In addition, some isolated cases of fulminant disease in immunocompetent individuals have been reported. As the presentation is frequently non-specific, it is important to maintain a high level of suspicion for these viral etiologies and start empiric therapy with antiviral agents as soon as possible.
Liver transplantation is the last resort. These variants are not confined to the Mediterranean region. The same nonsense mutation without a second mutation in the adjacent codon has been observed in patients from Japan and elsewhere, along with rarer examples of defective precore regions caused by frameshifts or loss of the initiation codon for the precore region.
In many cases, precore variants have been described in patients with severe chronic liver disease and who may have failed to respond to therapy with interferon.
This observation raises the question of whether they are more pathogenic than the wild-type virus. When tests for HBsAg became widely available, regions of the world where the chronic carrier state is common were found to be coincident with those where there is a high prevalence of primary liver cancer. Furthermore, in these areas, patients with tumor almost invariably are seropositive for HBsAg.
A prospective study in Taiwan revealed that cases of hepatocellular carcinoma occurred in 3, carriers of HBsAg at the start of the study, but only 10 such tumors arose in the 19, control males who were HBsAg negative. There is no similarity in the pattern of integration between different tumors, and variation is seen both in the integration site s and in the number of copies or partial copies of the viral genome.
Integration seems to involve microdeletion of host sequences and rearrangements and deletions of part of the viral genome also may occur. When an intact surface gene is present, the tumor cells may produce and secrete HBsAg in the form of 22 nm particles. Production of HBcAg by tumors is rare, however, and the core ORF is often incomplete and modifications such as methylation may also modulate its expression.
Cytotoxic T cells targeted against core gene products on the hepatocyte surface seem to be the major mechanism of clearance of infected cells from the liver, and cells with integrated viral DNA which are capable of expressing these proteins also may be lysed. The mechanisms of oncogenesis by HBV remain obscure. HBV may act non-specifically by stimulating active regeneration and cirrhosis which may be associated with long-term chronicity. However, HBV-associated tumors occasionally arise in the absence of cirrhosis, and such hypotheses do not explain the frequent finding of integrated viral DNA in tumors.
In rare instances, the viral genome has been found to be integrated into cellular genes such as cyclin A and a retinoic acid receptor. Translocations and other chromosomal rearrangements also have been observed. Although insertional mutagenesis of HBV remains an attractive hypothesis to explain its oncogenicity, there is insufficient supportive evidence. Like many other cancers, development of hepatocellular carcinoma is likely to be a multifactorial process.
The clonal expansion of cells with integrated viral DNA seems to be an early stage in this process and such clones may accumulate in the liver throughout the period of active virus replication. In areas where the prevalence of primary liver cancer is high, virus infection usually occurs at an early age and virus replication may be prolonged, although the peak incidence of tumor is many years after the initial infection. Delta hepatitis was first recognized following detection of a novel protein, delta antigen HDAg , by immunofluorescent staining in the nuclei of hepatocytes from patients with chronic active hepatitis B.
HDV is coated with HBsAg which is needed for release from the host hepatocyte and for entry in the next round of infection. Two forms of delta hepatitis infection are known. Vaccination against HBV also prevents co-infection. This may cause a second episode of clinical hepatitis and accelerate the course of the chronic liver disease, or cause overt disease in asymptomatic HBsAg carriers. In areas of low prevalence of HBV, those at risk of hepatitis B, particularly intravenous drug abusers, are also at risk of HDV infection.
The HDV genome is a closed circular RNA molecule of nucleotides and resembles those of the satellite viroids and virusoids of plants and similarly seems to be replicated by the host RNA polymerase II with autocatalytic cleavage and circularization of the progeny genomes via trans -esterification reactions ribosome activity. Consensus sequences of viroids which are believed to be involved in these processes also are conserved in HDV.
This is encoded in an open reading frame in the antigenomic RNA but four other open reading frames which are also present in the genome do not appear to be utilized. The antigen, which contains a nuclear localization signal, was originally detected in the nuclei of infected hepatocytes and may be detected in serum only after stripping off the outer envelope of the virus with detergent.
