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Hepatitis B: A case Based Approach to Mx

Mar 07 | 3:30 PM

Chronic hepatitis B (CHB) is a public health problem worldwide. HBsAg positivity for more than six months associated with HBV replication documented by either HBeAg positivity or HBV-DNA in the serum accounts for the diagnosis of CHB. Physicians must activate the specific antiviral immune response or inhibit viral replication for overcoming HBV infections. To understand this topic better, Dr. Aniket Shah will cover the basics of immunology, diagnostic protocols, and recommended line of Mx of CHB!

[Music] they want greetings to one and on hereby netflix welcomes you we are glad you are here please make sure you are comfortable and the discussion will be starting right now and here by uh dr aniket shah is a consultant in infectious diseases hospitals and sar has a decade experience regarding the infectious diseases so i would think like he is the one person who can speak better about uh the current topic of hepatitis b case-based management and this is dr lakshman says the moderate obsession presently in jesus miserable medical college good evening everybody uh so today we are going to discuss uh important points regarding uh diagnosis and management of hepatitis b and what a physician should know uh a lot of you would be seeing a lot of hepatitis b patients in your day-to-day practice and it's indeed a very complex very dynamic very heterogeneous sort of infection and it's really not easy to treat this infection you know there are various guidelines for the management of hepatitis b like american association of study of liver disease and european association of study of liver disease but you know if you actually go and read the actual guidelines it gets very confusing so it's really very difficult to interpret specifically in a day-to-day scenario when you know all our physicians are really busy with their routine practices so when they come across a hepatitis b patient you know i would like to make very important take away points from this session so that most of you would get it a little easier for you to treat hepatitis b in your clinical practice so that should be my aim that i am not going to go into significant details about the pathophysiology and all those things but you know when you come across a patient of hepatitis b how are you going to manage this should be the take a home message uh from this session for all of you right so uh before going into the content of my talk these are the few agendas that i am going to discuss over the next 40-45 minutes so first of all we will discuss about history and how the virus behaves what is the pattern of the virus what is the structure of the virus it has been a big global health issue so we'll touch a few things about epidemiology of this infection uh modes of transmission what are the at-risk population who should be tested uh what is the clinical presentation what are the signs and symptoms of the disease what is the battery of investigation that you are going to order when you come across a patient of hepatitis b and how are you going to manage this patient so this is how we are going to move uh moving on to the first thing that is you know how the virus actually looks like so basically this is the structure of the virus if you see the outermost part it is called as a hepatitis b surface antigen which is hbsag coming from out to win we will see hdpe antigen then there will be hpc antigen uh there will be a partially double stranded hpv dna and that is going to be hbv dna polymerase so this is something about the structure as all of us know it's been a very ancient disease which was first described in fifth century before christ and it was earliest recognized blood uh the earliest recognized blood borne outbreak of hepatitis was in germany in 1883 uh it was started after receiving the smallpox vaccine uh so basically you know in hepatitis b you have to remember two things that uh basically it comes as three variants the virus comes as three variants one uh which is called as an inactive carrier where the person will be having the virus but it will remain inactive and that person will not have any injury on the liver so that patient would be inactive the important thing to remember in hepatitis b is that those stages like inactive stage or a chronic stage or a chronic active stage these are all dynamic sort of infections so the one person who is inactive today may get active infection maybe a year or five years later so once we label that this person is inactive we cannot stop following that person because it's it's interchangeable interchangeable so person might go from inactive to chronic immune tolerant or chronic active stage of hepatitis so we have to once hepatitis b is positive we have to monitor that patient throughout the life at least at six monthly in some patients we can do it every yearly so coming to the mutants why the mutants are important so originally the most common strain of hepatitis b was wild type of virus which we call it as hbe antigen positive now more and more cases are coming with hbe antigen negative so hbe antigen negative it is basically a mutant of a wild type which is called as a pre core mutant or basal core promoter mutant so this virus is prone to lot of mutation and this is the most dominant variant that we see in clinical practice that these patients they have hde antigen negative why it is important to understand these mutants it is because that more and more patients are coming with hbe antigen negative on your slide you can see on the right side that hbe antigen negative variant which is a predominant variant right now it has got significant increased risk of developing fibrosis cirrhosis as well as hepatocellular carcinoma so these are the patients who are at more risk of developing an active disease as all of us know about hepatitis it has got hepatitis a b c d and e out of this a and e r c coral root bc and d are mainly parenteral root d cannot survive alone so it is a super infection over hepatitis b and we are going to be going into the detail of hepatitis b and not the other viruses epidemiology as i said it is a significant public health problem uh before two years the actual uh number of patients who are suffering from hepatitis b are more than 350 million so they are all more than 350 million patients are suffering from hepatitis b and it comes with a lot of morbidity and mortality now you know this is very interesting slide if you see that most of the chronic hepatitis b patients in asia pacific region the total amount of patients like 75 percentage majority of the patients are coming from the asian pacific region while rest of the world is only 25 so why it is like this i will share it with you so this is a an epidemiological geographical slide where you will see the red zone is the one where there is a very high prevalence of hepatitis b so mainly china southeast asia you can see sub-saharan africa and few part of america mainly south america these are the regions which are called as endemic for hepatitis b virus and they have maximum amount of prevalence uh why it is like this why the west have comparatively uh lower rates of prevalence it is because that the data shows