Who is hepatitis b carrier

Chronic hepatitis B tends to be milder in children. Nevertheless, severe liver disease including cirrhosis may occur in a small proportion of patients during childhood [ 21 , 22 ]. Several studies have shown that seroconversion with marked reduction of HBV replication is associated with biochemical and histologic remission of inflammatory activity in the majority of patients [ 23 - 25 ]. Regression of fibrosis occurs gradually months to years after HBeAg seroconversion.

Older carriers and females are more likely to clear HBeAg [ 33 ]. These exacerbations usually last 2 to 4 months [ 34 ]. In some cases these spontaneous flares of hepatitis are not followed by subsequent HBeAg seroconversion and can be viewed as an abortive attempt at seroconversion.

These flares of hepatitis are usually asymptomatic and frequently unrecognized, but some are accompanied by symptoms of acute hepatitis and rarely, primarily in patients with cirrhosis or advanced fibrosis, may lead to hepatic decompensation and even death due to massive necrosis [ 34 ]. Other causes of liver disease, such as superinfection with other hepatitis viruses, alcohol abuse, hepatotoxic drug use, and autoimmune or metabolic liver disease, should be excluded [ 3 , 4 ].

The most frequent variant has a G-to-A change at nucleotide GA , which creates a stop codon in the precore region of the HBV genome and completely abolishes the production of HBeAg [ 35 ].

Other variants include changes in the start codon of the precore region or a two-nucleotide substitution AT, GA in the core promoter region, which reduces precore messenger RNA synthesis and HBeAg production [ 36 ]. Patient with HBeAg negative are older than patients with HBeAg-positive chronic hepatitis median 40, range 36—45 years. The older age and the high rate of advanced liver damage at presentation suggest that HBeAg-negative chronic hepatitis represents a late phase in the natural history of chronic HBV infection rather than de novo infection with HBV variants that do not produce HBeAg.

Thus, the increasing prevalence of HBeAg-negative. Fluctuation in level of viremia and ALT are more common and sustained response is rare. Delayed spontaneous HBsAg clearance has been estimated to occur at a low rate of 0.

Long-term follow- up up to 18 years of these carriers has indicated that the vast majority show sustained biochemical remission and very low risk of cirrhosis or hepatocellular carcinoma HCC [ 40 - 42 ].

Rarely, patients, even noncirrhotics, may develop liver cancer during the inactive HBsAg carrier state [ 40 - 43 ]. HBV reactivation is usually asymptomatic but on occasion can mimic acute viral hepatitis [ 44 ]. Acute flares of hepatitis should be differentiated from superinfection with other hepatotropic viruses.

Clearance of HBsAg has been reported to be higher in women than in men and in older than younger carriers. Prognosis is improved by loss of HBsAg as liver disease is usually inactive and nonprogressive, but HBsAg clearance does not completely prevent occurrence of decompensation or HCC in patients who have already developed cirrhosis [ 45 , 46 ].

Chronic HBV infection is a dynamic process with a wide spectrum of spectrum of affliction. On one hand patients are asymptomatic with no clinical evidence of liver diseases, while on other being end-stage cirrhosis and hepatocellular carcinoma.

For many decades the patients were considered to have a benign, non progression infection and were designated as hepatitis B "carriers". Probably the word 'carrier' was mistakenly chosen for hepatitis B as in true sense, a carrier is an individual who i harbors a specific infectious agent ii has no discernible clinical disease and iii serves as a potential source of infection.

For this infection the second and third points should be looked at carefully. One the basis of Asian collaborative survey the term 'carrier' was replaced by the term 'chronic hepatitis B virus infection' [ 47 , 48 ]. Later on for this infection the term 'Inactive HBsAg carrier' was adopted [ 49 ]. Treatment is not recommended as there is no evidence that available therapy affects HBsAg status.