Transmission studies in chimpanzees established that the main agent of parenterally acquired non-A, non-B hepatitis was likely to be an enveloped virus some 30 to 60 nm in diameter. These studies made available a pool of plasma which contained a relatively high titer of the agent. In order to clone the genome, the virus was pelleted from the plasma.
The resultant cDNA was then inserted into the bacteriophage expression vector lambda gt 11 and the libraries screened using serum from a patient with chronic non-A, non-B hepatitis. This approach led to the detection of a clone designated which was found to bind to antibodies present in the sera of several individuals infected with non-A, non-B hepatitis.
This clone was used as a probe to detect a larger, overlapping clone in the same library. It was possible to demonstrate that these sequences hybridized to a positive-sense RNA molecule of around 10, nt which was present in the livers of infected chimpanzees but not in uninfected controls. No homologous sequences could be detected in the chimpanzee or human genomes.
Thus, clones covering the entire viral genome were assembled and the complete nucleotide sequence determined. Successful cloning of portions of the viral genome permitted the development of new diagnostic tests for infection by the virus. Since the original antigen was detected by antibodies in the serum of an infected patient it was an obvious candidate for the basis of an ELISA to detect anti-HCV antibodies.
A larger clone, C, was assembled from a number of overlapping clones and expressed in yeast as a fusion protein using human superoxide dismutase sequences to facilitate expression, and this fusion protein formed the basis of first generation tests for HCV infection. The antigen comprises amino acid sequences from the non-structural, NS4, region of the genome and C contains both NS3 and NS4 sequences. It is now known that antibodies to C are detected relatively late following an acute infection.
Furthermore, the first generation ELISAs were associated with a high rate of false positive reactions when applied to low incidence populations, and there were further problems with some retrospective studies on stored sera. Data based on this test alone should, therefore, be interpreted with caution. Second generation tests include antigens from the nucleocapsid and further non-structural regions of the genome.
The former C22 is particularly useful and antibodies to the HCV core protein seem to appear relatively early in infection. These second generation tests confirm that HCV is the major cause of parenterally transmitted non-A, non-B hepatitis.
Routine testing of blood donations is now in place in many countries and prevalence rates vary from 0. Most of those with antibody have a history of parenteral risk such as a history of transfusion or administration of blood products or of intravenous drug abuse.
There is little evidence for sexual or perinatal transmission of HCV and it is not clear what are the natural routes of transmission. The availability of the nucleotide sequence of HCV made possible the use of the polymerase chain reaction PCR as a direct test for the genome of the virus. Whether the virus is cytopathic or whether there is an immunopathological element remains unclear.
HCV infection is also associated with progression to primary liver cancer. For example, in Japan, where the incidence of hepatocellular carcinoma has been increasing despite a decrease in the prevalence of HBsAg, HCV is now considered the major risk factor. There is no DNA intermediate in the replication of the HCV genome or integration of viral nucleic acid and viral pathology may contribute to oncogenesis through cirrhosis and regeneration of liver cells.
HCV rarely seems to cause fulminant hepatitis. It has been proposed that HCV should be the prototype of a third genus in the family Flaviviridae.
All of these genomes contain a single large open reading frame which is translated to yield a polyprotein of around amino acids in the case of HCV from which the viral proteins are derived by post-translational cleavage and other modifications. The amino acid sequence of the nucleocapsid protein seems to be highly conserved among different isolates of HCV.
The next domain in the polyprotein also has a signal sequence at its carboxyl-terminus and may be processed in a similar fashion. These glycoproteins have not been visualized in vivo and the molecular sizes are estimated from sequence data and expression studies in vitro. Other post-translational modifications, including further proteolytic cleavages, are possible.
These proteins are the focus of considerable interest because of their potential use in tests for the direct detection of viral proteins and for HCV vaccines. Nucleotide sequencing studies reveal that both domains contain hypervariable regions.
It is possible that this divergence has been driven by antibody pressure and that these regions specify important immunogenic epitopes. In the flaviviruses, NS3 has two functional domains, a protease which is involved in cleavage of the non-structural region of the polyprotein and a helicase which is presumably involved in RNA replication. Motifs within this region of the HCV genome have homology to the appropriate consensus sequences, suggesting similar functions.
