This module will discuss the epidemiology, pathophysiology, and transmission of the hepatitis C virus, and the clinical course and treatment of hepatitis C infection.
After finishing this module, the learner will be able to:
Hepatitis C is a very common disease. The progression from infection with the virus to fibrosis, cirrhosis, and cancer takes decades to develop, and many cases are undiagnosed. As the population ages, the number of people needing treatment for hepatitis C will increase (Davis, Alter, El-Serag, Poynard, & Jennings 2010). Nurses now and in years to come will need to understand the disease and the treatments for it.
The hepatitis C virus has been in existence for a long time. The virus was not isolated and identified until 1989 (Alter, 2011), (Choo, et al., 1989). Prior to that, cases of hepatitis that were not caused by the hepatitis A virus or by the hepatitis B virus were classified as non-A, non-B hepatitis. Since the identification of the hepatitis C virus, a test for screening blood supplies has greatly reduced the risk of transmission of the virus by transfusion and effective treatments have been developed. Even with these developments Hepatitis C infections are still a major cause of morbidity.
Hepatitis C is the most common blood-borne disease in the United States (CDC, 2011). There are approximately 5.2 million cases of hepatitis C infection in the United States (Grebely, Dore, 2011). Infection with hepatitis C is the leading cause of hepatocellular carcinoma in most Western countries (Velosa, Serejo, Marinho, Nunes, Glria, 2011). It is the third leading cause of cancer world-wide (Horner, Gale, 2009), and approximately 40% of all liver transplantations are performed because of complications associated with hepatitis C infection (Perrakis, et al, 2011), (Rubn, Aguilera, Berenguer, 2011).
The progression from infection with the hepatitis C virus to fibrosis, cirrhosis, liver failure, and/or hepatocellular cancer takes decades. Presently, there is no vaccine for hepatitis C. The number of people needing medical care for the complications associated with hepatitis C has increased in the past few years and the number of cases is expected to increase dramatically in the next 20 to 30 years (Davis, Alter, El-Serag, Poynard, Jennings, 2010). Effective treatment is available, but side effects of the medications can be very serious, unpleasant, and therapy can take almost a year to complete. Patients must balance the risk of developing liver failure and/or liver cancer and the side effects of completing a long course of therapy that is not guaranteed to work.
A 44-year-old male has made an appointment with a primary care physician. He is in good health, has no major medical problems, and does not take any prescription medications. He is moderately overweight, drinks alcohol (occasionally to excess), and smokes. He has no specific complaints, but has started a new job. The job requires strenuous activity, and his employer has requested that a physician exam him to determine if he can tolerate this level of physical stress. During the interview, the man admits to the physician that he had experimented with IV drugs, but has not used any illicit substances for over 20 years. Laboratory tests reveal that his serum AST is 115 IU/L, his serum ALT is 190 IU/L. A test for hepatitis C antibodies is positive, the antibody test is confirmed with a positive RIBA test, and he has a hepatitis C viral load of 3 x 106 copies per mL, genotype 1. He does not have an infection with HIV or hepatitis B, and his CBC is normal. The physician tells the patient that because he is male, because he has probably had the infection for a long time, is overweight, occasionally drinks to excess, and he is at risk for cirrhosis and, possibly liver cancer. The physician recommends treatment with interferon, ribavirin, and a protease inhibitor. She advises the patient that the drug therapy may need almost a year to complete, significant and very unpleasant side effects are common, and there is a 30% chance the therapy will not be successful.
A 55-year-old female is diagnosed with hepatitis C. She had worked as a registered nurse 30 years earlier, before universal precautions were standard protocol, and had numerous percutaneous exposures to blood. The patient has no physical complaints, does not smoke or drink, is not overweight, and does not have an infection with either HIV or hepatitis B. She has genotype 1, her viral load is 8 x 106 copies per mL, and her serum transaminases are mildly elevated. An ultrasound of her liver did not show evidence of hepatocellular cancer. A biopsy of her liver revealed moderate fibrosis. Her physician prescribes interferon, ribavirin, and boceprevir. Six weeks after initiation of the therapy, the patient complains of profound fatigue, nausea, and she states that she is very depressed. She is finding it difficult to function in her daily life. Her hemoglobin is 9.0 mg/dL, her serum glucose is 112 mg/dL, her thyroid function is normal, and there has been a significant drop in the viral load.
The hepatitis C virus is an RNA virus. RNA viruses (e.g., HIV, hepatitis C, Ebola) use RNA to replicate, they have very high replication rates, are genetically very diverse, and mutate very quickly (Lauring, Randino, 2010). These qualities - among other characteristics of the hepatitis C virus - make it very difficult for the hosts immune system to eradicate the virus or for therapeutic drugs to be effective in treating an infection with hepatitis C. Although the body and the liver react to an infection with a strong cellular and humoral immune response, the virus rapidly replicates and only 25% of all people who are infected spontaneously clear the virus. It is not known exactly why the virus survives despite this immune response, but its persistence and the chronic infection that is so common is due to a complex, multi-factorial host-virus interaction (Lauring, Andino, 2010), (Wang, J.H., et al., 2011). Once the infection becomes chronic the virus damages hepatocytes and stimulates an inflammatory response; the result is fibrosis which can progress to cirrhosis, liver failure, and/or liver cancer.
