Rebetol SPC as it gives further details on the dosing (based on weight and genotype)

Note that pregnancy must be excluded before treatment and effective contraception is essential during therapy and for 4 months after for women and 7 months after for men.

Common side effects when using PEG-IFN plus ribavirin include flu like symptoms, low mood, rash, dry skin, fatigue, anaemia, ophthalmic disturbance and GI disturbance. See summary of product characteristics for further information www.medicines.org.uk.

Boceprevir (Victrelis®)


NS3/4A protease inhibitors interfere with the ability of HCV to replicate by inhibiting a key viral enzyme, NS3/4A serine protease. Boceprevir inhibits replication of the hepatitis C virus by binding reversibly to NS3 serine protease. Boceprevir must be administered in combination with PEG-INF alfa and ribavirin. The dosage is 800 mg orally 3 times daily. Boceprevir is indicated for the treatment of chronic hepatitis C (CHC) genotype 1 infection, in combination with peginterferon alfa and ribavirin, in adult patients with compensated liver disease who are previously untreated or who have failed previous therapy.

Telaprevir (Incivo®)


Telaprevir inhibits HCV NS3/4A protease needed for proteolytic cleavage of the HCV-encoded poly-protein into mature forms. It is indicated for chronic hepatitis C genotype 1 infection in combination with peginterferon alfa and ribavirin. Indication is specifically for adults with compensated liver disease, including cirrhosis, who are treatment-naive or who have been previously treated with interferon-based treatment, including prior null responders, partial responders, and relapsers.

Newly licensed agents in 2014

Directly Acting Antiretrovirals


Contributor Information and Disclosures

Author


Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA  Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center

Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada

Disclosure: Pfizer Inc Honoraria Speaking and teaching

Chief Editor



Julian Katz, MD  Clinical Professor of Medicine, Drexel University College of Medicine

Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law, Medicine & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

Additional Contributors



Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership



George Y Wu, MD, PhD Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine

George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians

Disclosure: Springer Consulting fee Consulting; Gilead Consulting fee Review panel membership; Gilead Honoraria Speaking and teaching; Bristol-Myers Squibb Honoraria Speaking and teaching; Springer Royalty Review panel membership

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment


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  96. Gane EJ, Stedman CA, Hyland RH, Ding X, Svarovskaia E, Symonds WT, et al. Nucleotide polymerase inhibitor sofosbuvir plus ribavirin for hepatitis C. N Engl J Med. Jan 3 2013;368(1):34-44. [Medline].

 



 

Hepatitis C. Causes of chronic liver disease. Courtesy of the US Centers for Disease Control and Prevention.



Hepatitis C viral genome. Courtesy of Hepatitis Resource Network.

Natural history of hepatitis C virus infection.

Diagnostic algorithm for hepatitis C virus infection.

Evolution of the treatment of hepatitis C virus infection.

Pegylated interferon alfa-2b plus ribavirin therapy for chronic hepatitis C.

Cold agglutinin disease indistinguishable from cryoglobulinemia. Courtesy of Walter Reed Army Medical Center Dermatology.

Cryoglobulinemia, palpable purpura, dysproteinemic purpura, and leukocytoclastic vasculitis (small vessel vasculitis). Courtesy of Walter Reed Army Medical Center Dermatology.

Cutis marmorata. Courtesy of Walter Reed Army Medical Center Dermatology.

Erythema multiforme, bull's-eye lesions. Courtesy of Walter Reed Army Medical Center Dermatology.

Erythema dyschromicum perstans. Courtesy of Walter Reed Army Medical Center Dermatology.

Erythema dyschromicum perstans. Courtesy of Walter Reed Army Medical Center Dermatology.

Erythema nodosa. Courtesy of Walter Reed Army Medical Center Dermatology.

Erythema nodosa. Courtesy of Walter Reed Army Medical Center Dermatology.

Erythema multiforme. Courtesy of Walter Reed Army Medical Center Dermatology.

Erythema multiforme. Courtesy of Walter Reed Army Medical Center Dermatology.

Erythema multiforme. Courtesy of Walter Reed Army Medical Center Dermatology.

Erythema multiforme of the oral mucosa. Courtesy of Walter Reed Army Medical Center Dermatology.

Erythema multiforme (Stevens-Johnson syndrome). Courtesy of Walter Reed Army Medical Center Dermatology.

