OK, hi everyone. So today we are going to discuss about hepatitis, hepatitis B, management in adults. So myself, Dr. Lapey Shanan, I'm a consultant gastroenterology and hepatopulmonary sciences at Mani Hospital, Dharaka. And with me, Dr. Sufla, we'll be discussing about neonatal hepatitis subsequently. So to begin with, my talk will cover the following topics. First is the natural history, epidemiology, goals, and indication of therapy. How are we currently managing hepatitis B? How do we monitor the therapy? What are the stopping rules? And how do we do the surveillance for liver cancer? What are the various treatment guidelines and certain clinical case business? So globally, just chronic hepatitis is a health problem. It is the most common chronic viral infection in the world. And there are certain, according to the prevalence, various cases are divided. And our country is somewhere in the intermediate group. And China comes in the high group. Overall, in Asia, it is very high prevalence group. And estimated around 240 million people worldwide are living with chronic hepatitis B. As regards India, chronic hepatitis B, again, is a public health problem. And around 40 million HPV carriers are there. 10% to 15% of all the pool in the world is in India. And there are 43 to 45 million new cases per year. One lakh deaths annually are attributable to hepatitis B. And of the 25 million newborns, annually one million run lifetime risk for hepatitis B. So let's discuss briefly about the roots of transmission. So there are broadly two roots of transmission. One is the horizontal transmission. And another is the vertical transmission. Horizontal transmission, it is by the sexual contact exposure to bladder, body fluids, immunalysis, organ blood and semen donors, IV drug use and prolonged close contact. Whereas the vertical transmission is from the infected mother to the child. Approximately 25 to 50% of acute infection in the children aged one to five years and less than 5% in older children and adults progress to chronic hepatitis B. And 90% of the infants born to positive mothers develop chronic hepatitis B. So if we discuss only in India, then the mother baby transmission is the commonest. And there are various studies which have shown around 80 to 90% rate of transmission. This was one study way back in 1987, another study in 2011, which have shown that patients who have a high DNA, they have 100% risk of transmission. 3 fourth of the hepatitis B in India is through the mother baby transmission and thus the role of pediatrician is paramount. So this another study in 2006, in which 116 hepatitis B positive children were studied and it was seen that 74% mother had evidence of hepatitis B virus infection. And thus they postulated that any adult who come to us with hepatitis B, their mother and their siblings should be checked for anti-hepatitis B E titer, anti-HB code total and anti-HBS. And if we do this screening, it is found that 18% family members are found to be hepatitis B positive. Therefore the message is that we should screen all patients and the screening should mean not only HBS AG, it should mean these four tests before vaccinating anyone. And if any patient come to you with hepatitis B positive, HBS AG positive to all the family members, these four tests should be advised by you. Now, when does HBV transmission occur during pregnancy? The one is during gestation. So now the studies initially it was thought that it is the delivery when the transmission is there during delivery, which is called the perinatal transmission. But now it is seen that the transmission occurs throughout the gestation, that is intra-eutrine transmission. And it is now considered more important route of transmission than only the delivery. And even in the postnatal period, the transmission can occur, which is considered important. And this transmission is prevented by immunoprophylaxis. We give hepatitis B vaccination to the newborn and also HB, that is hepatitis B immunoglobulin at the time of birth. But what happens during transmission during gestation? To prevent that, we need to give antivirals to the pregnant female during pregnancy itself. Now we come to the natural history of hepatitis B. Now, natural history very much depends on the postimmune response. So if we see that if the patient has a very good immune response, vigorous immune response, it leads to acute hepatitis. In acute hepatitis, there will be high transaminitis, that is ELT will be more than 1400, and in most of these cases, around 95% of the cases, they will be full recovery. In few of these patients, they can also present to us with fulminant hepatitis or acute liver failure, which can lead to death or it can also recovery. But the rule is that if the patient has a good immune response, it will lead to either full recovery or in few cases death. But if there is a weak immune response, then it leads to persistent infection. Patient can come to us either in the carrier stage, chronic hepatitis, cirrhosis or liver cancer. There are two different stages in that. One is the immune tolerant stage in which the ELT is normal and one is the immune active stage in which the ELT will be high. And there is rotation between this ELT immune tolerant phase and immune active phase, which happens every 4.3 months. And the best example of this weak immune response is the infants in which the immunity is not well developed. Therefore they do not have immunity