Hepatitis C virus consists of a family of highly related but nevertheless distinct genotypes, numbering at present 6 genotypes and various subtypes with differing geographical distribution, and with a complex nomenclature. The C, NS3 and NS4 domains are the most highly conserved regions of the genome, and therefore these proteins are the most suitable for use as capture antigens for broadly reactive tests for antibodies to HCV.
The sequence differences observed between HCV groups suggest that virus-host interactions may be different, which could result in differences in pathogenicity and in response to antiviral therapy. It is important, therefore, to develop group- and virus-specific tests. The degree of divergence apparent within the viral envelope proteins implies the absence of a broad cross-neutralizing antibody response to infection by viruses of different groups.
Indeed, sequence changes within this region may occur during the evolution of disease in individual patients and may play an important role in progression to chronicity. Neutralizing antibodies have not been identified so far. The virus has not been cultivated in vitro cf. Yellow fever flavivirus, which has been cultured and from which vaccines have been prepared. Nevertheless, approaches to vaccine development could be based on techniques used for the development of vaccines against the Flaviviruses and Pestiviruses.
About 30 years ago, a series of transmission studies of human viral hepatitis were initiated in small South American tamarins or marmosets, which were chosen because of their very limited contact with man, implying that they were unlikely to have been infected with human viruses. A serum which was obtained on the third day of jaundice from a young surgeon GB with jaundice-induced hepatitis in each of four inoculated marmosets and was passaged serially in these animals.
These important observations remained controversial until the application recently of modern molecular virological techniques. Cross-challenge experiments showed that infection with the original infectious tamarin inoculum conferred protection from reinfection with GBV-B but not GBV-A. The organization of the genes of the GBV-A, B, and C genomes shows that they are related to other positive-strand RNA viruses with local regions of sequence identity with various flaviviruses.
Diagnostic reagents were prepared with recombinant antigens, and limited testing was carried out in groups of patients, blood donors and other selected individuals: patients with non-A, B, C, D, E hepatitis, multitransfused patients, intravenous drug addicts and other populations with a high incidence of viral hepatitis.
The development and availability of specific diagnostic reagents will establish the epidemiology of these newly identified viruses, their pathogenic significance in man and their clinical and public health importance. Turn recording back on. National Center for Biotechnology Information , U. Show details Baron S, editor. Search term. Chapter 70 Hepatitis Viruses Arie J. General Concepts Viral hepatitis has emerged as a major public health problem throughout the world affecting several hundreds of millions of people.
The hepatitis viruses include a range of unrelated and often highly unusual human pathogens. Hepatitis A virus Hepatitis A virus HAV , classified as hepatovirus, is a small, unenveloped symmetrical RNA virus which shares many of the characteristics of the picornavirus family, and is the cause of infectious or epidemic hepatitis transmitted by the fecal-oral route. Hepatitis C virus Hepatitis C virus HCV , is an enveloped single-stranded RNA virus which appears to be distantly related possibly in its evolution to flaviviruses, although hepatitis C is not transmitted by arthropod vectors.
Hepatitis E virus Hepatitis E virus HEV , the cause of enterically-transmitted non-A, non-B hepatitis, is another non-enveloped, single-stranded RNA virus, which shares many biophysical and biochemical features with caliciviruses. Patients with ascites with suspicion for spontaneous bacterial peritonitis should be treated with antibiotics empirically.
Liver transplantation can be an option in end-stage liver disease, but patients must abstain from alcohol for at least six months before they are candidates for transplantation. Many other disorders can present with similar symptoms and signs commonly found in patients of hepatitis. Patients with acute and chronic active viral hepatitis infections usually present with malaise, fatigue, low-grade fever, anorexia, loss of weight, nausea, vomiting, etc. Patients can be completely normal on physical exam or may have right upper quadrant pain with hepatomegaly, urticarial rash and may show signs of dehydration.