that in asian population this virus has started vertically so in asian population this virus is transmitted from mother to the infants and because the immunity the maturity of immune system is very less very immature for infants there are very high chances of this virus to get into the chronic infection while in other western part of the world this virus you know it is uh acquired mainly by uh either by sexual root or iv drug abuser you know or parentally and because it is mainly acquired in adulthood all the adults who have comparatively strong immunity so they have very high chances of getting an spontaneous resolution compared to the asian population so this is something important epidemiologically that most of the population uh who are from asia they are more long-term carriers company compared to the western world modes of transmission i think everyone of us know that sexual root parental root and perinatal vertical transmission these are the three common roots no point in going into much of the details very important who should be tested again all those patients all those persons who are at actual risk of acquiring hepatitis b should be tested so it's a logical answer so any uh person who have iv drug abuser iv drug history those who have multiple sexual partners or those who have history of sexually transmitted diseases homosexually active men inmates of jail or correctional facilities individuals who have chronically unidentified undiagnosed elevated liver enzymes patients who are suffering from hiv or hcv it is very important that all hcv all hiv patient must be uh tested for hepatitis b because if there is hiv hps co-infection or if there is a hcd hbs aging co-infection then the regimen differs from a person who only has hepatitis b infection so all hiv at cv remember you should not forget to test for hepatitis b all individuals who are on chronic hemodialysis they are at very high risk of developing hepatitis b all pregnant women as we know the vertical transmission risk is always there people coming from endemic region like i said uh southeast asia china sub-saharan africa south america so all this they have very high endemicity of this infection babies of mothers of chronic hbv infection which goes without saying uh all health care personnel specifically to those who are coming in very regular contact with the blood all residents and staff members of the institution who takes care of mentally population because there are going to be accidents in such facilities uh all family members specifically spouses of hbsag positive person so this is the list of infection all of you must be aware about this but then again it was a quick revision for all of you so that you know you you should not forget testing hbsag in if the person is falling into this group this is presentation again in very short this is presentation see everyone knows hepatitis b comes either as an acute hepatitis b and if there is persistence of hbsag for more than six months then we can labor it to be chronic hepatitis b so acute hepatitis b usually after an exposure to this hbsag virus usually it takes around 60 to 110 days for the infection to start developing and it basically has a spectrum you know starting from completely asymptomatic uh infection person who are completely feeling absolutely fine no symptoms at all might be having acute hepatitis b starting from that spectrum until uh acute feminine liver failure so person can the spectrum is really wide wide starting from asymptomatic to fulminant hepatic failure uh as for all basic symptoms of any hepatitis like anorexia decrease oral intake weakness pruritus a colic stool jaundice anorexia nausea vomiting all common symptoms of jaundice would be there uh after acute infection most of the patient around 85 to 90 percentage of the patient would completely take care of that infection they would develop immunity and they would not go into the chronic hepatitis b say we are taking 100 patients who are exposed to hepatitis b virus and they are getting acute hepatitis b infection 85 to 90 will get a spontaneous resolution and they will have a permanent antibodies to hepatitis b and they would not develop chronic hepatitis around 10 to 12 percentage of uh patients would go on to develop chronic hepatitis b and only one percentage of uh this patient may have acute feminine illness specifically if there is hdv co-infection that is hdb super infection those are the patients who are at very high risk of developing acute feminine hepatic failure moving on to the next slide as i said there will be either a complete resolution of infection patient would you know variably go from one stage to another like immune tolerant chronic hepatitis b hbe antigen positive active hepatitis h b e antigen negative hepatitis and inactive chronic hepatitis b so like i i'm seeing one hand raised anyone has a question lakshman said you want to take any question here uh it was a hand raised they have to keep the question but they didn't keep the question as such sir fine fine sure so i'm moving on right okay so whatever the question is you can just write down and we'll take uh all the questions uh uh once the session is over all right so i'm moving on uh so again as i said what is chronic hepatitis b it is defined as persistence of hbsag for more than six months this is how you are going to label this patient as a chronic hepatitis b again you know i'm trying to revise one thing again and again because you know it's it's not easy to remember so you might be seeing some repetition of slides but i want to make sure that at the end of session it's pretty clear what you are going to do when you come across such a patient okay so again acute hepatitis b as i said 90 percentage of them will get a complete resolution nine percent uh would go on to develop a chronic hepatitis b infection and one percent will go into the fulminant hepatic failure as i said it's a very heterogeneous very dynamic very complex in complex infection you know it is because see on your slide in the middle hbe antigen positive so now we are entering into the chronic hepatitis b discussion so how are we going to approach a patient of chronic hepatitis b so to understand that we should understand some sort of pathophysiology uh so that our management is going to get easier so most of uh you know that the commonest strain right now is hbe antigen negative but previously it was a wild type of virus that is hpe and then positive so in the middle of the slide you will see a group which is hbe antigen positive now because it's a dynamic disease dynamic infection one particular person is going to keep on changing the group he once his wild type hbe antigen positive might be an active carrier he might mutate into hbe antigen negative he might be immune tolerant or he might be shifting to immune active stage very important that once uh in patients who are inactive carrier and who are you know you are following it for 6 months 12 months now you are following yearly and every time the viral load and everything is remaining under control but always remember that whenever such patients of inactive carrier they are planned for any uh chemotherapy transplant biologicals say for example any immunosuppressive therapy there is going to be