There are six major hepatitis C genotypes - genotypes 1 through 6 - and there are more than 100 subspecies (Bostan, Mahmood, 2010). The most common genotype worldwide is type 1, and this is the most common genotype in the United States. Approximately 75% of all patients in the United States with a hepatitis C virus infection are infected with the type I genotype and approximately 25% are infected with genotype 2 or 3 (Schiff, 2011).
Learning Break: Genotype is an important factor in the prognosis of a hepatitis infection. Genotypes 2 and 3 are more easily eradicated than genotype 1, and the treatment protocol for genotypes 2 and 3 differs slightly from the treatment protocol for genotype 1 (CDC, 2011).
Hepatitis C is primarily transmitted by exposure to infected blood. In developed countries this happens most often by IV drug use when people share needles (Mukherjee, Dhawan, 2010), and the Centers for Disease Control and Prevention (CDC) has estimated that 33% of people between the ages of 18-30 who use IV drugs are infected with hepatitis C, and the rate of infection is approximately 70 - 90% in older person who used, or still use IV drugs (CDC, 2011).
Sexual transmission of hepatitis C is a controversial topic. Hepatitis C virus RNA has been isolated in semen and cervical smears (Tohme, Holmberg, 2010) (Wang, C.C., et al., 2011), although not consistently. The current literature clearly states that in monogamous, heterosexual couples in which one partner is infected with hepatitis C but the other is not, sexual transmission does not happen (Wang, C.C., et al., 2011), (Alter, 2011). The CDC does not recommend that monogamous, heterosexual couples need to use condoms (CDC, 2011). The sexual transmission of hepatitis C is clearly less efficient than the sexual transmission of hepatitis B and HIV (Alter, 2011), but sexual transmission of hepatitis C can, and does occur in specific populations.
A concurrent HIV infection sharply increases the risk of sexual transmission (Tohme, Holmberg, 2010), especially among men who have sex with men (Gamage, Read, Bradshaw, 2011). People who have multiple sex partners have an increased risk of sexual transmission of the virus, and people who engage in sexual practices that involve exposure to blood and/or tearing of mucosal membranes are at a higher risk. Exposure to genital ulcerations and the presence of a sexually transmitted disease also increases the risk of sexual transmission of hepatitis C (Thome, Holmberg, 2010).
Learning Break: An HIV infection may increase the risk of sexual transmission of hepatitis C by increasing the viral load of hepatitis C in blood or semen or by compromising the immune system (van de Laar, Paxton, Zorgdrager, Cornelissen, de Vries, 2011).
Hepatitis C can be transmitted from an infected mother to a fetus, and the rate of transmission by this route has been estimated to be 2-6% (Hurtado, et al., 2010). If the mothers viral load is high, she has an infection with HIV, there is birth trauma, or an amniocentesis was performed, the transmission risk is increased. The virus has been found in breast milk, but breastfeeding is not contraindicated (Valladares, Chacaltana, Sjorgen, 2010).
The risk of developing transmission of hepatitis C from a blood transfusion is approximately 1 in 2 million, the risk of transmission of hepatitis C from a needle stick is approximately 1.8-3% (Mukherjee, Dhawan, 2010), and the risk of transmission of the virus during invasive medical procedures such as colonoscopy, endoscopy, etc. is very low. Hepatitis C infections are more common in patients who undergo maintenance hemodialysis, but this increased rate of infection is due to poor compliance with infection control protocols (Fabrizi, Messa, Martin, 2008). Hepatitis C is not transmitted by insect bites, food, water, inhalation, or causal contact.
Approximately 25% of hepatitis C infections spontaneously resolve and the virus is cleared (Grebely, Dore, 2011). Some people who are infected develop an acute infection with jaundice and other signs and symptoms. However, in the great majority of cases the patient is asymptomatic in the initial period after infection and remains so for many, many years. The infection becomes chronic and silent, the patient is asymptomatic, and there is a slow progression over decades. In worst cases, the infection may progress from fibrosis (very common), to cirrhosis. Eventually it could progress to end-stage liver disease with decompensation and/or hepatocellular cancer (Schiff, 2011), (Grebley, Dore, 2011).
Learning Break: The risk for developing fibrosis is not associated with the genotype or the viral load (Rosen, 2011).
The risk of developing cirrhosis or other complications over 30 years of infection is approximately 5-25% (Schiff, 2011), and the level of risk increases with:
Mortality from hepatitis C varies. Many people who have an infection of hepatitis C die from other causes and if the patient does not use IV drugs and does not have an infection with HIV, there is probably no difference in the all-cause mortality rate of people infected with hepatitis C and those who are not (Schiff, 2011). However, there is some epidemiological evidence that the risk of mortality is increased even if the patient does not use IV drugs or have an infection with HIV (Grebely, Dore, 2011).
Learning Break: Cirrhosis is a common consequence of hepatitis C infection. The histological definition of cirrhosis is: a diffuse hepatic process characterized by fibrosis and conversion of normal liver architecture into structurally abnormal nodules interlacing bands of fibrous tissue in the liver. Fibrosis is an increase in the amount of the extracellular collagen supporting framework of the liver. It is the first step in the development of cirrhosis. Fibrosis is potentially reversible; cirrhosis is not.