In advanced stages of liver disease from chronic viral hepatitis, patients may present with hematemesis, ascites, pedal edema, encephalopathy, etc. These symptoms and signs are observable with many other acute or chronic infectious or non-infectious conditions. Patients who have viral or bacterial gastroenteritis, acute cholecystitis, acute cholelithiasis, tuberculosis, HIV, liver abscess, malignancies such as pancreatic cancer, lymphoma, and hepatocellular cancer, small bowel obstruction, peptic ulcer disease can all have an overlap of these signs and symptoms.
Patients with severe congestive heart failure can present with pedal edema, ascites, and hepatomegaly due to hepatic congestion. Patients who have gastrointestinal bleeding from other causes, including cirrhosis due to advanced non-alcoholic steatohepatitis, can present similarly like patients with advanced liver disease due to viral, autoimmune, or alcoholic hepatitis. Patients with hereditary hemochromatosis can present in their 50s or 60s with abdominal pain, fatigue, weakness, and symptoms and signs of liver failure.
Hereditary hemochromatosis is an autosomal recessive disease that disrupts the body's iron regulation, and excess iron becomes deposited in various organs of the body, including the liver. Diagnosis is usually by checking serum iron, serum ferritin, and serum transferrin levels. A liver biopsy may become necessary to evaluate for the degree of fibrosis and to differentiate it from other disorders of the liver, including viral or autoimmune hepatitis. Patients can present with joint pain, and some patients complain of pain in the knuckles of the first two fingers called the "iron fist" sign.
This sign is specific to hereditary hemochromatosis but is not present in all the patients. Drug-induced liver injuries have become more common, and more than a thousand drugs have been identified, and studies are underway to find out more about them.
Patients with drug-induced liver injuries can be completely asymptomatic, with only lab abnormalities of elevated aminotransferases to acute or chronic hepatitis or acute liver failure and remain one of the biggest causes of emergency liver transplants. The unregulated use of herbal and dietary supplements has created a new challenge to identify and treat patients promptly.
Patients with autoimmune hepatitis and alcoholic hepatitis can also have similar symptoms as in viral hepatitis, especially when the disease is advanced, and patients experience severe liver dysfunction. A careful history, laboratory studies, and liver biopsy, when necessary, should be obtained to differentiate them. Further information on how to diagnose and differentiate these conditions are obtainable from the evaluation section of this article.
Since there are so many conditions that can present with similar symptoms and signs, it is not within the scope of this article to discuss every condition listed in the differential diagnosis. Hepatitis A infection is usually a mild self-limiting illness. Patients infected with hepatitis A virus develop lifelong immunity against subsequent infection from hepatitis A.
Overall, mortality is very low, and complications including relapse, jaundice, and fulminant liver failure are rare. Patients who are immunocompromised, the elderly, and young children are at higher risk compared to healthy adults.
Patients with hepatitis B infection are at risk of developing chronic hepatitis and cirrhosis as well as hepatocellular carcinoma as a consequence. Fulminant hepatic failure happens in about 0. Chronic liver disease from chronic hepatitis B infection is responsible for approximately fatalities per year globally. These patients are at high risk of developing chronic active hepatitis, cirrhosis, and hepatocellular carcinoma.
Chronic hepatitis C infection remains one of the leading reasons for liver transplantation. The hepatitis C related mortality rate in the United States increased till but has been declining since but remains elevated in developing countries. Patients who have chronic hepatitis B virus infection and then get coinfected with hepatitis D virus tend to develop chronic hepatitis D infection and leads to the development of chronic hepatitis more commonly compared to patients who only chronic hepatitis B infection and a majority of those patients end up developing end-stage liver disease and cirrhosis.
Hepatitis E infection is a mild self-limiting illness like hepatitis A infection. The exact mechanism of how it causes a high mortality rate in pregnant patients is not clear. Most patients are asymptomatic in acute infection with normal aminotransferase levels.
Fulminant hepatic failure and chronic infections are rare with hepatitis G infection. The prognosis of autoimmune hepatitis is directly related to the severity of liver inflammation. Patients who have severe symptoms and signs of extensive liver damage on the initial presentation have a high mortality rate and bad prognosis compared to those patients in whom the initial disease is mild. Patients who frequently relapse or do not respond to treatment also have a worse prognosis. About half of the patients who have severe autoimmune hepatitis die within five years without treatment.
