Chronic Viral Hepatitis B Without Delta Agent

Hepatitis D Viral Infection

Hepatitis D viral infection concerns a distinct subgroup of simultaneously HBV-infected individuals usually presenting with severe chronic liver disease. HDV is a defective RNA agent needing the presence of HBV for its life cycle. Two major specific patterns of infection can occur, namely HDVâHBV coinfection or HDV superinfection of a chronic HBV carrier status. Prevention and therapeutic strategies for HDV are similar to those applied in HBV recipients . As most of these recipients present with a nonreplicating HBV status, results of LT are outstanding with survival rates exceeding 90%.

Kenneth E. Sherman MD, PhD, Halim Muslu MD, in, 2010

Hepatitis B Surface Antigen Test

A hepatitis B surface antigen test shows if youre contagious. A positive result means you have hepatitis B and can spread the virus. A negative result means you dont currently have hepatitis B. This test doesnt distinguish between chronic and acute infection. This test is used together with other hepatitis B tests to determine the .

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You can use it for research or reference.

The following cases of disease should be notified:

• Confirmed acute
• Although it is recognized that chronic hepatitis B infections are not reportable in all provinces and territories, where possible, chronic and unspecified infections should be notified to the national level.

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Acute Hepatitis B Infection

An acute hepatitis B infection may last up to six months and infected persons are able to pass the virus to others during this time. A simple blood test can let a person know if the hepatitis B virus is in their blood or if they have successfully gotten rid of the virus. Until your health care provider confirms that the blood test shows that there is no more hepatitis B virus in your blood, it is important to protect others from a possible infection.

It is also important to have your sexual partner and family members get tested for hepatitis B. If they have not been infected and have not received the hepatitis B vaccine then they should also start the hepatitis B vaccine series.

Symptoms of an acute infection may include loss of appetite, joint and muscle pain, low-grade fever, and possible stomach pain. Although most people do not experience symptoms, they can appear 60-150 days after infection, with the average being 90 days or 3 months. Some people may experience more severe symptoms such as nausea, vomiting, jaundice , or a bloated stomach that may cause them to see a health care provider.

If treatment for an acute hepatitis B infection is required, a person may be hospitalized for general support. Rest and managing symptoms are the primary goals of this medical care. A rare, life-threatening condition called fulminant hepatitis can occur with a new acute infection and requires immediate, urgent medical attention since a person can go into sudden liver failure.

Development Of Tools To Screen For Viral Hepatitis

With the confirmed association between viral hepatitis and the presence of the AuAg, Blumberg and Alter, along with others at the NIH, engaged in the development of screening and diagnostic tests to prevent hepatitis following blood transfusions. Initially, Ouchterlony was found to be fairly sensitive and specific, and it was subsequently used as a crude screening tool that became the first-generation test for viral hepatitis screening. This was rapidly followed by more sophisticated tests, such as radioimmunoassay that were more objective and quantitative measurement methods as opposed to using Ouchterlony, which was somewhat subjective . These initial screening efforts contributed to the greatest decrease in incidence of transfusion-associated hepatitis, from 30% to 10% during the 1970s .

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A Tabular Or Chart Listing Of Features And Signs And Symptoms

HBV or HDV infection does not have any pathognomonic or characteristic features.

Some less common clinical presentations

Extrahepatic manifestations occur in approximately 10% of patients with chronic HBV infection. Mediated by circulating immune complexes, acute hepatitis may be heralded by a serum sickness-like syndrome manifested as fever, skin rashes, arthralgia, and arthritis, which usually subside with the onset of jaundice.

Hepatitis B virus-related glomerulonephritis, most commonly membranous glomerulonephritis, is another manifestation.

Other extrahepatic manifestations include rarely essential mixed cryoglobulinemia and aplastic anemia.

Other diseases and conditions that might mimic the signs, symptoms, or clinical features of HBV infection

Other viral hepatitis , perform HCV antibodies, and HCV RNA.