Screening for hepatitis C should be done if someone:
The first step in screening/diagnosing is a blood test for antibodies to the core protein of the virus (anti-HCV test). If this is positive, a recombinant immunoblot assay (RIBA) blood test is done to confirm the antibody test. If that test is positive, the presence of an active infection is confirmed by a test for viral RNA: at that point the genotype is determined and the viral load is measured (Note: Viral load is frequently referred to as the number of copies).
After the diagnosis is made, the patient should be checked for liver damage. Serum transaminases should be measured, but it is important to note that these may be normal even if there are serious hepatic lesions. A complete blood count, serum glucose, blood urea nitrogen, serum creatinine, thyroid function studies, and tests for HIV and hepatitis B should be obtained. These tests are needed to check for risk factors that make for a poor prognosis (e.g., HIV and possibly hepatitis B) and for complications associated with hepatitis C infection (these complications will be discussed in a subsequent section of the module).
Learning Break: Concurrent infection with hepatitis C and hepatitis B is relatively common. It is not clear at this point if an infection with hepatitis B has a negative influence on the clinical course of a hepatitis C infection; there is some evidence that it does not (Jang, et al., 2011), but some authors feel that it may (Fernandez-Rodriguez, Gutierrez, Lled, Casas, 2011).
An ultrasound of the liver and a serum α-fetoprotein test should be done to check for hepatocellular cancer (Noda, et al., 2010) and if the patient has a chronic infection. Treatment for a liver biopsy is recommended, (Schiff, 2011). The tissue sample from the liver biopsy is assessed for fibrosis. The degree of fibrosis is determined using either the Ishak scoring system or the Metavir scoring system (Moradpour, Mllhaupt, & Swiss, 2012). Assessing the degree of fibrosis is important. People who have mild or no fibrosis have a low risk of developing cirrhosis, but people with specific patterns of fibrosis (e.g., portal fibrosis or septal fibrosis) are more likely to develop cirrhosis and develop it relatively quickly.
Learning Break: α-fetoprotein is a protein produced by the liver. The level of α-fetoprotein is often elevated when a patient has liver cancer, so it is considered to be a tumor marker.
Liver biopsy has long been considered to be the definitive test for assessment of the degree of fibrosis caused by hepatitis C. A direct histological assessment is then obtained. However, a liver biopsy is expensive, invasive, complications are possible, and there can be sampling errors and observer errors. Complications of the procedure are uncommon and death is rare, but sampling and observer errors are not uncommon. A recent review noted that there can be 33.1% difference in the fibrosis score assigned to the same sample, and that cirrhosis may be missed in 10-30% of liver biopsies (Sebastiani, Alberti, 2012).
Non-invasive tests for assessment of liver fibrosis are available. These include:
These noninvasive tests show promise, but at this point there is no universal agreement on when and for whom they should be used in place of liver biopsy (Sebastini, Alberti, 2012).
There are many complications associated with hepatitis C. This module will discuss the most serious and the most common ones.
Infection with hepatitis C increases the risk of developing insulin resistance and type II diabetes. This association was first noted and confirmed not long after the hepatitis C virus was first isolated (Allison, et al., 1995).
The prevalence of an infection with hepatitis C is higher in people with diabetes (Eslam, Khattab, Harrison, 2011), and people who have a hepatitis C infection have an increased risk for developing type II diabetes. This risk has been estimated to be 11 times higher than in uninfected people (Eslam, Khattab, Harrison, 2011), (White, Ratziu, El-Serag, 2008). The prevalence of type II diabetes in the population infected with hepatitis C has been estimated to be between 24-50% (Parvaiz, et al., 2011). Insulin resistance occurs in approximately 25% of all people who have an infection with hepatitis C (Parvaiz, et al., 2011).
Learning Break: Insulin resistance is a condition in which insulin is produced, but the body cannot use it properly. A given amount of insulin does not produce the expected result and higher than normal amounts are required to maintain euglycemia.
The mechanism(s) by which hepatitis C infection causes type II diabetes and insulin resistance is not completely understood (Eslam, Khattab, Harrison, 2011). Infection with hepatitis C increases the production and activity of inflammatory cyotkines and reactive oxygen species in the hepatocytes and this appears to affect intracellular insulin signaling mechanisms and the activity of the GLUT 4 insulin transporter (Parvaiz, et al., 2011). An infection with hepatitis C may increase glucose production and decrease glucose uptake.
Diabetes and insulin resistance associated with hepatitis C infection increase the progression of liver fibrosis (Hsu, et al., 2010). Insulin resistance is associated with a decreased rate of rapid virological response (RVR) and a decreased rate of sustained virological response (SVR) in patients treated with ribavirin and pegylated interferon-? (Dai, et al., 2009), (Khattab, et al., 2010), (Mizuta, et al., 2010). Insulin resistance increases the risk of developing hepatocellular cancer (Konishi, et al., 2009).
The risk of developing hepatocellular carcinoma is 15 to 20 times higher for people infected with hepatitis C than for those who are not (Harnoise, 2012). The incidence of hepatocellular cancer in the United States has tripled in the last three years. This increase has been attributed to infections with hepatitis C (Harnoise, 2012).The primary risk factor for the development of this cancer is cirrhosis. A chronic infection with hepatitis C increases the incidence of cirrhosis. Patients with cirrhosis caused by an infection with hepatitis C have a 2-8% chance per year of developing hepatocellular carcinoma (Nash, Woodall, Brown, Davies, Alexander, 2010). It is not clear how the hepatitis C virus causes this cancer. It may be that the virus impairs the livers ability to regenerate and repair itself, or it may be caused by the insulin resistance, oxidative stress, and steatosis that complicate an infection with hepatitis C (Nash, Woodall, Brown, Davies, Alexander, 2010), (Jahan, et al., 2012).