a very uh significantly increased chance of converting from inactive carrier to active hepatitis b so you should be pretty pretty careful uh with your all inactive carrier patients even though you have labeled them in active carrier you must be following them and you must be keeping a track that if at all such scenario occurs they should come to you and you should take a call about whether these patients require treatment or not so reactivation in an active carrier is very important as i said uh what are the battery of investigations that you are going to order when you see a patient of hepatitis b so we will obviously obviously do complete blood count we will do complete lft with ptinr hbsag hpe antigen hbv viral load hepatitis c hepatitis d hiv hiv hcv as i said because co-infection the regimen is going to be different hdb because those are the patients who have uh again the oral nucleoside analogues which are the usual drug of choice for hepatitis b are not going to work so it is always important to know whether this hpsag patient is actually suffering from hdb or not liver biopsy and fibroscan will go through one by one and at what stage what investigation should be ordered but this is the complete battery of investigation that you might need when treating a patient of hepatitis b another two slides are very interesting very complex again i'll take i'll go slow here i want you uh to understand what is hbsag what is hbc antigen uh what is hepatitis b surface antibody you know once these things are clear you know it will be very easy for you to decide whether this patient actually requires treatment or not you know what happens why this is important i am telling you is that yesterday only i was referred a patient from a gynecologist uh because they found that patient is having hps antibody positive so patient was pregnant and they got so uh frightened you know that there is something called hepatitis b they just got it tested i don't know for what reason but they were referred because they were hb is antibody positive so i have to reassure that see this is nth bs antibody you are actually immune so maybe because of previous infection or may be because of vaccination so nt hbc igm anti-hbc total hbs antigen and hbs antibody viral loads these are the few things that might confuse you so i hope that another two three slides i'll take five seven minutes but uh it will be very clear for all of you to understand that what report and what is the interpretation of this particular report so first definition is uh hbs antigen so it is a most common test because to label someone to be having chronic hepatitis b it has to be hbs ag positive and it should be persistent for more than six months so hbs8 basically means infection coming to the second one hepatitis b or antibody so this is hbc antibody igg again it has two parts igm and total so where whenever there is an exposure to hepatitis b virus these patients are going to have anti-hbc antibody total for life long see if i i go to the one slide yeah so this is a natural history of a particular patient who was exposed to hbs ag was exposed to hepatitis b and this patient without any treatment without any intervention through natural course ultimately at the end of 32 weeks his own immune system took care of the virus and he become immune so if you see at around four weeks after the exposure to this infection hbs ag antigen would start coming up it would peak at around eight weeks and it would start waning off and it would go away in 24 weeks so this we are talking about patients who are getting recovered okay these are not the patient who have been converted to chronic hepatitis b this we are talking about 90 percentage of the patients who got the exposure to the virus but because of their strong immune system the virus has been taken care of without the intervention so according to the natural history hbsag would go he can gradually go away by 24 weeks once patient is exposed to this virus as you see in your screen in this chart total nth bc it is going to remain high forever it is never going to go to the baseline so once you are exposed to this virus even though hbs ag has gone now because there is resolution of infection but in these patients you will see anti-hbc lifelong well igm of nthbc would peak after hbsag and would go down after hbsag so igm basically uh as a for every infection it's basically an acute marker so after a while it will go away but total anti-hbc is going to remain positive forever and then the anti-hbs antibody would start developing by 32 weeks and it is going to remain forever so once exposed these patients would have total anti-hbc and anti-hbs antibody for lifelong if this patient is not converting into chronic hepatitis b hbs ag is going to get cleared from the blood so if we taste this patient at around 52 weeks from the exposure you will see that nt hbc is positive and thds antibody is positive and patient we will declare this patient as an patient is immune to hepatitis b okay so this patient got the exposure but now patient is immune what is the difference when the patient is vaccinated so vaccinated population they would definitely have anti-hbs antibody but because there was never an exposure to the virus they will not have anti-hbc antibody in the blood so for vaccinated population you will only and only see anti-hbs antibody positive while those who have exposed but now about immune would have total nth bs hbc and nth base antibodies so this i think is clear uh coming to the next slide which as i said that patients who are not able to take care of the virus on their own and those who are developing into chronic hepatitis b infection so if you see once hbs ag has started developing in the blood it is going to remain more than six months so this patient is now convert now be labeled as a chronic hepatitis b positive coming to a total anti-hbc again the rule remains the same once exposed to the virus nt hbc is going to remain forever and hbc igm is going to peek and come back and this patient this group of patients where we are labeling them to be chronic hepatitis b infection they will never develop anti-hbs antibody so you will not see nth base antibody because there is no immunity and these are the patients who are called as chronic hepatitis b infection so this is a major difference between getting the exposure and getting read of the infection and the patients who actually develop the chronic hepatitis b so coming back to the slide again uh so chronic hepatitis b infection patient as i said hbsag will be positive as they have the exposure nth bc antibody total is going to be positive and they will never develop anti-hbs antibodies so this is the group which will be called as a chronic hepatitis b infection and this is the group who actually needs treatment depending upon if they fit into the criteria of the treatment second point patients who have developed immunity from previous infection so remember our first graph they will have hbs ag negative because the immune system has taken antibody total you you might have seen a lot of hepatologists ordering this test and you get confused you know what are these tests whether should i treat this patient or not another important thing that in all your pathology