Discovery Of Hdv And Other Viral Hepatidities

Following the discovery of components of the HBV virion, efforts increased to identify other viral pathogens that cause viral hepatitis, and these subsequent discoveries aided in the eventual identification of HDV. The hepatitis A virus was discovered in 1973, using immune EM, as was similarly performed previously for visualization of HBV. Preceding epidemiologic and direct human experimentation showed that HAV was transmissible by oral inoculation with filtered stool extracts from infected patients. Using this information, Feinstone, Kapikian, and Purcell discovered HAV in fecal samples obtained from human volunteers with appropriate clinical histories for hepatitis A . Specifically, stool specimens from these patients were incubated with convalescent serum from other distinct patients with hepatitis A, leading to the visualization of virus particles heavily coated with serum antibody. With the discovery of both HAV and HBV, research on viral hepatitis progressed, permitting isolation of more elusive viral pathogens with less distinctive clinical phenotypes.

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Diagnostic And Clinical Features

Active HDV infection is diagnosed by the finding in serum or liver of the HDV RNA or of the HDAg. Viremia can be detected with genetic probes that hybridize with complementary HDV RNA transcription polymerase chain reaction can detect in serum 10 to 100 copies of the viral genome.

The clinical course of acute HBV/HDV coinfections varies according to the degree of HBV and HDV expression and the interplay between the two viruses, ranging from icteric hepatitis, with full but transient expression of both viruses, to milder anicteric forms associated with diminished HDV expression. Early repression of HBV can inhibit HBsAg synthesis to the extent that this marker is not detectable in serum.

Acute hepatitis D is clinically and histologically indistinguishable from ordinary hepatitis B distinction requires specific serologic testing. The markers of HBV infection are the HBsAg and IgM anti-HBc finding the latter is required for diagnosing HBV/HDV coinfection as opposed to superinfection. Coinfection hepatitis is diagnosed from the increase of IgM anti-HD the IgG antibody also increases but is usually elevated after a delay of several weeks, compared to the IgM antibody.

Severe forms of the illness are accompanied by the full battery of HDV markers, including early HD antigenemia. HDV RNA can be detected in serum very soon during the course of infection and disappears with resolution of disease.

Quirino Lai, … Jan P. Lerut, in, 2014

Treatment Options For Hepatitis B

Acute hepatitis B usually doesnt require treatment. Most people will overcome an acute infection on their own. However, rest and hydration will help you recover.

Antiviral medications are used to treat chronic hepatitis B. These help you fight the virus. They may also reduce the risk of future liver complications.

You may need a liver transplant if hepatitis B has severely damaged your liver. A liver transplant means a surgeon will remove your liver and replace it with a donor liver. Most donor livers come from deceased donors.

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Clinical Manifestations And Pathogenesis Of Viral Hepatitis

Clinical manifestations of acute infection from agents causing viral hepatitis vary from asymptomatic or mild flulike illness without jaundice to fatal liver failure, depending on the patients immune response, the viral pathogen involved, and other unknown virushost factors. Acute viral hepatitis can be characterized by a prodromal phase of profound anorexia, nausea, vomiting, malaise, and fever. In addition, urticaria and arthralgia occur occasionally. Subsequently, the icteric phase may begin and jaundice, if present, usually peaks in 12 weeks and fades during a 2- to 4-week recovery phase. Acute liver failure , a rare syndrome characterized by rapid clinical deterioration with the onset of hepatic encephalopathy and coma without known preexisting liver disease, may develop in some patients . ALF, also designated as fulminant hepatitis, carries a high morbidity and mortality. With regards to acute viral hepatitis, as with many other etiologies of ALF, care is mainly supportive. Lamivudine may be considered for treatment of patients with acute HBV, although evidence of efficacy is questionable .

Discovery Of The Australian Antigen

The early 1960s marked several important milestones in the history of viral hepatitis, catapulted by the discovery of the HBV surface antigen by Blumberg and Alter. Although it was a peculiar and serendipitous discovery, Blumbergs previous exploits had enabled the initial experiments to be conducted. In the 1950s, he collected blood samples from several indigenous populations located throughout the world. His goal was to study the inherited diversity in humans with a focus on finding the basis behind variability in disease susceptibility and outcomes. After these initial blood collection efforts, Blumberg assumed a position at the National Institutes of Health , where at the same time Alter was studying patients who had undergone a blood transfusion and subsequently developed febrile transfusion reactions. Using agar gel double diffusion, also known as Ouchterlony, Alter began testing serum from patients who had received multiple transfusions against serum that Blumberg had collected from individuals during his travels . Initial efforts were focused on identifying new serum lipoproteins because Blumberg had already established that lipoproteins were polymorphic between individuals .