The development of hepatocellular carcinoma is less common in patients who have cirrhosis from autoimmune hepatitis compared to those patients who have cirrhosis from other causes. The prognosis of patients who have alcoholic hepatitis depends on whether they abstain from alcohol and the degree of liver injury.
Patients who abstain from alcohol strictly show improvement in liver function over months to years and liver biopsy also reveals the resolution of histologic changes. Patients who continue to drink alcohol continue to get worse with the development of cirrhosis. A discussion on these prognostic scoring methods is beyond the scope of this article. Complications of viral hepatitis include chronic infection with chronic active hepatitis, acute or subacute hepatic necrosis, cirrhosis, liver failure, hepatocellular carcinoma in patients with hepatitis B or C infection.
Patients who have hepatitis B infection are at high risk of developing chronic infection. Cirrhosis developing from hepatitis C infection is a leading cause of liver transplantation in the United States. Cirrhosis itself can cause multiple complications, including hepatic encephalopathy, portal hypertension, ascites, spontaneous bacterial peritonitis, variceal bleed, hepatorenal syndrome, etc.
Patients who have chronic hepatitis C infection also have a high risk of developing extrahepatic complications including cryoglobulinemia which can lead to rash, vasculitis, and glomerulonephritis secondary to deposition of immune complexes in the small vessels, non-Hodgkin lymphoma, focal lymphocytic sialadenitis, autoimmune thyroiditis, porphyria cutanea tarda, lichen planus, etc.
Complications of autoimmune hepatitis are similar to complications of viral hepatitis, or patients can develop end-stage liver disease with cirrhosis, which can lead to complications like ascites, hepatic encephalopathy, coagulopathy, variceal bleed, portal hypertension, and severe malnutrition.
Hepatocellular carcinoma can occur but is not as common as seen in patients with chronic hepatitis B or C infection. Some patients can develop primary biliary cirrhosis and eventually developed hepatocellular carcinoma.
Complications of alcoholic hepatitis are similar to that of cirrhosis. Patients can develop variceal bleeding with portal hypertension, hepatic encephalopathy, coagulopathy, and severe thrombocytopenia, ascites, and spontaneous bacterial peritonitis.
Patients developing cirrhosis and its complications many times require close monitoring with hospitalization and emergency treatment. Patients with variceal bleed require immediate resuscitation, protection of the airway, endoscopy with sclerotherapy or band ligation of the varices. Many patients require administration of somatostatin or octreotide.
Patients with hepatic encephalopathy are usually put on rifaximin or lactulose as an outpatient and require close monitoring. Worsening of encephalopathy involves hospitalization. These patients are typically maintained on a low protein diet. Patients with severe coagulopathy require vitamin K administration and platelet transfusion if necessary.
Patients with ascites are treated with diuretics, control of dietary salt intake, and may need frequent paracentesis with intermittent use of intravenous albumin. Some patients develop spontaneous bacterial peritonitis and require antibiotics. The majority of patients require frequent hospitalizations due to complications of cirrhosis, and their quality of life is significantly altered. Patients who develop hepatocellular carcinoma may require chemotherapy, radiation therapy, and liver transplantation.
Patient education is key to preventing and controlling hepatitis, especially viral and alcoholic hepatitis. Patients who have viral hepatitis must obtain education educated regarding the importance of routine follow-up and the importance of monitoring the disease progression and development of complications.
They should learn about the importance of personal hygiene, including frequent handwashing. People who are traveling to endemic areas should be advised not to drink untreated water or ingest shellfish or raw seafood, and fruits and veritable should always be eaten after being cooked or after being peeled. Patients who have hepatitis A should not handle food for others until they stop shedding the virus. Patients should receive instruction about not sharing any articles, including toothbrushes, razors, or needles that have the potential for contamination with saliva, semen, or blood.