laboratory reports you when you get hvac positive there will be a value in the bracket 5000 point something or 2 000 points something but see it has got no significance it won't tell you whether this value needs treatment that i am going to discuss in the next slide but only hepatitis b surface antigen positive or negative that is what is important not the value inside moving on to the next slide this already we have covered coming to the most important part see i wanted to clear you know basics about this uh few things but the major uh core of this session is this this is what you should remember it's really very easy and i would like to repeat if anyone wants but once these things are clear it's going to be pretty black and white clear that this is the patient i'm going to treat this is the medicine that i'm going to use this is the patient i'm only going to observe and this is the medicine i'm not going to use in this question right so moving on before going into the content of how to evaluate patient for management let me first put four four or five questions that this is the common scenario that you will have and then from this uh we will gradually decide whether this particular patient needs treatment or not so case number one goes like this mr a who is a 54 5 year old gentleman who did not or does not have any past medical history comes to your opd with a positive report of hbs antigen he comes with few reports ordered by a general physician so he has hbs antigen positive he has hbe antigen positive he has hbv viral load of 3 500 international units per ml and he has also done lft and as if it is 15 so this is one scenario coming to the next scenario again mr b who is a 50 year old gentleman without any past medical history comes to you with reports of hbs antigen positive hb e antigen negative hbv viral load of 4 800 international units per ml and scpd of 87. coming to number three scenario the patient is hbs ag positive hbe antigen negative with scpt of 28 and who has viral load of 5000 5000 and the last patient who has hbs ag positive hbe antigen positive viral load of more than 25000 and hcpt of 102. so you know mostly you will come across one of this scenario high viral load normal scpt high viral load high scpt hbe antigen positive negative so these are the things that the patient is going to bring when he comes to you and then from these reports how are we going to decide whether this patient requires treatment or not so the most important point to remember here is that all the antivirals which are available currently which are called as nucleoside nucleotide analogues are suppressive and none of them are curative hardly you will see one percent patient every year who get actual conversion of hbs aeg so they will become hbs ag negative on treatment only one 99 percentage of the patient usually will require long-term therapy we will also discuss in which patients to stop the therapy when to stop the therapy but in nutshell you have to remember that most of the antivirus which are available are suppressive they are not curative even in a particular instance when the patient falls into the category of stopping the treatment that does not mean stopping the management this once hbs8 positive you have to monitor the patient throughout his life so it's not a pure cure sort of a thing okay so moving on so what were the criteria and how it was decided following will follow this criteria to see whether this particular patient requires treatment or not so until 2006 where this revolutionary study called reveal study came from taiwan you know where they studied all chronic hepatitis b patients untreated for 15 years and what they actually found out is that a single most independent marker to guide the injury the scarring the fibrosis and chances of cirrhosis and hepatocellular carcinoma of liver in a hepatitis b patient was hepatitis b viral load not the age not the sex not the history of alcohol not the lft derangement only and only viral load was the single most important factor which actually decided that how liver is going to behave in a patient of chronic hepatitis b and from this day onwards after the release of these guidelines everyone understood that viral load is something that we have to control and then the you know all these different antivirus nucleoside nucleated analogues came up and the treatment has completely took off from there so the river study was really a benchmark study uh which started and guided all of us in selection of antiviral therapy so what are our aims of starting a particular antiviral therapy in a patient is we want complete elimination and sustain suppression of hepatitis b it's not a cure elimination or sustained suppression of hepatitis b virus we would definitely like to prevent development of fibrosis cirrhosis and liver failure and we would also like to prevent the chances of hepatocellular carcinoma which again is an independent risk factor irrespective of development of cirrhosis this again one should remember hbsag chronic hepatitis b is an independent risk factor for developing hepatocellular carcinoma irrespective of development of cirrhosis or not moving on so whenever you come across a patient of hepatitis b always divide your patient into one of these three categories whether your patient is hde antigen positive whether the patient is actually antigen negative and whether this patient is suffering from cirrhosis or not again if the patient is suffering from cirrhosis you have to divide into two groups group a compensated cirrhosis group b decompensated cirrhosis so first of all this is a benchmark you have to divide your patient into these categories and coming then two criterias hbv viral load and hdpt lt is scpt these are two important markers to guide us regarding starting of the treatment so what are the names of uh different antivirals as all of us know lemmy budding started from lambivity in edifore telburidine pagelited interferon and takavir tinofole again in tinofoil the pro drugs you know for elephantamide which is the latest one uh is more beneficial because it has got comparatively less renal toxicity and less chances of development of osteopenia compared to tdf which was the conventional drug of dino format currently the first generation uh first line of choice uh drugs for treatment of hepatitis b are you know forever and anti-cavity there is no need of going into the details of the other other drugs uh because all these drugs have got very high resistance and the drugs that i mentioned tinophobia and techni are the only two drugs which are commonly used right now in the treatment of hepatitis b so you only have to remember things about xenophobia and anticarbonate so coming to the important part what are the criteria to start the treatment as i said first we are going to decide whether this patient is having cirrhosis or no cirrhosis okay so we have started the patients who does not have seroc so i am not talking about cirrhosis right now patient with hepatitis b without cirrhosis again as we already discussed we will divide the patient into the groups whether hbe antigen positive or hbe antigen negative first i am talking about patients without cirrhosis with hbe antigen positive okay so this is the group no cirrhosis