macTT
Forum Senior
Topics: 32
Posts: 86
|
Dear members,
My question in complete recovery from hep. B infection, would your serum also show + Anti Hbe Ab? Or would you just have postivie Anti HbsAb and Anti HbcAb?
Thx in advance
PS: ALSO the common cause of heptatis in US after a blood transfusion is it Hep C or Hep B.
Thx for the help.
JACK
|
| brutus25
Forum Junior
Topics: 13
Posts: 62
|
The MCC of posttransfusion hepatitis and chronic hepatitis is HepC ( Goljan 100pg HY pg71)
Diagnosis of HBeAg-Negative/HBeAb-Positive Patient
Question
I have a 32-year-old patient who is hepatitis B e antigen (HBeAg)-negative/HBe antibody (HBeAb)-positive, with normal serum aminotransferases and a high hepatitis B virus (HBV)-DNA titer (> 100,000 copies/mL; test repeated twice within 6 months with same result). What is your diagnosis?
Response from Paul Martin, MD
Professor of Medicine, Associate Director of the Division of Liver Disease, Recanati/Miller Transplantation Institute, Mount Sinai Hospital, New York, NY
Much of the liver injury in HBV infection reflects host immune response rather than a direct cytopathic effect of the virus. During the course of chronic HBV infection, biochemical dysfunction may be absent for protracted periods despite active replication. Lok and colleagues[1] described in a large cohort of Chinese patients a number of phases of chronic HBV infection. The term "immune tolerant" was used to describe the conundrum of failure of the virus to provoke a hepatic inflammatory response, and was typically seen in the first 2 decades of life following perinatally or childhood-acquired infection. In contrast, the "immune reactive" phase was characterized by hepatic necroinflammatory activity, reflected by elevated serum aminotransferases and other clinical manifestations of active hepatitis, and was observed in young adulthood following a spontaneous increase in immune response. As a result of enhanced immune response over time, viral activity may be suppressed with clearance of HBeAg, a major target of the host immune response and evolution into an "inactive carrier" phase.
This patient's blood tests, however, are notable, despite the absence of HBeAg and normal liver chemistries, for the presence of HBV DNA in serum and, I presume, hepatitis B surface antigen. This serologic profile suggests that chronic HBV infection has evolved into the e antigen (HBeAg)-negative form of chronic hepatitis B. Generally, in patients with chronic HBV infection, HBeAg loss and development of anti-HBe antibody -- either spontaneously or due to antiviral therapy -- result in a reduction of necroinflammatory activity in the liver in the inactive carrier phase. However, in about a quarter of chronically infected patients, spontaneous HBeAg loss is complicated by the emergence of a mutant form of HBV, most frequently as a result of a mutation in the core or precore region of the viral genome. This mutation results in continuing viral replication and liver damage. Currently available antiviral therapies for chronic hepatitis B are indicated in chronically infected patients with active replication and HBeAg, or in its absence, HBV DNA present in serum. The role of antiviral therapy in the treatment of patients with actively replicating virus and normal aminotransferases, as in this patient, is less well defined, with some authorities recommending liver biopsy to determine whether liver injury (such as fibrosis) is occurring in order to initiate treatment. If treatment is not started, continued close follow-up, including serial liver chemistries, is an appropriate consideration in this patient, with an increase in serum aminotransferases as an indication of the need to treat.
I looked it up on the net but no results , if you get to the bottom of this please post I`m also intrigued.Hope it helps you becase it most certainly confused me
|
| Ancylostoma
Forum Guru
Topics: 42
Posts: 642
|
Mac the only way to determine if someone is a completely recoverd is the presence of anti hbsAb . The presence of this ab, shows that you have recovered completely, or that you have been vaccinated against Hep B. The presence of anticore antibody, shows that this immunity came via being infected. If a patients serology has hbsAB without HBcAB then you know the patients immunity came via vaccination. Finally when you consider HBeag and HBdna as a measure of infectiviy and active viral infection. The presence of HBeag in someone who is HBS + means that the person is actively producing virus and is highly infectious. If he has completely recovered you should see HBeAb. However it doesnt exacly work the other way, a person with hepatitis can have hbeag or ab.
In short when answering a question on the step look for HBSAG. It presence means he has the disease. If he has HBSab , then that person is now immune from infection. Now you have to find out where his immunity came from, presence of core antibody, means it came from an infection(IgM- acute, IgG- chronic). A vaccinated person will only have HBSab. Finally equate HBeAg(HBDna) to active viral production and infectivity. A person with hepatitis can have HBeAG indicating that they are highly infections and actively producing the virus. Or they can be HBeAb positive and not producing hte virus but still have the disease They are not highly infections. Finally HBsag >6 months means that he is a chronic hep b infection
As example we will do the question that brustus put up.
I have a 32-year-old patient who is hepatitis B e antigen (HBeAg)-negative/HBe antibody (HBeAb)-positive, with normal serum aminotransferases and a high hepatitis B virus (HBV)-DNA titer (> 100,000 copies/mL; test repeated twice within 6 months with same result). What is your diagnosis?
1)We look for the presence of HBsAg or HBsAb, but this question doesnt provide that information. However it does say that the viral load was checked twice within 6 months and came up positive. We must therefor assume that the man is HBsAg + within the last 6 months.
2) Now because he has hbsAg, he will have anti core ab (hbcAb) but at this moment it is unimportant.
3) Now he has something unusual, he has HBeAb and a positive HBDNA. These signs are contradictory. Remember that HBeab + should mean is not infective, but the presence of hbDNA means he is infective. How can this be? Dr paul, says that in 25 % of people that develop a chronic carrier state, will also develop a mutated HBV causing damage and active viral replication.
The synopsis, you have chronic hepatitis , chronic because of the presence greater then 6 months. Liver transminases should be monitored closely of better yet you should treat is like chroniv active hepatitis If you want to know about the mutation , the 2nd chapter in Dr, Paul martins response in burstus post explains it all.
Good post brustus, really helpful
Edited by Ancylostoma on 12/26/06 - 11:34 AM
|
| macTT
Forum Senior
Topics: 32
Posts: 86
|
Hey Ancylostoma and brustus,
Thx very much for the detailed explanation, I appreciate the effort. PLz correct me if I am wrong,
So to sum it up....basically HbeAb can mean 2 different conditions
1) A patient who is a chronic carrier or
2) A paitent who is fully recovered
Howver, to be certain if the patient is recovered or not, we have to take a look at the HbsAb and the HbcAb to make sure. Is this basically it? Sorry for all the haslte guys.
|
| Ancylostoma
Forum Guru
Topics: 42
Posts: 642
|
No your getting confused. Surface antigen is by far the most important antigen, it detemins if you have the disease, and antibidy to it means you dont. Read the explanation again.
|
|
| |
| | | | | |