All the patients should avoid using hepatotoxic agents, including alcohol and acetaminophen. Patients who are having a disease progression with liver disease should be referred to a gastroenterologist or hepatologist promptly. Patients with features of liver damage that includes liver fibrosis, cirrhosis, hepatocellular carcinoma, and features of portal hypertension should be monitored with routine labs.
All pregnant women should have screening for hepatitis B infection and HIV infection. If they test positive for hepatitis B infection, then both the mother and newborn should be treated appropriately.
Neonates who are born to mothers who have hepatitis B infection should be given hepatitis B vaccination within 12 hours of birth to prevent the transmission of the virus.
Sometimes the mother needs to be treated actively during pregnancy, also depending on her viral load and HIV status. Healthcare workers should maintain strict infection control practices, and those at risk of contracting hepatitis C virus infection should be offered appropriate health education, testing, and treatment as required. Healthcare providers should be able to identify the individuals at risk and test them for hepatitis C infection. These individuals include people who have a history of injection drug use, persons infected with HIV, individuals with blood-borne exposure to hepatitis C virus, and certain healthcare workers.
Patients with autoimmune hepatitis should be tested for other autoimmune diseases and should be referred early in their illness to a gastroenterologist or a hepatologist. Referral to other specialists like endocrinology or rheumatology is necessary if the clinician finds evidence for other autoimmune disorders during the workup. Patients should have counsel about the importance of side effects of treatment, including corticosteroids, as many of them would require long term treatment.
Patients who are at risk of developing alcoholic hepatitis or who already have alcoholic hepatitis should be educated about abstaining from alcohol completely and about serious health consequences of continued alcohol use.
Patients should be referred to rehabilitation programs and should be encouraged to attend them regularly. Patients should understand the importance of preventing hepatitis, and it requires emphasis that preventing hepatitis is much easier than treating hepatitis. Viral hepatitis is preventable with vaccination. Individuals traveling to areas where hepatitis A is endemic should be offered hepatitis A vaccine one month before traveling.
Other patients who should be offered hepatitis A vaccine are individuals who use illicit drugs, men who have sex with men, patients with chronic liver disease, patients who are awaiting liver transplant or are recipients of a liver transplant, patients receiving clotting factor concentrates, and individuals who work with hepatitis virus-infected primates in laboratories.
Patients can receive inactivated hepatitis A virus vaccine through the intramuscular route with a booster dose recommended after six months. Patients exposed to hepatitis A virus can also be given postexposure prophylaxis with hepatitis A immunoglobulin and should have it within 48 hours of exposure for higher effectiveness. Typically it is recommended for individuals who are in close contact with the patients of hepatitis A infection at home or in daycare centers. Hepatitis B vaccine is recommended for all the infants as a part of the routine immunization schedule.
It should also be given to the adults at high risk of infection including patients on dialysis, healthcare workers who are at risk of exposure to blood and body fluids, people with sexual partners who have hepatitis B infection, sexually active persons who are not in a long-term monogamous relationship, persons who are being evaluated or treated for sexually transmitted infections, men who have sex with men, individuals who share needles or syringes, household contacts of individuals who have hepatitis B infection, residents and staff of facilities for developmentally disabled persons and in correctional facilities, victims of sexual assault or abuse, people with chronic liver disease, HIV infection or diabetes, individuals who have a known sexual or household contact with an acutely infected patient, and those individuals who had an inadvertent percutaneous or mucosal exposure.
Infants are given initial vaccination at the time of birth with repeat vaccination at 1 to 2 months and 6 to 18 months. For the adults, after the initial vaccination, it is repeated at one month and six months.
Some clinicians recommend booster dose at 5 to 10 years. Individuals can also receive postexposure prophylaxis with hepatitis B immunoglobulin. It is usually given after liver transplantation to those patients who were infected with the hepatitis B virus to reduce the damage to the liver allograft. Patients requiring frequent transfusion of blood products or factor concentrates like patients of hemophilia should also receive the vaccination; however, with higher usage of recombinant factor and better techniques for the viral elimination process have decreased the risk of infection significantly.
Vaccine for hepatitis C is currently not available, and immunoglobulin is not proven to be effective in preventing transmission. It is, therefore, of high importance to put infection control practices in place and prevent the contamination of blood, organs, and semen and prevent the transmission of the virus into donor pools with better screening and improved viral elimination techniques.