hbe antigen positive so scenario number one patient whose viral load is less than 20 000 international units per ml patience sgpt is normal both red signals viral load of less than twenty thousand red sept normal red two red signals we are not going to treat this patient and we are going to monitor this patient every six monthly to see if there is any change in the viral load or if there is any change in the sapd again how do you define normal sgpt again there are a lot of discrepancy with different guidelines but what i personally follow is that uh 35 for male and 25 uh for female is considered to be a normal scpt uh if the scpt is more than two times uh the upper limit of normal uh then the indication will definitely change so you have to remember more than two times upper limit of normal that is 35 for male and more than two times upper limit of normal that is 25 for female moving on so this was scenario one low viral load normal scpt weight we are not rating next scenario viral load of more than twenty thousand scpt elevation of more than two times upper limit of normal green plus green signal both the green we are definitely going to treat this patient again remember take a moment we are talking about patients who don't have cirrhosis patients who have hd antigen positive right so hb antigen positive again i am repeating viral load of less than 20 000 so for hbe antigen positive cut off viral load is 20 000 when i will discuss about hbe entj negative the cutoff is 2000 so two figures you have to remember for positive twenty thousand for hbe integer negative two thousand okay so coming to this scenario very easy high viral load more than two times upper limit of normal we have to treat coming to third category hbv viral load of more than twenty thousand with normal sgpt and this is the scenario that we are coming across more often you know they have high viral load they have normal sgpt so conventionally we used to actually tell you know label this patient as immune tolerant they have high viral load but because of the immune tolerance the liver is not getting scarred but now those terminology has got no importance in selection criteria for treatment so there is no point in remembering those things but yes high viral load normal sgpt what are you going to do so ideally theoretically all these patients should undergo liver biopsy to decide whether this particular patient requires therapy of antiviral or not now patient is completely asymptomatic he is coming to you with a hbcg positive you get all these stress and you tell him your liver is absolutely fine but i have to do a liver biopsy to evaluate whether you need a treatment or not that patient is never never going to come back to you see liver biopsy in a healthy walking patient i don't think majority of the patients are going to get agreed for getting a liver biopsy and it's not a practical solution so the guidelines have come with different options other options which are obviously non-invasive right so there are three methods to decide whether a person who has high viral load and normal scpt whether we need a treatment in this patient or not so first is dr tong's criteria these are the point system age of more than 40 will have one point sex of male 1 point recipient mutation bcp that is basal core promoter region mutation hepatocellular carcinoma in the first degree relatives which have three points albumin of less than three point five and platelets of less than one point three so if point are more than three more than equal to three this patient requires treatment again this is a little crude method you have to you know all the time you know calculating all those things so the easiest and most accepted method in this group is a fibro scan see fibro scan is very very widely available easily accessible uh and very easy to interpret all the technicians who use fibro scans are very well hours with the scan and after it's around 20 25 minutes procedure completely non-invasive not very costly and it will ultimately the result will be showing either as f0 f1 f2 f3 f4 depending upon the stage of fibrosis amount of fibrosis it works on the principle of shear wave velocity it basically tells us about the stiffness of the lever caused by the virus so if the patient is falling into the category of f0 or f1 that is the earliest stage okay so that shows that this patient is at minimum risk of developing scarring in the liver later on so this patient they do not require treatment if the patient on fibroscan falls into the category of f2 f3 or f4 they definitely require the treatment so again we are talking about patients who do not have cirrhosis who have hbe antigen positive who have high viral load who have normal sgpt we have to decide on the basis of fibroscan whether this patient requires an antiviral therapy or not again there is one more index called an april index which will have a few calculation to do and if the index is less than 0.5 you have to wait monitor if the index is more than one treat so dr tong's criteria and every index were used before the easy accessibility of fibro scan now that the fibroscan is very easily accessible uh everyone follows the criteria of fibroskin okay so we are done here with hbe antigen positive group moving on to group b that is hbe antigen negative group okay no cirrhosis but hde antigen negative which is again a commoner group now as i said in the first slide this is basically a pre core mutation and more and more patients are now shifted from wild type virus to hp antigen negative so these are the patients you are going to see more and more in your opd's so again as i said for hpe antigen positive the criteria of viral load was 20 000 for hbe integer negative the cut off value is 2000 international units per mm okay so scenario one vital load of less than 2000 normal scpt monitor this patient every six months don't do anything viral load of more than 2000 scpt of more than two times of upper limit of normal you have to treat both green treat the patient coming again third commoner scenario in between scenario high viral load with normal scpt again the same thing fibroscan go for a fibrous scan if the patient is falling into the category of f 0 f 1 you have to wait monitor if the patient is falling into the category of f 2 f 3 f 4 you are definitely going to treat this patient okay again uh for now huh yes moving into cirrhosis so hp what we discussed right now was patients who do not have celosis now patients who do have cirrhosis again there are some debate going on about this but easy to remember is that all the compensated cirrhosis patients even one episode of decompensation in the past those patients they would require treatment and you should never stop the treatment irrespective of what we achieve after starting the antiviral therapy and that stands through even for a compensated cirrhosis so one syllosis has developed there is no question of stopping the therapy after whatever goal we have achieved difference between compensated and decompensated syllosis is therefore decompensated cirrhosis irrespective of viral load irrespective of sgpt patient must be on an antiviral while cirrhotic patient who have undetectable hpv viral load with completely normal lfd you can still wait again