against this infection which is transmitted to them from the mother and thus they have chronic infections which persist throughout life in them and come to us many times incidentally. So this is termed as IDAHS, which is called Incidentally Detected Asymptomatic HBaseG Positive Subjects. Many a times you must have encountered that a patient says that he went for blood transfusion, blood donation and on screening he was found to be HBaseG positive, but he's asymptomatic. So such patients these instead of saying have HBaseG carriers or chronic hepatitis B, the term now is IDHS. This was one study in 2008 in which it was seen that HBV DNA in such patients of normal ELT can be very high in 60% and in patients who had intermittently normal ELT, it was 72% had a high HBV DNA. And even in these 40% of these IDHS patients had with normal ELT had a hepatic fibrosis ranging from F2 to F4. Even 3.7% had F4 fibrosis which means that they are either preserotic or serotic. So it is important to detect these patients to evaluate these patients because these patients may turn up directly into cirrhosis or liver cancer to you someday. Now chronic HBV carrier is a misleading term. It is now replaced by chronic hepatitis B virus infection. So what happens in this chronic hepatitis B? Around 8 to 40% of the patients, they go to cirrhotic state. Cirrhosis means there's a irreversible damage. How do we define chronic infection? It is defined as the persistence of positive test result for HBaseG or HBV DNA for at least six months. Of these, cirrhotic patients 10 to 17% can cause hepatic cancer. 15% can go to decompensated liver disease or liver failure. And both of these ultimately require liver transplantation. Otherwise, there is 70 to 80% chances of death. Now what are the various factors that lead to this hepatitis B progression? There are certain post factors, viral or disease factors and environmental factors. Most factors important is more than 40 years of age, male gender, family history of hepatocerebral cancer and African or Asian race. Thus, we are at a higher risk of this progression. Viral factors are the high DNA level, high HBaseG quantitative level, prolonged time to HBE antigen zero conversion. Zero conversion means conversion of HBE antigen to anti-HBE. Development of E negative chronic hepatitis B, genotype C or D, there are various genotypes for hepatitis B. So just genotype C or D has a higher risk of progression and in Indians have more of genotype D than a basal core promoter mutations, elevated ALT levels and presence of fibrosis or cirrhosis. There are certain environmental factors like co-infection with hepatitis C, hepatitis D or HIV, uncommitted alcohol consumption, cigarette smoking, aflatoxins, obesity and or diabetes. So in these risk factors, there are certain causes of HCC development also. And these include the high level of HBaseG, again genotype C or D, pre-core or basal core promoter mutations, increased alpha-phytoprotein, decreased baseline ALT and family history of HCC or alcohol consumption. Apart from that, there are certain non-HCC liver deaths and the cause for that are increased ALT and reduced albumin platelet count, which indicates CLD, acytis and enkephalopathy. And for both of these, there are certain common things like older age, as we have seen more than 40, male sex, cirrhosis, increased DNA load and HBE antigen status. Now we come to this course of HBV infection, many of them we are aware of this thing that there are various stages. Chronic hepatitis V, this follow a variable clinical course, but it is not necessary that all patients will go through each phase. So we have immune tolerant phase. In this immune tolerant phase, there will be a high DNA level and low ALT level. This is often seen in perinatally infected children and it may last for several decades. And in infection acquired during adults, put or in late childhood, this phase is short or absent. And as there is a high DNA, HBE antigen is positive in these cases and there is very low rate of HBE antigen, zero clearance. ALT will be normal. So when the patient will get this LFT done, it is normal, but it doesn't means that the patient is normal, but because the DNA level is very high in these patients. And as older age predict adverse outcomes, it is important to monitor older immune tolerant patients who may show minimally or intermittently elevated ALT. The next phase is immune clearance phase. Immune clearance phase, this occurs when there's a ALT starts increasing and the DNA starts decreasing. The patient again, maybe will have HBE CT positive and HBE antigen will start showing some zero conversion. And when there's a HBE antigen zero conversion, it's a serological marker of the end of the immune clearance phase. 