Since the hepatitis D virus occurs as a coinfection when hepatitis B virus infection is present, transmission can be prevented by immunizing patients against hepatitis B virus. Currently, it is not possible to prevent hepatitis D virus superinfection in patients with chronic hepatitis B infection. Vaccine for hepatitis E virus infection does not exist at this time, and the administration of immunoglobulin does not prevent the disease. Patients who are transplant recipients or get frequent transfusions, injection drug users, hemodialysis patients, and men who have sex with men are the groups that are at increased risk.
However, there is currently not a vaccine available for hepatitis G. This article discusses hepatitis, which is a complex disease and requires an interprofessional approach from healthcare providers to tackle it. The article discusses strategies to prevent hepatitis through patient education and vaccination and the importance of closer monitoring for disease progression and complications. These strategies require significant interprofessional communication and care coordination by physicians, including primary care physicians and specialists, nurses, pharmacists, and other health professionals, to enhance patient-centered care.
Nursing needs to work closely with the patient to ensure they understand their disease, are compliant with medications and vaccines, and note progress or lack thereof. Pharmacists are crucial to ensuring the proper medications at the correct dose are in the therapy regimen, and that there are no interactions. Any issues noted by any member of the interprofessional healthcare team need to be shared and charted, so everyone operates from the same data.
These measures can help improve the outcomes and aid to patient safety and can also help enhance team performance. Hepatitis D stages and serological markers. Contributed by Umair Masood, MD. Chronic inflammation in a distorted portal space is a feature of chronic hepatitis. Contributed by Fabiola Farci, MD.
This book is distributed under the terms of the Creative Commons Attribution 4. Turn recording back on. National Center for Biotechnology Information , U. StatPearls [Internet]. Search term. Affiliations 1 University of Illinois. Continuing Education Activity The term hepatitis means inflammation of the liver — hepatitis most commonly results from viruses.
Introduction Hepatitis is defined as inflammation of the liver that can result from a variety of causes such as heavy alcohol use, autoimmune, drugs, or toxins. Hepatitis C Hepatitis C virus is an RNA virus and is a member of the Flaviviridae family with one serotype, but at least six major genotypes and more than 80 subtypes. Autoimmune Hepatitis The exact etiology of autoimmune hepatitis is unknown. Alcoholic Hepatitis The exact mechanism of how alcoholic hepatitis is not well defined; many factors play a role that includes genetic factors, metabolism of ethanol and its metabolite acetaldehyde causing damage to hepatocyte cell membranes, malnutrition, immunologic factors such as stimulation of cytokines accelerating cell death, steatotic changes, free radicals, and oxidative injuries, etc.
Epidemiology Viral Hepatitis Viral Hepatitis is considered a major public health issue. Hepatitis C Hepatitis C virus is the most prevalent cause of parenteral hepatitis worldwide. Hepatitis D Hepatitis D occurs in patients who are positive for HBsAg, and hepatitis D either occurs as a coinfection with Hepatitis B or patients who are chronic Hepatitis B virus carries can get superinfection with hepatitis D virus.
History and Physical Clinical Presentation Viral Hepatitis Clinical presentation of viral hepatitis can be different in every individual depending on the type of virus causing the infection. Typically patients with viral hepatitis go through 4 phases. Hepatitis B Patients with hepatitis B virus infection enter the prodromal phase after the incubation period and have symptoms of anorexia, malaise, and fatigue which are the most common initial clinical symptoms.
Hepatitis C Patients infected with the hepatitis C virus develop similar symptoms after the incubation period to those of hepatitis B virus infection during the acute infection phase with symptoms of anorexia, malaise, and fatigue. Hepatitis D The majority of patients who have a simultaneous infection with the hepatitis B virus and hepatitis D virus have a self-limited infection.
Hepatitis E Patients with acute hepatitis E virus infection develop an acute self-limited illness similar to hepatitis A virus infection.