Palmar erythema. Courtesy of Walter Reed Army Medical Center Dermatology.

Granuloma annulare. Courtesy of Walter Reed Army Medical Center Dermatology.

Disseminated superficial (actinic) porokeratosis. Courtesy of Walter Reed Army Medical Center Dermatology.

Disseminated superficial (actinic) porokeratosis. Courtesy of Walter Reed Army Medical Center Dermatology.

Lichen planus. Courtesy of Walter Reed Army Medical Center Dermatology.

Lichen planus. Courtesy of Walter Reed Army Medical Center Dermatology.

Lichen planus. Courtesy of Walter Reed Army Medical Center Dermatology.

Lichen planus (hypertrophic type). Courtesy of Walter Reed Army Medical Center Dermatology.

Lichen planus (oral lesions). Courtesy of Walter Reed Army Medical Center Dermatology.

Lichen planus (volar wrist). Courtesy of Walter Reed Army Medical Center Dermatology.

Lymphoma cutis. Courtesy of Walter Reed Army Medical Center Dermatology.

Henoch-Schönlein purpura. Courtesy of Walter Reed Army Medical Center Dermatology.

Palpable purpura. Courtesy of Walter Reed Army Medical Center Dermatology.

Purpura in hemophilia (factor VIII deficiency). All ecchymoses and bland petechiae are in the differential diagnosis of thrombocytopenic purpuras, including thrombocytopenia secondary to hepatitis C virus in which an autoantibody to platelets is present. Courtesy of Walter Reed Army Medical Center Dermatology.

Progressive pigmented purpuric eruption. Courtesy of Walter Reed Army Medical Center Dermatology.

Progressive pigmented purpura (photo rotated 90°). Courtesy of Walter Reed Army Medical Center Dermatology.

Progressive pigmented purpura (Gougerot-Blum disease). Courtesy of Walter Reed Army Medical Center Dermatology.

Progressive pigmented purpura (Schamberg disease). Courtesy of Walter Reed Army Medical Center Dermatology.

Thrombocytopenic purpura. Courtesy of Walter Reed Army Medical Center Dermatology.

Prurigo nodularis. Courtesy of Walter Reed Army Medical Center Dermatology.

Prurigo nodularis. Courtesy of Walter Reed Army Medical Center Dermatology.

Prurigo nodularis. Courtesy of Walter Reed Army Medical Center Dermatology.

Chronic urticaria. Courtesy of Walter Reed Army Medical Center Dermatology.

Urticaria (secondary to penicillin). Courtesy of Walter Reed Army Medical Center Dermatology.

Nodular vasculitis. Courtesy of Walter Reed Army Medical Center Dermatology.

Henoch-Schönlein purpura, palpable purpura, and leukocytoclastic vasculitis. Courtesy of Walter Reed Army Medical Center Dermatology.

Vitiligo. Courtesy of Walter Reed Army Medical Center Dermatology.

Vitiligo. Courtesy of Walter Reed Army Medical Center Dermatology.

Waldenström hypergammaglobulinemic purpura. Courtesy of Walter Reed Army Medical Center Dermatology.



 

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Sofosbuvir - NS5B Polymerase Inhibitor (Available June 2014)


Sofosbuvir (SOF) is an HCV-specific uridine nucleotide prodrug that blocks replication of HCV by inhibiting the HCV NS5B polymerase and terminating the generation of HCV RNA chains.
Unlike the majority of available drugs, SOF and its major metabolite, GS-331007, are not metabolised by the cytochrome (CYP) P450 enzymes or by uridine biphosphate glucuronosyltransferase (UGT) and do not act as inducers or inhibitors of these enzymes.
SOF, but not GS-331007, is a substrate of both drug transporters P-gp and BCRP, therefore medicinal products which are potent inducers of these pathways have the potential to affect SOF metabolism and reduce its concentration and therapeutic efficacy. Although interactions have not been directly studied, co-administration with the analeptic modafinil, with certain anticonvulsants (e.g. carbamazepine, phenytoin, phenobarbital, oxcarbazepine), with some antimycobacterials (e.g. rifabutin, rifampin, rifapentine) or with St John’s Wort, all potent inducers of P-gp, is expected to decrease the concentration of SOF leading to reduced therapeutic effect. Sofosbuvir should not be used with such products.


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