you will take this with a pinch of salt because most of the experts they open that once there is a development of cerosis irrespective of viral load you should put the patient on antiviral so if you take my word no need to confuse your cells cirrhosis compensated or decompensated cirrhosis put your patient on antibiotic because these are otherwise very very safe drugs and don't stop because we see patients with cirrhosis compensated or decompensated cirrhosis if the patient is on antiviral medicine and if you stop the medicine in between there is going to be sudden flare and there would be sudden decompensation and it would turn into an acute on chronic liver failure so never never ever stop patients of cirrhosis uh this i am getting few questions here but i'll take all these questions uh at the end of the session we are almost uh on the verge of completion around seven eight minutes now uh so hbb hdb uh co-infection there are limited data uh to uh guide because it's the more of more severe infection more chances of permanent hepatic failure more chances of fibrosis uh only antiviral that is actually effective for hbv hdb co-infection is pagilated interferon no nucleoside analog like anticoagulant you know which are usually used for chronic hepatitis b they are not useful for hdb infection so it is that is why it is important to get hdb in all question of hbs hd positive because once there is super infection with hdb there is no point of putting the patient on standard drugs uh now again what are the end points okay so once you have decided that this is the group of patient where i need the patient to put on the therapy if i can actually stop the treatment or not as i said once cirrhosis there is no stopping so we are only talking about the patients with chronic hepatitis b who have not developed cirrhosis how are we going to decide whether these patients require two-year therapy three-year therapy or a lifelong therapy so what are the criteria what are the end points that we want to achieve so again for patients who are hbe antigen positive that is group a what we are going to do the first criteria is to see that hbe antigen should turn to hbe antigen negative and patients who should have hd ent body positive once we achieve hbe antigen zero conversion that is from hbe antigen positive to hbe antigen negative we have to continue therapy for another six to twelve months which is called as a consolidation therapy and after that if patient hb eag still remains negative there is no again 0 conversion to sb antigen positive we can actually stop the treatment 75 percentage of the this patient would remain they maintain the suppression for a longer period of time in the absence of antiviral therapy but in 25 percentage of the patient we see uh reappearance of active infection so again as i said once positive you cannot stop following them even or even if you stop the treatment you should never stop following these patients while for hde antigen negative patient it has not been defined so once hbe ant is a negative patient falls into the criteria for starting antiviral therapy you have to continue for life long similarly again similar slide after antiviral therapy first we want hpv viral load to get undetectable scp to get normal hbe antigen to be lost consolidation first take 6 to 12 months all things remain good we can stop and as i said around 75 to 90 percent would have a suppress maintained response why not uh other antiviral and only anti-covariant you know forward because all this previous first and second generation antivirals they have very high chances of development of resistance one point to remember about enter cavity is the patient who already had received laminin in the past there are very high genetic chances of development of resistance to enter cavity if patient is already exposed or experienced lamibudin or there is a confirmed resistance to laminin so all those patients who have previously uh experienced lemon building those patients should be receiving pinot phobia and not in technology this is the same enter cavity dose 0.5 milligram per day those patients who have received laminid in the past as i said preferred drug is you know forever but just in case you have by because if there is some contraindication of using tino4 and you are using enter cavity the dose should be one milligram side effects are very very minor like headache nausea some abdominal discomfort some difficulty in sleep again for tinnophobia there are you know forward uh dysproxial fumarate there is tdf a conventional drug and a pro drug which has been recently developed which is called as a tinophobial elephant amide uh the dose of tdf is 300 and for taf it is 25 and as i said in the previous slides that taf is comparatively lesser renal toxicity and lesser chances of development of osteopenia patient interferon after the development of uh wonderful drugs like enter cover and you know forward the usage of pagilated interferon alpha 2 has gone down drastically only in the cases of hdb super infection which in india we hardly see we don't use vaginal interferon just in case we have to use the doses are 180 microgram to be given subcutaneous once a week for 48 weeks pregnancy with hepatitis b uh even though the patient did not fall into the criteria of treatment before the pregnancy but now that patient has got pregnancy we have there are chances that there is a sudden rise in the viral load so the criteria which has been decided is in the pregnancy if the viral load is more than two lakhs international units per ml very very high viral load only in this scenario they should be treated with you know forward in third trimester and takeover is group c class c drug for pregnancy while tenofovir is class b so whenever required you have to treat with you know forward in pregnancy if indicated children who are born to hbs ag positive mother as all of us know that all the routines scheduled at zero one six months and apart from that they must receive 0.06 ml per kg of hepatitis b immunoglobulin at the birth all patient of hepatitis b specifically these four uh criteria are there to screen them for uh development of hepatocellular carcinoma how are we going to screen two methods sonography alpha fetal protein every six months specifically if the patient has developed cirrhosis patient has a first degree relative history of liver carcinoma uh age of more than 14 male and 15 female and there is hdb co-infection these are the patients who have higher chances of development of hcc so we should you know screen them every six months because as all of us know earlier we diagnosed the hcc there are very good response to chemotherapy and chances of complete resolution of the hcc and the diagnosing it later is comes with a lot of problems uh what are the indications of vaccines of hepatitis b few things about vaccines as i said the remember the slide that we discussed initially who are the at-risk population of development of hepatitis b same all at this population we need to vaccinate them so i'm not repeating those things uh healthcare workers hemodialysis correctional facilities uh msm stds uh unexposed sex iv drug abusers pregnant female all these they definitely require the vaccination person who have chronic liver