Autoimmune Hepatitis Autoimmune hepatitis can clinically present in various ways. Alcoholic Hepatitis Patients with alcoholic hepatitis usually are malnourished and have physical signs of hepatomegaly and splenomegaly. Physical Examination Physical findings vary in individual patients depending on the time of presentation. Evaluation Baseline evaluation in a patient suspected to have viral hepatitis can be started by checking a hepatic function panel.
Viral Hepatitis Hepatitis A The standard test for diagnosing acute infection with hepatitis A virus is the presence of immunoglobulin M IgM antibody to the hepatitis A virus. Hepatitis B Work-up for hepatitis B virus infection divides into work-up for acute infection and chronic infection.
Acute Infection In patients who have an acute hepatitis B virus infection, the first serum marker to appear is the hepatitis B surface antigen HBsAg. Hepatitis A Treatment for acute hepatitis A infection is supportive. Acute Hepatitis B Infection Treatment of acute hepatitis B virus infection is supportive and similar to the treatment of acute hepatitis A infection.
Acute Hepatitis C Infection Acute hepatitis C infection is usually not detected frequently, but when detected, early interferon therapy is an option. Differential Diagnosis Many other disorders can present with similar symptoms and signs commonly found in patients of hepatitis. Liver abscess. Prognosis Viral Hepatitis Prognosis of viral hepatitis depends on the virus, causing the infection. Complications Viral Hepatitis Complications of viral hepatitis include chronic infection with chronic active hepatitis, acute or subacute hepatic necrosis, cirrhosis, liver failure, hepatocellular carcinoma in patients with hepatitis B or C infection.
Deterrence and Patient Education Patient education is key to preventing and controlling hepatitis, especially viral and alcoholic hepatitis. How long does it last? How is it spread? Hepatitis A Hepatitis B Hepatitis C Hepatitis A is spread when a person ingests fecal matter—even in microscopic amounts—from contact with objects, food, or drinks contaminated by feces or stool from an infected person.
The hepatitis B virus can also be transmitted from: Birth to an infected mother Sex with an infected person Sharing equipment that has been contaminated with blood from an infected person, such as needles, syringes, and even medical equipment, such as glucose monitors Sharing personal items such as toothbrushes or razors Poor infection control has resulted in outbreaks in health care facilities.
The hepatitis C virus can also be transmitted from: Sharing equipment that has been contaminated with blood from an infected person, such as needles and syringes Receiving a blood transfusion or organ transplant before when widespread screening virtually eliminated hepatitis C from the blood supply Poor infection control has resulted in outbreaks in health care facilities Birth to an infected mother. Who should be vaccinated? All infants All children and adolescents younger than 19 years of age who have not been vaccinated People at risk for infection by sexual exposure including: people whose sex partners have hepatitis B, sexually active people who are not in a long-term, mutually monogamous relationship, people seeking evaluation or treatment for an STD, and men who have sex with men People at risk for infection by exposure to blood including: people who inject drugs, people who live with a person who has hepatitis B, residents and staff of facilities for developmentally disabled people, health care and public safety workers at risk for exposure to blood or blood-contaminated body fluids on the job Hemodialysis patients and predialysis, peritoneal dialysis, and home dialysis patients People with diabetes aged 19—59 years; people with diabetes aged 60 or older should ask their doctor.
International travelers to countries where hepatitis B is common People with hepatitis C People with chronic liver disease People with HIV People who are in jail or prison All other people seeking protection from hepatitis B virus infection. There is no vaccine available for hepatitis C. How serious is it?
Hepatitis A Hepatitis B Hepatitis C People can be sick for a few weeks to a few months Most recover with no lasting liver damage Although very rare, death can occur. Who should be tested? CDC recommends hepatitis C testing for: All adults aged 18 years and older All pregnant women during each pregnancy People who ever injected drugs and shared needles, syringes, or other drug preparation equipment, including those who injected once or a few times many years ago.
Regular testing is recommended for people who currently inject and share needles, syringes, or other drug preparation equipment. People with HIV People who have ever received maintenance hemodialysis. Regular testing is recommended for people who currently receive maintenance hemodialysis. ABC Table What causes it?
0コメント