Acute Vs Chronic Hepatitis B
A hepatitis B infection can result in either an acute infection or a chronic infection. When a person is first infected with the hepatitis B virus, it is called an acute infection . Most healthy adults that are infected do not have any symptoms and are able to get rid of the virus without any problems. Some adults are unable to get rid of the virus after six months and they are diagnosed as having a chronic infection. A simple blood test can diagnose an acute or chronic hepatitis B infection.
The risk of developing a chronic hepatitis B infection is directly related to the age at which a person is first exposed to the hepatitis B virus. The younger a person is when they are first infected, the greater the risk of developing a chronic hepatitis B infection:
- More than 90% of infants that are infected will develop a chronic hepatitis B infection
- Up to 50% of young children between 1 and 5 years who are infected will develop a chronic hepatitis B infection
- 5-10% of healthy adults 19 years and older who are infected will develop a chronic hepatitis B infection
The recommendation for hepatitis B vaccination of babies and children is so important because they are at the greatest risk of developing a chronic infection if they are not protected against the hepatitis B virus as soon as possible.
Who Is At Risk For Hepatitis B
Anyone can get hepatitis B, but the risk is higher in:
- Infants born to mothers who have hepatitis B
- People who inject drugs or share needles, syringes, and other types of drug equipment
- Sex partners of people with hepatitis B, especially if they are not using latex or polyurethane condoms during sex
- Men who have sex with men
- People who live with someone who has hepatitis B, especially if they use the same razor, toothbrush, or nail clippers
- Health care and public-safety workers who are exposed to blood on the job
- Yellowish eyes and skin, called jaundice
If you have chronic hepatitis B, you may not have symptoms until complications develop. This could be decades after you were infected. For this reason, hepatitis B screening is important, even if you have no symptoms. Screening means that you are tested for a disease even though you dont have symptoms. If you are at high risk, your health care provider may suggest screening.
Age And Sex Distribution
Historically, notification rates have consistently been highest in young adults aged 1519 years, 2024 years and 2529 years . Since 2001, notification rates in these three age groups have declined, particularly in 1519 year olds, where for the first time in 2005 rates fell below 1 per 100,000 to 0.8 per 100,000. Rates have remained fairly stable in the other age groups from 1993 to 2005. As in previous years, there were more male than female notifications in almost all age groups in 2003, 2004 and 2005, with an overall male:female ratio of 1.7:1.
During the period 2002/2003 to 2004/2005, rates for hospitalisations with a principal diagnosis of acute hepatitis B were highest in adults aged 2529 years and 2024 years . Like notifications, and as in previous years, hospitalisations occurred predominantly in males with an overall male:female ratio of 1.8:1.
Figure 8. Acute hepatitis B notification rates, Australia, 1993 to 2005,* by age group
* Notifications where the month of diagnosis was between January 1993 and December 2005.
Figure 9. Acute hepatitis B hospitalisation rates, Australia, 2002/2003 to 2004/2005,* by age group and sex
* Hospitalisations where the principal diagnosis was acute hepatitis B and the month of separation was between 1 July 2002 and 30 June 2005.
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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
How Long Does It Last
Hepatitis A can last from a few weeks to several months.
Hepatitis B can range from a mild illness, lasting a few weeks, to a serious, life-long condition. More than 90% of unimmunized infants who get infected develop a chronic infection, but 6%10% of older children and adults who get infected develop chronic hepatitis B.
Hepatitis C can range from a mild illness, lasting a few weeks, to a serious, life-long infection. Most people who get infected with the hepatitis C virus develop chronic hepatitis C.
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What Is Hepatic Encephalopathy
Hepatic encephalopathy is an often-temporary neurological disorder due to chronic, severe liver disease. A diseased liver struggles to filter toxins from the bloodstream. These toxins build up in the body and travel to the brain. Toxicity affects brain function and causes cognitive impairment.
People with hepatic encephalopathy may seem confused or have difficulty processing their thoughts. Treatments can remove the toxins and reverse the problem. As liver disease progresses, the condition may worsen and become less treatable. Hepatic encephalopathy is also known as portosystemic encephalopathy .