People who are infected with hepatitis C have an increased risk for the development of renal disease (Morales, Kamar, Rostaing, 2012). The most common renal disorder in patients with a hepatitis C infection is membranoproliferative glomerulonephritis (MPGN). Membranoproliferative glomerulonephritis is a form of nephritis that can result in azotemia, hematuria, and nephrotic syndrome. The incidence of MPGN associated with hepatitis C has been approximately 40% (McGuire, et al., 2006).
Cryoglobulinemia is the most common extrahepatic complication of hepatitis C infection. The disease is an immune-mediated process that causes deposition of immune complexes into the endothelium of small and medium-sized arteries and veins. This results in widespread inflammation and vasculitis. Cryoglobulinemia affects approximately 10-70% of people with a hepatitis C infection (Charles, Dustin, 2009), and the presence of the disease increases the risk of developing cirrhosis. The signs and symptoms of cryoglobulinemia vary depending on the organs that are affected.
People who are infected with hepatitis C and HIV deserve special consideration. The incidence of infection with hepatitis C is much higher in people who are also infected with HIV. Up to one-third of people infected with HIV are also infected with hepatitis C (Hernandez, Sherman, 2011) and concurrent infection with these viruses changes the natural progression of a hepatitis C infection for the worse. The virus is more easily transmitted, the viral load is higher, liver damage occurs more often, progresses more quickly, and the response to treatment is attenuated in this population (Danta, Rodger, 2011). HIV-induced suppression of the immune system (e.g., CD4 T-cells depletion, impairment of cell-mediated immunity to the hepatitis C virus), infection of, and damage to the hepatocytes by HIV, or an increase in systemic inflammation may explain why HCV/HIV-infected people have a higher incidence of liver damage and a more rapid progression of the disease (Page, Nelson, Kelleher, 2011). The exact mechanism by which this process occurs is not known.
Learning Break: The high incidence of concurrent infection with hepatitis C and HIV can be explained in part by IV drug use in this population (the risk of percutaneous transmission of hepatitis C is 10 times higher than that of HIV), and unsafe, risky sex practices.
Chronic hepatitis C infections are treated with drug therapy. The basic goal of therapy is a sustained viral response (SVR). Sustained viral response is defined as absence of detectable hepatitis C RNA at the end of the treatment and at six months after the end of the treatment. A SVR decreases the risk of developing liver cancer and reduces the mortality associated with hepatitis C (Wilkins, Malcolm, Raina, & Schade, 2010) (Singal, Volk, Jensen, DiBisceglie, Schoenfeld, 2010). Most authorities recommend at least a trial of therapy for patients who have a chronic infection, patients who have some evidence of fibrosis or cirrhosis, and if the patient has renal function and does not have anemia or neutropenia. Once the decision has been made to treat the patient who has a hepatitis C infection, the goal is to try and eradicate the virus and by doing so, prevent the progression to cirrhosis, severe liver damage, and/or liver cancer. Some patients are fortunate and have a rapid virological response (RVR): HCV RNA is undetectable after four weeks of therapy. If the patient does not have a RVR and the patient does not have a > 2 log10 drop in viral load after 12 weeks of therapy, the chances of attaining a SVR are virtually nil and treatment will be stopped.
Until 2011, patients were prescribed oral ribavirin (common trade names are Rebetol® and Ribasphere®) and injectable, pegylated interferon alfa-2a (common trade name Pegasys®). Ribavirin and interferon are immunomodulators that have anti-viral activity, but it is not completely understood how they work when used to treat hepatitis C. The ribavirin is taken twice a day and the patient self-administers the interferon injection, subcutaneously, once a week.
Learning Break: The interferon used to treat hepatitis C infections is attached to a molecule of polyethylene glycol - the peg. Attaching the drug to the polyethylene glycol molecule sustains absorption of the drug, decreases its volume of distribution, increases the half-life of the drug, and decreases its renal clearance. This modification allows for once a week dosing.
Unfortunately, the success rate of ribavirin/interferon therapy for patients with an infection with genotype 1 is only 40% (Rosen, 2011), (Alkhouri, Zein, 2012). In 2011, the Food and Drug Administration (FDA) approved two oral protease inhibitors for use in the treatment of hepatitis C infection. These drugs - boceprevir (Victrelis®) and telaprevir (Incivek®) - inhibit hepatitis C virus replication. They are given along with ribavirin and interferon (this is often called triple drug therapy), and the combination has increased the success rate of treatment of genotype 1 hepatitis C to approximately 70%. The triple drug therapy is recommended for treating patients who have a chronic hepatitis C infection unless the patient is pregnant, has uncontrolled thyroid dysfunction, is severely anemic, has severe and uncontrolled depression, has decompensated cirrhosis, or has several other less common medical conditions. The treatment protocols for the triple drug therapy are complex. The specific medication regimen that will be prescribed depends on many factors and the different regimens will not be discussed here in detail, but depending on the response to therapy, patients are treated for 24-48 weeks (See the article by Moradpour D, Mllhaupt B, Swiss A. for details).