Family screening with HBsAg and anti-HBs, if negative vaccinate them and success of vaccination should be confirmed with anti-HBs testing. Protected sexual intercourse until partner has developed protective antibodies. The offspring need active and passive vaccination [ 4 , 47 ]. Use of alcohol should be avoided, possibility of reactivation or super infection by other viruses and advised if there is jaundice, malaise or increased fatigue. Regular follow-up at every 6—12 months intervals with ALT [ 4 ].

If the age of the patient is more than 50 yrs family history of HCC-AFP and ultrasonography every 6—12 monthly should be done. For some people, hepatitis B infection becomes chronic, meaning it lasts more than six months. Having chronic hepatitis B increases your risk of developing liver failure, liver cancer or cirrhosis — a condition that permanently scars of the liver. Most adults with hepatitis B recover fully, even if their signs and symptoms are severe.

Infants and children are more likely to develop a chronic long-lasting hepatitis B infection. A vaccine can prevent hepatitis B, but there's no cure if you have the condition. If you're infected, taking certain precautions can help prevent spreading the virus to others. Signs and symptoms of hepatitis B range from mild to severe.

They usually appear about one to four months after you've been infected, although you could see them as early as two weeks post-infection. Some people, usually young children, may not have any symptoms. If you know you've been exposed to hepatitis B, contact your doctor immediately. A preventive treatment may reduce your risk of infection if you receive the treatment within 24 hours of exposure to the virus. There is a problem with information submitted for this request.

Subscribe for free and receive your in-depth guide to digestive health, plus the latest on health innovations and news. You can unsubscribe at any time. Error Email field is required. Error Include a valid email address. Studying the incidence of liver complications in inactive carriers is likewise hindered by the small number of prospective studies which correctly define this state. In two longitudinal studies of strictly defined inactive carriers followed for a median of 3. Liver-related outcomes in inactive carriers incidence per person-years.

In a larger scale sample of Taiwanese inactive carriers, annual rates of HCC and liver-related mortality were 0. Interestingly, its prognostic value for HCC was greater in HBe-negative patients with normal ALT and no cirrhosis when compared with the whole HBsAg-positive cohort; this greater association was not found for prediction of cirrhosis. Due to its general excellent prognosis, antiviral treatment is not generally recommended for HBV patients in the inactive carrier state.

To this end, transient elastography appears an advantageous fibrosis assessment tool that can easily be used for baseline and even serial monitoring of liver fibrotic changes. Though a rare complication, HCC is a possible life-threatening event; however, guidelines only recommend screening in high-risk patients.

HBsAg inactive carriers represent the majority of hepatitis B virus carriers who have seroconverted to anti-HBe, 5 making them an especially important subpopulation of chronic HBV patients, both due to their significant number but also because of the particularities in their management. Specifically, they are not candidates for any of the current hepatitis B therapies available.

The clinician's main goals when faced with an inactive carrier must be A confirming inactive carrier status, B monitoring for reactivation and C screening for liver complications. However, we believe that this particular subset of patients has an important risk of active disease and according to guidelines warrants different management from true inactive carriers, deserving therefore clinical distinction.

Guideline recommendations for these patients vary between tighter follow-up with ALT determination every 3 months and HBV DNA measurements every 6—12 months for 3 years and liver fibrosis assessment with a non-invasive method such as transient elastography or even liver biopsy. In recent years, HBsAg quantification has been gaining prominence as a tempting substitute for the yearlong follow-up necessary to diagnose inactive carriers.

It provides additional information about the patient's immune control over the disease and possibly about the extent of affected hepatocytes: HBsAg loss represents optimal viral suppression and lower HBsAg levels as well as higher rate of HBsAg decline during the course of the disease appear to be predictive of this outcome. As for the assessment of liver fibrosis in this subset of HBV-infected patients, it seems to us that despite being the gold-standard, liver biopsy does not constitute an optimal first-line exam in this population, mainly because it is invasive, observer-dependent and carries a small risk of serious complications, making its use in asymptomatic patients with low risk of severe liver disease very questionable.