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How Can I Confirm The Diagnosis

What tests should be ordered first?

BsAg is the hallmark of HBV infection. It is usually detectable 1 to 10 weeks after an acute exposure to HBV, and approximately 2 to 6 weeks before the onset of clinical symptoms. Most patients who recover from acute hepatitis B clear HBsAg in 4 to 6 months. Persistence of HBsAg in serum for more than 6 months implies chronic infection. Anti-HBs can be detected in individuals who recovered from HBV infection and in those who successfully responded to hepatitis B vaccination.

The antigen HBeAg is a marker of HBV replication and infectivity. Its presence is usually associated with the detection of HBV DNA in serum and a high risk of transmission of infection. However, HBeAg-negative and anti-HBe-positive patients may continue to have active liver disease and moderate levels of HBV DNA in serum. These patients usually have HBV variants with diminished or abolished production of HBeAg.

In patients with acute hepatitis B, serum HBV DNA appears early and may precede the detection of HBsAg.

Chronic hepatitis B is categorized into four phases based on the virus activity and the patientâs immune response to the virus activity . Patients may evolve through some or all phases with variable duration.

• Inactive carrier: HBeAg , HBV DNA low, ALT normal

• Immune tolerant: HBeAg , HBV DNA elevated, ALT normal

• Immune active: HBeAg , HBV DNA elevated, ALT elevated

• Immune reactivation: HBeAg , HBV DNA elevated, ALT elevated

Certain Infectious And Parasitic Diseasesincludes

• certain localized infections – see body system-related chapters

• carrier or suspected carrier of infectious disease
• infectious and parasitic diseases complicating pregnancy, childbirth and the puerperium
• infectious and parasitic diseases specific to the perinatal period
• influenza and other acute respiratory infections

• code to identify resistance to antimicrobial drugs

• herpesviral hepatitis

• Chronic hepatitis b with hepatic coma
• Chronic type b viral hepatitis
• Hepatitis b, chronic
• Hepatitis b, chronic, with hepatic coma

• Inflammation of the liver in humans caused by hepatitis b virus lasting six months or more. It is primarily transmitted by parenteral exposure, such as transfusion of contaminated blood or blood products, but can also be transmitted via sexual or intimate personal contact.

• 441 Disorders of liver except malignancy, cirrhosis or alcoholic hepatitis with mcc
• 442 Disorders of liver except malignancy, cirrhosis or alcoholic hepatitis with cc
• 443 Disorders of liver except malignancy, cirrhosis or alcoholic hepatitis without cc/mcc
• 791 Prematurity with major problems
• 793 Full term neonate with major problems

• : New code
• 2017

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What Other Diseases Conditions Or Complications Should I Look For In Patients With Hepatitis B Virus Infection

Acute HBV infection can lead to fulminant hepatitis. Acute liver failure develops in approximately 0.1% to 0.5% of patients.

Prothrombin time, which reflects hepatic synthetic function, is the best indicator of prognosis.

Progression to cirrhosis occurs in up to 20% of patients with untreated chronic hepatitis B. Annual incidence of hepatic decompensation is 5-8% and hepatocellular carcinoma is 2-4% in patients with cirrhosis. Rates of cirrhosis and HCC increase substantially with HBV DNA level, alt levels, HBeAg positivity, and genotype C. Additional risk factors include advanced age, male gender, immunocompromised state, concomitant viral infection , alcohol use, and metabolic syndrome. Furthermore, risk of HCC is higher in patients from Sub-Saharan Africa, positive family history, and smoking.

What Is Hepatitis Delta

Hepatitis delta, also known as hepatitis D or HDV, is a liver infection caused by the hepatitis delta virus that results in the most severe form of viral hepatitis known to humans. Only those already infected with hepatitis B can acquire hepatitis delta, however, as it is dependent on the hepatitis B virus to reproduce.

Worldwide, more than 296 million people live with hepatitis B and of this number, an estimated 15-20 million are also infected with hepatitis delta. Coinfections lead to more serious liver disease than hepatitis B infection alone. They are associated with faster progression to liver fibrosis, increased risk of liver cancer, and early decompensated cirrhosis and liver failure.