disease uh person who have hiv and cv infection uh coming to the post exposure prophylaxis uh so you must be coming along a lot of scenario your infection control team from the institute that you are working you know i am getting call every week that you know ex-staff or uh y staff has developed a needle prick uh and patient is found to be hvac positive whatever what i'm going to do so always remember irrespective of the vaccination history just get the anti-hbs antibody tighter than 10 is the magic number if the anti-hbs antibody tighter are more than 10 that this that it means that this patient is completely immune and there is no need to do anything just forget about it if the virus if the antibody uh hbs antibody titer is less than 10 then this patient they require 0.06 ml per kg of hepatitis b and the complete vaccination series of zero one month and six months so last two slides what are the take home message from this session number one most of the hepatitis b patients would be asymptomatic initially so because patient is not feeling anything that doesn't mean that this patient is not at risk of developing cirrhosis or hcc uh pre core mutant there is hbe antigen negative hepatitis b is gradually becoming a predominant strain now hbv viral load is the single most important marker for guiding the management fibroscan is an ideal alternative to liver biopsy to decide the starting therapy for patients who are falling into the borderline groups you know forward enter with the third generation antiviral are the most commonly used and should be the only thing should be used treatment of hepatitis b is suppressive it's not curative so do not forget to monitor your patient life long all serious patient must be certain antiviral and all serotic patients must never be stopped on antiviral therapy timely diagnosis and early treatment of hepatitis b can effectively prevent the development of cirrhosis and hepatocellular carcinoma regular screening of hepatitis c is essential in selected group of patients with chronic hepatitis b thank you very much for uh patient listening and i hope that uh after this session uh it will be a little easier for you to manage patients with chronic hepatitis b in your day to day practice uh laxman said please take on from here yes that's a very great elaborate session sir so nice you guys given everything yes thank you so yeah he's asking a question should we treat the acute hepatitis b with anti-virus as we discussed about when to treat uh all right so uh any acute viral hepatitis should never require the treatment except only one indication that patient is going into the acute feminine hepatic failure again the guidelines are debatable most of the guidelines they say if there is an acute decompensation acute viral hepatitis even if you start the antivirus the prognosis is not going to change so you only have to do the basic uh supportive care and liver transplantation whenever required but uh yes in patients who are actually personally with hepatitis b and going towards acute solving and hepatic failure there is no harming starting the antivirus why personally patients going into ferment and hepatic failure i would personally start antibiotics yes there is no harm yes uh one more question by dr uh uh sir what should be the symptoms so that we should start test for the diagnosis as it is very important yes so as i said you know it has it comes with a spectrum from completely asymptomatic to a feminine hepatic failure so all of all the persons who are falling into the risk factors as we discussed all these patients should be tested otherwise if you have a symptoms of uh hepatitis like jaundice and or excessive definitely you are going to test there are undiagnosed or unidentified elevation of liver enzyme then you should think about hvac but otherwise more or less it's many a times an asymptomatic illness so the patients who are at risk of development of hepatitis b you should screen them for hvac yes one more question by dr uh chahal also what is the difference in hbb dna ultra and rtpcr test i don't see there is any other any difference in ultra and rdpcr i think rtpcr is the standard dna rtpcr is the only recommended test right now it comes as two readings one is international units per ml and other is copies per ml but the standard is international units per mls you should always ask your laboratory to give you international units per ml and because that is the only single most criteria to decide tell us about guidance whether to start the treatment or not yes sir yeah uh one more question by dr nassim uh patient come for lscs with hb uh hb positive positive need treatment when the baby needs the treatment any new guidelines when does the baby need treatment for the treat that is like mother is positive and the baby so simple see mother is positive you know the mother is positive she is coming for lsca so immediately at the time of birth as i said we have to give the baby 0.06 ml per kg of hepatitis b immunoglobulin and start the vaccination series 99.99 of the chances that people will not develop hepatitis b infection but this baby should be monitored until the age of 18 months for uh hbs ag if at all baby remains hbs hd positive beyond 18 months then again you have to use the same guidelines as we used for adult in deciding whether that particular requires the therapy or not and one more question by dr nk week uh is there any significance of sjot by sgbt ratio in this no so yes initially initially uh when the guidelines were not very clear that there used to be seo tic-pt ratio but now the criteria they have you know try that they try to simplify so only two things you should remember doctrine one is viral load other is scpt more than two times upper limit of normal don't go into any other details it is going to confuse you try to simplify yes and one more question by himself again uh what about the transplant prognosis in such cases definitely see transparent prognosis irrespective of hepatitis b for any acute feminine hepatic failure transplant prognosis comparatively remains foreign compared to a routine cirrhosis of liver patients chronic patients going into the transplant but i think that is the only way out so if uh if the transplant process has started at a particular time i think a lot of patients can be saved so i would personally advise all these patients of acute feminine liver failure should be sent to the center where they do have transplant facility at the earliest yes yes one more question by american day what is the duration of tino forward in pregnancy positive hbs hd cost duration so so as i said that only to be given in third trimester if the viral load is very very high until the pregnancy is there patient should be on you know forward i think uh again there are no very clear guidelines on this but patient should be maintained on you know forward for another six months if that particular pregnant female was not falling into the criteria of tree starting the treatment before pregnancy there are very high chances that this patient after the pregnancy is done she may not require antivirus so again after six months you do the uh the same protocol the end points will remain the same that patient should lose hbv dna viral load patient should