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Deltavirus Antigens And Editing Of The Amber Codon
One key feature of HDV is the expression of two viral proteins from a single ORF. A 19-amino acid carboxyl-terminal extension differentiates the S-HDAg from the L-HDAg in human HDV. This extension is the result of antigenomic editing by cellular adenosine deaminase acting on RNA 1 at a site corresponding to the amber stop codon in the S-HDAg ORF of the circular antigenomic HDV RNA, edited from a UAG to a UIG codon. Following HDV RNA replication, the UIG codon is converted into a tryptophan codon during subsequent HDV messenger RNA synthesis, allowing expression of the L-HDAg . Interestingly, a 19-amino acid carboxyl-terminal extension is present in RDeV, though different in 15 of the 19 amino acids. To investigate potential RDeV large antigen expression, the full RDeV genome was cloned as a tandem head-to-tail fusion construct in genomic orientation downstream of a CMV promoter and transfected into HuH7 cells. As positive controls, S- or L-RDeAg was expressed under the control of a CMV promoter. Specific S- or L-RDeAg expression was examined with antibodies from rabbits immunized with synthetic peptides against S-RDeAg or the putative 19-amino acid extension of L-RDeAg . The tandem genome construct expressed S-RDeAg but not L-RDeAg .
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Hcc Incidence Among Linked
Among the 553,085 study population, 354,499 subjects did not have any history of malignancy at baseline and they were included in the incident HCC analysis. During the follow-up period , 71,765 patients developed new HCC over a mean follow-up of 14.5 years . Cumulative incidence for HCC development at 15 years was significantly higher in male . . By age, the 40s age group had the highest proportion of patients who developed HCC while linked-to-care , followed by the 30s group , with also higher rates among males .
Cumulative incidence rate and survival rates of patients who newly developed HCC during LTC. Cumulative incidence of HCC development according to sex. The distribution of age group who developed HCC during LTC. Kaplan-Meier plots for survival estimates after HCC development by sex. Kaplan-Meier plots for survival estimates after HCC development by age. All the p-values were less than 0.0001 in the comparison between 20s vs. 30s, 20s vs. 40s, 20s vs. 50s, 30s vs. 40s, 30s vs. 50s, and 40s vs. 50s. Kaplan-Meier plots for survival estimates after HCC development by income levels.
What Are The Treatments For Hepatitis B
If you think you may have been exposed to hepatitis B, its important to talk with a healthcare professional as soon as possible.
A doctor or other healthcare professional may administer the first dose of the hepatitis B vaccine and a shot of hepatitis B immunoglobulin. This is a combination of antibodies that provide short-term protection against the virus.
Though both can be given up to a week after exposure, theyre most effective at preventing infection if administered within 48 hours.
If you receive a diagnosis of acute hepatitis B, a doctor may refer you to a specialist. They may advise you to get regular blood tests to ensure you dont develop chronic hepatitis.
Many people with acute hepatitis B dont experience serious symptoms. But if you do, it can help to:
- get plenty of rest
- take over-the-counter pain mediation, like naproxen, when needed
Other lifestyle changes may also be needed to manage your infection, such as:
- eating a nutritious, balanced diet
- avoiding substances that can harm your liver, such as:
- certain herbal supplements or medications, including acetaminophen
If blood tests show you still have an active infection after 6 months, your doctor may recommend further treatment, including medications to help control the virus and prevent liver damage.
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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.
What Is The Right Therapy For The Patient With Hepatitis B Virus Infection
Treatment with antiviral therapy is recommended in patients with chronic hepatitis B in the immune active phase with elevated HBV DNA levels and ALT greater than 2x the ULN. Patients with cirrhosis and HBV DNA > 2,000 IU/mL should be treated regardless of ALT levels. If patients do not meet these cutoff criteria, antiviral therapy should still be considered if older age, positive family history, presence of extrahepatic manifestations, or prior treatment).
Treatment with antiviral therapy is generally not recommended for patients with immune tolerant chronic hepatitis B. However, patients should have labs checked every 6 months to look for evidence of activation. Additionally, in spite of normal ALT levels, patients should be treated with antiviral therapy if there is evidence of necroinflammation or fibrosis.
What treatment options are effective?
Several agents are currently approved for the treatment of chronic hepatitis B: interferon alpha , pegylated interferon alfa 2a, lamivudine, adefovir, entecavir, telbivudine, and tenofovir. Each agent has inherent limitations.