Learning Break: Protease is an enzyme that breaks down proteins. Viruses use protease to cleave proteins so that the virus can construct its own vital proteins. This breakdown of the host proteins is one of the important steps in the replication step of the viral life cycle.
The drug therapy protocol for hepatitis C infection can be difficult to complete. The treatment course is long, the side effects are very unpleasant, serious adverse effects are possible, and approximately 15-17% of patients withdraw from treatment (Arase, et al., 2007), (Alkhouri, Zein, 2012). Reducing doses of the drugs can make the therapy easier to tolerate, but can decrease the effectiveness of the therapy (Stickel, et al., 2012), (Goh, et al., 2011).
The most common side effects of therapy with the ribavirin/interferon therapy or the ribavirin/interferon and protease inhibitor therapy are anemia and other hematologic complications, dermatologic complaints, dysgeusia, fatigue, flu-like signs and symptoms, mood disorders, nausea, and thyroid dysfunction (Moradpour, Mllhaupt, Swiss, 2012), (Park, et al., 2012).
The three common, serious side effects anemia, thyroid dysfunction, and mood disorders - will be discussed here.
Hemolytic anemia is the most frequent medical reason for discontinuation of therapy (Stickel, et al., 2012). The drop in hemoglobin is caused by the ribavirin: the drug accumulates in the red blood cells and makes them vulnerable to oxidative stress. The maximum decrease in hemoglobin level usually occurs four weeks after the therapy is started. The incidence of anemia caused by peg-interferon/ribavirin therapy is 11-12% (Hu, et al., 2012); the incidence of anemia caused by peg-interferon/ribavirin and protease inhibitor therapy is approximately 36-50% (Moradpour, Mllhaupt, Swiss, 2012). If the patients hemoglobin decreases to < 10 g/dL, the dose of ribavirin can be decreased, and if the hemoglobin decreases to < 8.5 g/dL the drug therapy with ribavirin should be stopped (Stickel, et al., 2012). Erythropoietin can be used to treat hemolytic anemia caused by the drug therapy. After discontinuation of the drugs, the anemia slowly resolves and the patients hemoglobin and hematocrit return to pre-treatment levels.
Thyroid dysfunction occurs in many patients who have a hepatitis C infection and who are receiving interferon alfa-2a. The exact incidence is not known, but it has been reported to be from 1-54%, and women are more susceptible than men (Danilovic, et al., 2011), (Vasiliadis, et al., 2011). The thyroid dysfunction can be clinical or overt, and the patients can develop hypothyroid or hyperthyroid disorders. Infection with the hepatitis C virus itself may be a cause of thyroid damage, but the interferon has a direct toxic effect on the thyroid cells and it appears to induce the immune system to attack thyroid cells (Vasiliadis, et al., 2011). Thyroid function may return to normal after therapy has stopped, or it may not. One investigator found that 57% of all patients with a hepatitis C infection who were treated with interferon alfa-2A had permanent thyroid dysfunction (Vasiliadis, et al., 2011).
Mood disorders - especially depression - are a common reason for discontinuing drug therapy for hepatitis C. Severe, uncontrolled depression is a contraindication for the drug therapy for this disease, and the incidence of major depression associated with ribavirin/interferon therapy has been noted in up to 35% of all patients (Leutscher, et al., 2010). Depression and mood changes are very common reasons for the cessation of drug therapy.
Learning Break: Before administering boceprevir or telaprevir, it is very important to know what medications the patient is currently receiving. The effectiveness of many commonly used medications, e.g., anticonvulsants, digoxin, the statin drugs, and warfarin can be affected by boceprevir and telaprevir.
If drug therapy is successful and a SVR has been attained, the risk for liver damage and/or liver cancer is greatly reduced, and there is evidence that even if a SVR has not been attained, drug therapy decreases the risk for these problems (Ahmad, Eng, 2011), (Kwon, Lok, 2011). In either case, continued screening is recommended to check for liver cancer. There is no universally agreed upon screening schedule, but an ultrasound and measurement of serum α-fetoprotein every six months is commonly recommended (Nash, et al., 2010), Ahmad, Eng, 2011).
Nursing care is an essential part of the treatment of patients with hepatitis C. Nurses caring for patients who have an infection with hepatitis C should focus on a) patient education, b) monitoring for the complications of therapy, and c) helping the patient manage and cope with the side effects of therapy. Each patient will have differing needs for education, but the nurse should focus on safety, diet and exercise, safe administration of medications, and patient self-monitoring for complications of the disease and the therapy.
Make sure that the patient understands how hepatitis C is transmitted and what activities, in terms of contact with others, are safe and which activities are not. As regards diet and activity, no special diet is recommended for patients with hepatitis C, but alcohol should be avoided, and the patient should be encouraged to exercise as tolerated. Most patients will need to be taught sterile technique, injection technique, and the proper methods of disposing of hazardous material. There are many signs and symptoms associated with the complications of the disease and the drugs. Because the treatment often causes anemia and neutropenia, the patient should be instructed to notify a nurse of physician if they are exceptionally fatigued or have any signs or symptoms of infection. Self-monitoring for disease complications is not as easy, but patients should be taught about the signs and symptoms of hyperglycemia.