be hde antigen negative and then you can stop tinnophobia but you monitor the patient every six months and see if there is any uh reactivation of the disease then only you can withstand but if the pregnant female say before pregnancy was not fitting into the group of patients who actually requires treatment and only because of pregnancy there is sudden surge in hp viral load most of this pregnant female after pregnancy is settled they would start losing the virus the viral load and you may be actually able to stop thinophone okay uh one more question by shivong mixer why hb dna cutoff is different in hb e antigen positive group and negative group is there is a confidence yes so the data shows that in hbe antigen positive to virus to cause scarring necrosis macro inflammation into the liver more number of virus was required where in hbe integer negative lower the virus even with the lower copies there were higher chances of development of necro information because it is a mutated strain so even at a lower uh viral load there was chances of development of necro inflammation and this that is why uh this criteria has developed yes one more question like dr palaksha the father is hb is very positive and mother is negative and taken the vaccine what are the chances of having hbs aeg positive the child so again see if mother father is possible mother is negative mother is vaccinated vaccine usually gives around 95 to 99 percentage of protection to mother so now if mother remains negative during her pregnancy there are absolutely zero chance of baby getting it so even if the mother gets pregnant you have to screen her for hbsag if mother is aging negative then there is no point of baby getting infected right yes uh one more question by because sir comment about the booster dose of hepatitis vaccination yes so important question see there are again uh two schools of thought here one says that zero dose one one dose and six months dose is enough lifelong there is no added advantage of a booster dose because the thing is that why you need a booster dose is because which what we call it as a veining immunity so we see that x a person has taken three vaccines they do a anti-hbs antibody titer and the titer comes to be hundred international units per mm but that patient is immune now now if you again do it say just for your own knowledge for data purpose you repeat it after two years and it has gone down to only eight so ideally theoretically speaking logically we think that there is no harm in giving a booster dose uh for this patient because the immunity has gone down but what data shows is that even the cdc recommends that even if the anti-hbs antibody title has gone to less than 10 this patient is never going to develop uh hepatitis b even after the exposure once the three doses of vaccination is over but in our id group when we have one-to-one meetings and sessions all of us personally feel that even though this is a guideline if your antibody tighter is less than 10 after three doses of vaccination and if you are a person who is at risk of developing hepatitis b like a healthcare personal or the iv drug or the sexual or whatever the risk factor group patients that we discussed you should take there is an off-level guideline but theoretically speaking as per cdc there is no need of a repeat booster dose yes so one more thing i have a personal doubt like uh i hear like in a long time like uh some vaccines will give a good day uh immunogenicity some vaccines will not be given the cheaper vaccines will not be whereas johnson johnson's action will be given very good thing is there anything like that you came across sir for hypnotized b you are talking yes sir yes perhaps it is no no no no all the hebrew vaccines are definitely doing excellent their head to studies are pretty similar so there is no major uh statistically significant difference that is what i can say yes for all hbe antigen negative questions are precomputants yes so hbe integer negative is pre called simple uh yes one more question uh by dr vijay agarwal sure hepatitis b antigen positive mother can breastfeed her neonate yes absolutely no problems because already the baby has been vaccinated and i presume that he must have received the hb immunoglobulins as well so breastfeeding should not be an issue yes yes uh someone is asking uh we know doctors he's asking what guidelines to be followed actually american or european so that's what i said so so there are some things that i took from american association now study only disease and some i took it from es esl uh so it's a basically a combination of both the things but what i uh the presentation that i made is the most simplified version that i could make and i follow these guidelines there is there is minor variations if you actually study but then it is only going to confuse you so if you follow this you are on right right and you are doing a rational practice yes one more question by dr ashok body what is the significance of hp core and antibody okay so hb core antibody as i said it has got only to know that this whether this patient has ever got exposed to uh hepatitis b or not only this is the value uh so if this patient has got anti-hbs antibody from the vaccination then they would not have anti-hbc antibody total if they have got exposed then the nth hbs cnt body is going to remain forever but apart from that there is no other importance yes one more question right now by current so in the natural history there is a stage where patient becomes hb antigen negative and due to the viral reactivation to the increase in immunity patient represents with increased hpv dna and such patients are not pre-combutants but hb antigens are negative uh can you please repeat that he's telling like in a natural history there is a stage where patients of hpe antigen negative due to the viral reactivation there is a decrease in humidity such patients with increased hpv dna status such patients are not pre-core mutants but hb antigen negative okay so i uh as far as i know and what i have studied i i personally feel that i again have to deal with the literature because what he's saying is that that all not all hd antigen negative are pre-computed i think what is this is what he meant right so he has a doubt that probably there is some uh rare scenario in which patient through the natural history might be hp envision negative and he's still not precor mutant so i got the question he may be right i'm currently i'm not aware about any such scenario but again you know even if it is there or not i don't think it has got any clinical as clinical significance so i don't think there is any uh thing we should not go into the details but yes you may be right i really should go and check the effect okay [Music] so many wonderful thank you for the presentation answering the queries [Music] so many excellent talk sessions are given sir thank you thank you everyone for you know patient listening

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dr. Aniket Shah

Dr. Aniket Shah

Consultant in Infectious Diseases, Ahmedabad

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dr. Aniket Shah

Dr. Aniket Shah

Consultant in Infectious Diseases, Ahmedabad

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