With the drugs currently available, the physician may consider two different concepts for the treatment of chronic hepatitis B: the first concept is that of sustained response obtained after a limited duration of therapy with pegylated interferon the second concept is that of maintained response obtained during prolonged administration of therapy with analogues.
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Whats The Difference Between Acute And Chronic Hepatitis C
Hepatitis C is a contagious disease caused by HCV, which is spread through contact with blood and bodily fluids that contain HCV. This disease damages your liver. There are two types of hepatitis C infection: acute and chronic.
Acute hepatitis C is a short-term viral infection. People with acute hepatitis C carry the infection for a small window of time, often just several months . Most people with the acute form of hepatitis C will experience illness and mild symptoms such as fatigue and vomiting within the first six months after exposure. In many cases, the disease causes no symptoms at all.
Acute hepatitis C may improve or resolve without treatment. It leads to chronic infection in 75 to 85 percent of cases. The chronic form may cause long-term problems in your liver, including liver damage and liver cancer.
HCV is spread through direct contact with blood or certain bodily fluids that contain HCV. Its safe to engage in the following activities without worry of transmission:
If your doctor suspects that you have hepatitis C, they will draw blood to check for HCV antibodies. Antibodies are substances your body produces when its fighting an infection. If you have them, your doctor may order a second test to confirm that the virus is still present.
Hepatitis B: Diagnosis And Treatment
THAD WILKINS, MD DAVE ZIMMERMAN, MD and ROBERT R. SCHADE, MD, Medical College of Georgia, Augusta, Georgia
Am Fam Physician. 2010 Apr 15 81:965-972.
Patient information: See related handout on hepatitis B.
Globally, an estimated 350 million persons are chronically infected with hepatitis B virus , resulting in 600,000 deaths annually from cirrhosis, liver failure, and hepatocellular carcinoma.1,2 Approximately 88 percent of the worlds population live in regions where the prevalence of chronic HBV infection among adults is more than 2 percent.3 The prevalence of HBV infection in the United States is 0.4 percent, with an estimated 0.8 to 1.4 million persons chronically infected.3,4 With the implementation of vaccination programs in 1991, the incidence of new infections in the United States has declined from 11.5 cases per 100,000 persons in 1985 to 1.6 cases per 100,000 persons in 2006.3,4
SORT: KEY RECOMMENDATIONS FOR PRACTICE
High-risk populations should be screened for HBV infection.
HBV = hepatitis B virus.
A = consistent, good-quality patient-oriented evidence B = inconsistent or limited-quality patient-oriented evidence C = consensus, disease-oriented evidence, usual practice, expert opinion, or case series. For information about the SORT evidence rating system, go to .
SORT: KEY RECOMMENDATIONS FOR PRACTICE
High-risk populations should be screened for HBV infection.
HBV = hepatitis B virus.
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Treatment Of Hepatitis D
No treatments attenuate acute viral hepatitis, including hepatitis D. Alcohol should be avoided because it can increase liver damage. Restrictions on diet or activity, including commonly prescribed bed rest, have no scientific basis.
The only drug widely recommended for treatment of chronic hepatitis D is interferon-alfa, although pegylated interferon-alpha is likely equally effective. Treatment for 1 year is recommended, although whether longer treatment courses are more effective has not been established. Bulevirtide is available for treatment of hepatitis D in Europe. Hepatitis D is also treated in the context of clinical trials.
Organ Distribution Of Rdev Rna And Protein Detection
To obtain insight into the infection pattern caused by the rodent deltavirus, we tested for viral RNA in organs of 18 animals that were found dead during sampling . One of these animals tested RDeV RNA-positive in all available organs , but its organ-specific RNA concentrations did not suggest specific virus replication in the liver . Also, a commercial HDV antigen enzyme-linked immunosorbent assay that we found to cross-detect with RDeV did not identify organ-specific protein expression in the liver, lung, small intestine, heart, or kidney of this animal . To further understand potential virus excretion, fecal samples from 822 individuals were tested by RT-PCR, 10 of which were positive for RDeV RNA . This 1.2% detection rate was significantly lower than that in blood samples . The average virus concentration in fecal samples was 2.9 × 109 RNA copies per gram, with a maximum concentration of 2.2 × 1010 copies per gram. Average and maximum concentrations in blood were 1.8 × 108 and 2.1 × 109 copies per milliliter.
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.
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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