Helping the patient manage and cope with the side effects of therapy is a very important part of nursing care. Hepatitis C is a potentially dangerous disease, there is a risk of serious complications, and the treatment protocol is very difficult and it is not guaranteed to work. Patients often feel terrible - physically and psychologically - while they are receiving the double or triple drug therapy. Significant disruptions in life style are common because of drug side effects. Emotional and psychosocial support will help the patient cope with the illness and the adverse effects, and it can also help the patient stay the course and complete the treatment regimen.
Hepatitis C challenges us all and genotype remains an important factor in the prognosis of determining how to eradicate this disease which can cause fibrosis, cirrhosis, liver cancer, diabetes II with insulin resistance, and weakens our bodys resistance to other diseases. The development of tests which indicate if Hepatitis C is present, if liver cancer is present, and if the viral load is being sustained helps us to determine what treatment options to use. There is hope for the future as new drugs are being discovered to treat Chronic Hepatitis C infections and which can help to sustain viral response (SVR).
Healthcare professionals have to develop strategies to reduce transmission of HCV. Standard precautions, safe injection practice, and infection control practices need to be consistently followed. The public at all levels needs to be educated on methods to reduce transmission, ways to deal with an HCV infection, and ways to reduce liver damage if infected. Nurses need to keep up to date on current treatments and focus on safety, diet, exercise, safe administration of medications, patient self-monitoring for complications of the disease and the therapy being implemented.
Ahmad, J., & Eng, F.J. (2011). HCV and HCC: Clinical update and a review of HCC-associated viral mutations in the core gene. Seminars in Liver Disease, 31(4), 347-355.
Alkhouri, N, & Zein, N.N. (2012). Protease inhibitors: Silver bullets for chronic hepatitis C infection? Cleveland Clinic Journal of Medicine, 79(3). 213-222.
Allison, M.E., Wreghitt, T., Palmer C.R. & Alexander, G.J. (1994). Evidence for a link between hepatitis C virus infection and diabetes mellitus in a cirrhotic population. Journal of Hepatology, 21(6), 1135-1139.
Alter, M.J. (2011). HCV routes of transmission: What goes around comes around. Seminars in Liver Disease, 31(4), 340-346.
Arase, Y., Suzuki, F., & Suzuki, Y., Akuta, N., Kawamura, Y., Kobayashi, M., et al. (2007). Side effects of combination therapy of peg-interferon and ribavirin for chronic hepatitis-C. Internal Medicine, 46(22), 1827-1832.
Bostan, N., & Mahmood, T. (2010). An overview about hepatitis C: A devastating virus. Critical Reviews in Microbiology, 36(2), 91-133.
Centers for Disease Control and Prevention. (2011). Hepatitis C Information for Health Professionals. Retrieved January 10, 2012 from The CDC.
Centers for Disease Control and Prevention (2011). Hepatitis C Information for Health Professionals. Retrieved January 10, 2012 from The CDC.
Charles, E.D., & Dustin L.B. (2009). Hepatitis C virus-induced cryoglobulinemia. Kidney International, 76(8), 818-824.
Danta, M., & Rodger, A.J. (2011). Transmission of HCV in HIV-positive populations. Current Opinion in HIV & AIDS, 6(6), 451-458.
Choo, Q.L., Kuo, G., Weiner, A.J., Overby, L.R., Bradley, D.W., & Houghton, M. (1989). Isolation of a cDNA clone derived from a blood-borne non-A, non-B viral hepatitis genome. Science, 244(4902), 359-362.
Dai, C.Y., Huang, J.F., Hsieh, MY, Hour, N.J., Lin, Z.Y., Chen, S.C., et al. (2009). Insulin resistance predicts response to peg-interferon-alpha/ribavirin combination therapy in chronic hepatitis C patients. Journal of Hepatology. 50(4), 712-718.
Danilovic, D.L.S., Mendes-Correa, M.C., Chammas, M.C., Zambrini, H., & Marui, S. (2011). Thyroid hormonal disturbances related to treatment of hepatitis C with interferon-alpha and ribavirin. Clinics (Sao Paolo), 66(10), 1757-1763.
Davis, G.L., Alter, M.J., El-Serag, H., Poynard, T., & Jennings L.W. (2010). Aging of hepatitis C virus (HCV)-infected persons in the United States: A multiple cohort model of HCV prevalence and disease progression. Gastroenterology, 138(2), 513-521.
El-Zaydi, A.R., & Anis, M. (2012). Hepatitis C virus induced insulin resistance impairs response to anti-viral therapy. World Journal of Gastroenterology, 18(3), 212-224.
Eslam, M., Khattab, M.A., & Harrison, S.A. (2011). Insulin resistance and hepatitis C: An evolving story. Gut, 60(8), 1139-1151.
Fabrizi, F., Messa, P., & Martin, P. (2008). Transmission of hepatitis C virus infection in hemodialysis: Current concepts. International Journal of Artificial Organs, 31(12), 1004-1016.
Fernandez-Rodriguez, C.M., Gutierrez M.L., Lled, J.L., & Casas, M.L. (2011). Influence of hepatitis B virus infection in chronic hepatitis C outcomes. World Journal of Gastroenterology, 17(12), 1558-1562.