When available, liver transient elastography represents a more convenient screening test, both for health-care providers and patients, in diagnosing inactive carriers and even serially monitoring their degree of fibrosis. There are few prospective studies of inactive carriers defined according to the most recent guidelines.

Still, prognosis and outcomes are decidedly favorable in asymptomatic HBsAg carriers with normal ALT levels and low viremia. Reactivation rates in true inactive carriers are a very rare outcome: incidences were 0. Most longitudinal studies investigating reactivation in inactive carriers fail to mention HBeAg reversion rates; in those who do, these are negligible 0—0.

In isolated viremia in this range with persistently normal ALT levels, liver fibrosis stage should be investigated with transient elastography, since active liver inflammation is an unlikely confounding factor. Conversely, isolated ALT elevations Cirrhosis and hepatocellular carcinoma are rare but possible outcomes even after years of inactive disease and even after HBsAg loss.

It is interesting to note that HBV DNA has a proportionally greater predictor effect for HCC in inactive carriers compared to HBV chronic hepatitis in general, demonstrating the relevance of a viral-dependent, rather than fibrosis-dependent, oncogenic pathway in these patients. In conclusion, we consider hepatitis B inactive carrier state a relatively benign condition in the HBV infection spectrum, but only if accurately diagnosed.

Transient elastograhy and the promising HBsAg quantification in serum are the two most recent major advances that have contributed to more accurate diagnosis of this state and simplified its follow up, obviating the need for biopsy in many circumstances. After correct diagnosis, lifelong monitoring is warranted for early detection of possible reactivation and hepatic complications. The goal in clinical practice is to recognize all situations which mandate a change in management be it with tighter follow-up, further investigations or treatment , so it can be implemented as soon as possible in order to minimize liver damage and negative clinical outcomes.

The authors declare that no experiments were performed on humans or animals for this study. The authors declare that no patient data appear in this article.

No potential conflict of interest relevant to this article was reported. ISSN: Follow us:. Discontinued publication For more information click here. Previous article Next article. Issue 6. Pages November - December More article options. Hepatitis B inactive carriers: An overlooked population?.

Download PDF. Corresponding author. This item has received. Under a Creative Commons license. Article information. Table 1. Incidence of reactivation of hepatitis B in Hbe-negative patients.. Table 2. Table 3. Liver-related outcomes in inactive carriers incidence per person-years.. Show more Show less.

Diagnosis is made after at least one year of regular monitoring and requires lifelong follow-up to confirm that this state is maintained. Studying the natural history of inactive carriers is currently hindered by the small number of studies on patients correctly diagnosed according to current guidelines. Prophylactic antiviral treatment should be initiated as soon as possible in this latter case.

Despite some limitations, transient elastography appears an ideal approach for identifying such patients and for serial monitoring of liver changes in all inactive carriers. Overall, more longitudinal studies on larger cohorts of true inactive carriers would be helpful for establishing with greater certainty the most appropriate management strategy in these patients.

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Lok, B. Hepatology, 50 , pp. Chen, S. Huang, C. Chu, Y. Liaw, H. DNA levels in patients with persistently normal transaminase over 10 years following spontaneous HBeAg seroconversion. J Viral Hepat, 19 , pp. HBV-carriers: when is monitoring and surveillance sufficient? Clin Res Hepatol Gastroenterol, 35 , pp. Tai, S. Lin, I. Sheen, C. Chu, D. Lin, Y. Long-term outcome of hepatitis B e antigen-negative hepatitis B surface antigen carriers in relation to changes of alanine aminotransferase levels over time.

Hepatology, 49 , pp. Chen, H. Yang, U. Iloeje, S. You, S. Lu, L. Wang, et al. Carriers of inactive hepatitis B virus are still at risk for hepatocellular carcinoma and liver-related death. Martinot-Peignoux, M. Lapalus, T. Asselah, P. The role of HBsAg quantification for monitoring natural history and treatment outcome. Liver Int, 33 , pp.

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