Types of Infection

Hepatitis delta can be acquired either through coinfection or superinfection . A coinfection generally resolves spontaneously after about 6 months, but it can sometimes result in life-threatening or fatal liver failure.

A superinfection is the most common form of hepatitis delta and leads to a more severe liver disease than a chronic hepatitis B infection alone. Up to 90% of superinfected individuals will develop chronic infections of both hepatitis B and delta, of which approximately 70% will progress to cirrhosis , compared to 15-30% of those infected only with the hepatitis B virus.

Prevention

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Is Hepatitis B Contagious

Hepatitis B is highly contagious. It spreads through contact with infected blood and certain other bodily fluids. Although the virus can be found in saliva, its not spread through sharing utensils or kissing. It also doesnt spread through sneezing, coughing, or breastfeeding. Symptoms of hepatitis B may not appear for 3 months after exposure and can last for 212 weeks. However, you are still contagious, even

To screen for hepatitis B, your doctor will perform a series of blood tests.

A Listing Of A Subset Of Second

There are currently six medications approved for use in the United States. Choice of antiviral agent is driven by side effect profile, co-morbidities, prior therapy exposure, HBV genotype, costs, and pregnancy state.

Peg-IFN-2a: dose of 180 mcg weekly. Side effects include flu-like symptoms, mood disturbances, cytopenias, autoimmune disorders. Monitoring should include a CBC and TSH every 3 months, monitoring for infection, autoimmune disorders, neuropsychiatric complications, and infections. Pregnancy category C.

Entecavir: dose of 0.5 or 1.0 mg daily. Side effects include lactic acidosis. Pregnancy category C.

Tenofovir: dose of 300mg daily. Side effects include nephropathy, Fanconi-like syndrome, osteomalacia, lactic acidosis. Monitoring should include yearly creatinine clearance, serum phosphate, urine glucose and protein annually, as well as bone density scan if at risk. Pregnancy category B.

Lamivudine: dose of 100mg daily. Side effects include pancreatitis, lactic acidosis. Monitoring should include creatinine kinase and lactic acid if clinical concerns. Pregnancy category C.

Telbivudine: dose of 600mg daily. Side effects include creatine kinase elevations, myopathy, peripheral neuropathy, and lactic acidosis. Monitor creatinine kinase if symptoms. Pregnancy category B.

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Chronic Hepatitis B Infection

People who test positive for the hepatitis B virus for more than six months are diagnosed as having a chronic infection. This means their immune system was not able to get rid of the hepatitis B virus and it still remains in their blood and liver.

The risk of developing a chronic hepatitis B infection is also directly related to the age at which one first becomes exposed to the hepatitis B virus:

• 90% of infected newborns and babies will develop a chronic hepatitis B infection
• Up to 50% of infected children will develop a chronic hepatitis B infection
• 5-10% of infected adults will develop a chronic hepatitis B infection

Learning that you have a chronic hepatitis B infection can be very upsetting. Because most people do not have symptoms and can be diagnosed decades after their initial exposure to the hepatitis B virus, it can be a shock and a surprise to be diagnosed with a chronic hepatitis B infection. The good news is that most people with chronic hepatitis B should expect to live a long and healthy life.

There are effective drug therapies that can control and even stop the hepatitis B virus from further damaging a liver. There are also promising new drugs in the research pipeline that could provide a cure in the very near future. Although the risk of developing a serious liver disease or liver cancer is higher for those living with chronic hepatitis B than those who are not infected, there are still many simple things a person can do to help reduce their risks.

How Is Hepatitis D Diagnosed

Hepatitis D is diagnosed by an ELISA that detects the presence of antibody to hepatitis D in serum or plasma. The presence of the antibody in serum correlates with ongoing hepatitis D replication in the liver. Detection of hepatitis D antigen in liver tissue generally adds little to the diagnostic process. Early in the course of infection, acute hepatitis D may be detectable only by performing a test for the IgM form of the antibody. A PCR-based assay also may be performed to detect the presence of RNA from hepatitis D in serum or tissue. This assay is not commercially available, and its use seems to add little to the antibody testing. Because hepatitis D occurs only with concurrent acute hepatitis B infection or as a superinfection of chronic hepatitis B, there is little utility in testing for its presence at the initial workup for viral causes of liver enzyme abnormalities.

S.A. Weinman, R. Taylor, in, 2014

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