Gamage, D.G., Read, T.R.H., Bradshaw, C.S., Hocking, J.S., Howley, K. Chen, M.Y., et al. (2011). Incidence of hepatitis-C among HIV infected men who have sex with men (MSM) attending a sexual health service: a cohort study. BMC Infectious Disease, Feb. 3;11:39.
Goh, P.G., Kim, M.J., Kim, H.J., Eun, H.S., Kim, E.S., Kim, Y.J., et al. (2011). Importance of medication adherence to peg-interferon/ribavirin combination therapy in patients with chronic hepatitis C. Korean Journal of Gastroenterology, 57(5), 294-301.
Grebely, J., & Dore, G.J. (2011). What is killing people with hepatitis C virus infection? Seminars in Liver Disease, 31(4),331-339.
Harnoise, D.D. (2012). Hepatitis C virus infection and the rising incidence of hepatocellular carcinoma. Mayo Clinic Proceedings, 87(1), 7-8.
Hernandez, M.D., & Sherman, K.E. (2011). HIV/hepatitis C co-infection natural history and progression. Current Opinion in HIV and AIDS, 6(6), 478-482.
Hsu, C.S., Liu, C.H., Liu, C.J., Hsu, S.J., Chen, C.L., Hwang, J.J., et al. (2010). Association of metabolic profiles with hepatic fibrosis in chronic hepatitis C patients with genotype 1 or 2 infection. Journal of Gastroenterology & Hepatology. 25(5), 970-977.
Hu, C.C., Weng, C.H., Lin, C.L., Tien, H.C., Kuo, Y.L., Chien, C.H., et al. (2012). Predictors of changes in hemoglobin levels in patients with chronic hepatitis C treated with ribavirin plus pegylated interferon-α. Renal Failure, Jan 23 [Epub ahead of print].
Hurtado, C.W., Golden-Mason, L., Brocato, M., Krull M., Narkewicz, M.R., & Rosen H.R. (2010). Innate immune function in placenta and cord blood of hepatitis C-seropositive mother-infant dyads. PLoS One, 5(8), e12232.
Jahan, S., Ashfaq, U.A., Qasim, M., Khaliq, S., Saleem, M.J., & Afzal, N. (2012). Hepatitis C to hepatocellular carcinoma. Infectious Agents and Cancer, 7(1), 2-9.
Jang. J.Y., Jeong, S.W., Cheon, S.R., Lee, S.H., Kim, S.G., Cheon, Y.K., et al. (2011). Clinical significance of occult hepatitis B virus infection in chronic hepatitis C patients. Korean Journal of Hepatology, 17(3), 206-212.
Khattab, M., Eslam, M, Sharwae, M.A., Shatat, M., Ali, A., & Hamdy, L. (2010). Insulin resistance predicts rapid virologic response to peginterferon/ribavirin combination therapy in hepatitis C genotype 4 patients. Gastroenterology, 105(9), 1970-1977.
Konishi, I., Hiasa, Y., Shigematsu, S., Hirooka, M., Furukawa, S., Abe, M., et al. (2009). Diabetes pattern on the 75 g oral glucose tolerance test is a risk factor for hepatocellular carcinoma in patients with hepatitis C virus. Liver International, 29(8), 1194-1201.
Kwon, H., & Lok, A.S. (2011). Does antiviral therapy prevent hepatocellular cancer? Antiviral Therapy, 16(6), 787-795.
Lauring, A.S., & Andino, R. (2010). Quasispecies theory and the behavior of RNA viruses. PLoS Pathogens, 6(7), e1001005.
Leutscher, P.D., Lagging, M., Buhl M.R., Pedersen, C., Norkans, G., Langeland, N., et al. (2010). Evaluation of depression as a risk factor for treatment failure in chronic hepatitis. Hepatology, 52(5), 430-435.
McGuire, B.M., Julian, B.A., Bynon, J.S., Cook, W.J., King, S.J., Curtis J.J., et al. (2006). Brief communication: Glomerulonephritis in patients with hepatitis C cirrhosis undergoing liver transplantation. Annals of Internal Medicine,144(10), 735-741.
Mizuta, T., Kawaguchi, Y., Eguchi, Y., Takahashi, H., Ario, K., Akiyama, T., et al. (2010). Whole-body insulin sensitivity index is a highly specific marker for virological response to peg-interferon plus ribavirin therapy in chronic hepatitis C patients with genotype 1b and high viral load. Digestive Diseases and Sciences, 55(1), 183-189.
Moradpour, D., Mllhaupt, B., & Swiss A. (2012). Treatment of chronic hepatitis C genotype 1 with triple therapy compromising telaprevir or boceprevir. Swiss Medicine Weekly, Feb. 24;142:0. doi:104414.smw.2012.13516.
Morales, J.M., Kamar, N., & Rostaing L. (2012) Hepatitis C and renal disease: epidemiology, diagnosis, pathogenesis, and therapy. Contributions to Nephrology, 176, 10-23.
Mukherjee, S, & Dhawan, V.K. (2010). Hepatitis C. eMedicine, June 25, 2010. Retrieved March 14, 2012 from Medscape.
Nash, K.L., Woodall, T., Brown, A.S.M., Davies, S.E., & Alexander, G.J.M. (2010). Hepatocellular carcinoma in patients with chronic hepatitis C virus infection without cirrhosis. World Journal of Gastroenterology, 16(32), 4061-4065.
Noda, I., Kitamoto, M., Nakahara, H., Hayashi, R., Okimoto, T., Monzen, Y., et al. (2010) Regular surveillance by imaging for early detection and better prognosis of hepatocellular carcinoma in patients infected with hepatitis C virus. Journal of Gastroenterology, 45(1),105-112.
Page, E.E., Nelson, M., & Kelleher, P. (2011). HIV and hepatitis C co-infection: pathogenesis and microbial translocation. Current Opinion in HIV and AIDS, 6(6), 472-477.
Park, S.H., Park, C.K., Lee, J.W., Kim, Y.S., Jeong, S.H., Kim, Y.S., et al. (2012). Efficacy and tolerability of peg-interferon alpha plus ribavirin in the routine daily treatment of chronic hepatitis C patients in Korea: a multi-center, retrospective observational study. Gut & Liver, 6(1), 98-106.
Parvaiz, F., Manzoor, S., Tariq, H., Javed, F., Fatima, K., & Qadri, I. (2011). Hepatitis C virus infection: Molecular pathways to insulin resistance. Virology Journal, 18(8), 474-479. Gut and Liver 6(1), 98-106.
Perrakis, A., Yedibela, S., Schuhmann, R., Croner, V., Schellerer, R, Demir, W., et al. (2011). The effect and safety of the treatment of recurrent hepatitis C infection after orthotopic liver transplantation with pegylated interferon ?2b and ribavirin. Transplantation Proceedings, 43(10), 3824-3828.
Petrovic, D., Dempsey, E., Doherty, D.G., Kelleher D., & Long, A. (2012). Hepatitis C virus T-cell responses and viral escape mutations. European Journal of Immunology, 42(1), 17-26.
Rosen, H.R. (2011). Chronic hepatitis C infection. New England Journal of Medicine, 364(25), 2429-2438.
Rubn A., Aguilera V., & Berenguer, M. Liver transplantation and hepatitis C. (2011). Clinics and Research in Hepatology and Gastroenterology, 35(12), 805-812.
Schiff, E.R. (2011). Diagnosing and treating hepatitis C virus infection. American Journal of Managed Care, 17(Suppl. 4), S108-S115.
Sebastiani, G. & Alberti, A. (2012). How far is noninvasive assessment of liver fibrosis from replacing liver biopsy in hepatitis C? Journal of Viral Hepatitis, 19(Suppl. 1), 18-32.
Singal, A.G., Volk, M.L., Jensen, D., DiBisceglie, A.M., & Schoenfeld, P.S. (2010). A sustained viral response is associated with reduced liver-related morbidity and mortality in patients with hepatitis C virus. Clinical Gastroenterology & Hepatology, 8(3), 280-288.
Stickel, F., Helbling, B. Heim, M., Geier, C., Hirschi, B., Terziroli, K., et al. (2012). Critical review of the use of erythropoietin in the treatment of anemia during therapy for chronic hepatitis C. Journal of Viral Hepatitis. 19(2), 77-87.
Tohme, R.A., & Holmberg, S.D. (2010). Is sexual contact a major mode of hepatitis C virus transmission? Heptalology, 52(4),1497-1505.
Vallardes, D., Chacaltana, A., & Sjorgen M.H. (2010). The management of HCV-infected pregnant women. Annals of Hepatology, 9(Suppl.), S92-S97.
Vasiliadis, T., Anagnostis, P., Nalmpantidis, G., Soufleris, K., Patsiaoura. K., Grammatikos, N., et al. (2011). Thyroid dysfunction and long-term outcome during and after alpha-interferon therapy in patients with chronic hepatitis C. Annals of the Academy of Medicine of Singapore, 40(9), 394-400.
Van de Laar, T.J.W., Paxton, W.A., Zorgdrager, F., Cornelissen, M., & de Vries H.J.C. (2011). Sexual transmission of hepatitis C virus in human immunodeficiency virus-negative men who have sex with men: A series of care reports. Sexually Transmitted Diseases, 38(2), 102-104.
Velosa, J,, Serejo, F., Marinho, R., Nunes, J., & Glria, H. (2011). Eradication of hepatitis C virus reduces the risk of hepatocellular carcinoma in patients with compensated cirrhosis. Digestive Diseases and Sciences, 56(6), 1853-1861.
Wang, Y., Keck, Z.Y., & Foung, S.K.H. (2011). Neutralizing antibody response to hepatitis C virus. Viruses, 3(11), 2127-2145.
Wang, J.H., Pianko, M.J., Xe, K., Herskovic, A., Hershow, R., Cotler, S.J., et al. (2011). Characterization of antigenic variants of hepatitis C virus in immune evasion. Virology Journal, 8, 377-388.
Wang, C.C., Cook, L., Tapia, K.A., Krows, M., Bagabag, A., Santos, A., et al. (2011). Cervicovaginal shedding of hepatitis C viral RNA is associated with the presence of menstrual or other blood in cervicovaginal fluids. Journal of Clinical Virology, 50(1), 4-7.
Wilkins, T., Malcolm, J.K., Raina, D., & Schade, R.R. (2010). Hepatitis C: Diagnosis and treatment. American Family Physician, 81(11),1351-1357.