10 to 20% will have annual spontaneous HBE antigen zero conversion. This typically occurs during the second or third decade of life and may last for years, leading to progressive liver damage. When we do a liver biopsy, it will show necro inflammation and varying degree of fibrosis as a result of immune mediated liver damage. And the patients with active liver disease in the immune clearance phase are potential candidates for treatment. Now the next stage is inactive carrier. In the inactive carrier, there will be E antigen zero conversion. That means E negative and anti positive. The HBE DNA will be suppressed to very low or undetectable level and ALT will also get normalized. On biopsy, there will be mild hepatitis on minimal fibrosis, but it may have severe liver damage also, including cirrhosis. And the term healthy carrier is an erroneous term because a significant proportion of patients may have high viral load, hepatic fibrosis and other liver-related complications such as liver cancer. And around 20 to 30% of these patients may experience reactivation after E seroconversion. The next stage is reactivation and resolution. Reactivation may occur spontaneously or due to immunosuppression. The reactivation, what happens? Again, there will be high ELT, there will be DNA will increase. And these patients with reactivation are usually older with more advanced liver disease. And these patients may have increased risk of liver cirrhosis or FCC. Treatment is recommended for E negative chronic hepatitis B who experience reactivation. HPSHE laws, which is called resolution, this occurs in just 0.5 to 2% of Western patients and 0.1 to 0.8% of Asian patients. Some patients may still have detected HVB DNA in serum and are vulnerable to reactivation even in the resolution stage. So this is the natural history of hepatitis B. There is a change in the nomenclature. The old terminology of immune tolerant hepatitis B in which there is a high DNA, normal ELT, normal liver disease and E positive. They is now called E positive chronic infection. The previously term immune reactive E positive patients they have DNA ranging from 10 to 4 to 10 to 7. There is the elevated ELT level liver disease will be more to severe E positive and HBSHE higher. These patients are now called HBE antigen positive chronic hepatitis. The inactive carrier term which was used earlier in it, there was a low DNA level, ELT normal, no liver disease, E negative and HBSHE was also low, is now called HBE antigen chronic infection. And there's a previously used HBE antigen negative chronic hepatitis in which E was negative but DNA was high, ELT was elevated and there was more to severe liver disease. They are now called HBE antigen negative chronic hepatitis. So now how do we evaluate this treatment for medical management? So the patient needs to have a thorough history and physical examination like the risk factors for hepatitis risk factor for HIV co-infection, duration of infection, route of transmission, history of alcohol use, comorbid disease, family history of liver cancer. And on evaluation apart from LFT we need to have test for antibodies for HIV, HIV, HIV, HBE antigen and anti-HBE status and the HBE DNA level that has to be done at six month period. Patient should also be screened for HCC in high-risk patients. He may or may not require liver biopsy and if liver biopsy there are certain non-investing markers also for liver fibrosis like fibroscan and urine analysis. And patient should be counseled on risk of transmission, screening of the family members, vaccination of at-risk household and sexual contact and the family plan. So that becomes a treatment since 1990 when the interferon was first used for hepatitis B. There is a remarkable change in the treatment and there is now new way of oral therapy in which interferons are not used. The landmark change came from the discovery of Antecavir and Tinofevir and now the latest in the basket is Tinofevir elephanomide which is more nephrosafe than the earlier Tinofevir diastroproxen fumarate. There is also improvement in the efficacy of the seroconversion with these newer anti-nucleoside analogs and nucleotide analogs. Now, which nucleotide to be used? It depends on the safety, the barrier to resistance because the earlier nucleosides like the lime avidine, edifovir, they're a high antiviral potency but they also had increased chances of resistance, also the efficacy. So among them, the best are the Tinofevir and Antecavir because they have a good antiviral potency, their pharmacological barrier is very high and genetic barrier for resistance is also high. Only the Tinofevir, the earlier one had nephrotoxicity which the new TAF had very less incidence. So these both, these are the preferred nucleotide analogs and should be used as a first line therapy. So the 2018, the American guidelines, they say there is not much difference in which to use but like in pregnancy, this Tinofevir is a category B. It is more commonly used than Antecavir. There is no human data for TAF now. Regional disease, of course Antecavir is better and TAF can be used but for the bony diseases, all are good. And if there is HIV co-infection, the TDF was in the co-formulated in the retroviral regime. TAF is also in the co-formulated in the retroviral regime but if we use Antecavir, it is in addition to the complete ART regimen. The dose that is commonly used is 0.5 milligram for Antecavir, TAF 25 milligram per day and PDF 300 milligram per day. Is there any role of interferon nowadays? So there are certain roles. What are the favorable predictors of response? If the DNA is low, there is high ART and the genotype is ARB. But there are certain patient demographics also like in young people, in young women who want the pregnancy and there is absence of comorbidities, patient preference and concomitant delta infection or HCV. So in these, a course of peg interferon will be the most appropriate first-line treatment strategy and because it is a finite treatment, it is for one year of course and there is a sustained response and this patients who have a high LT and low DNA, there is a chances of seroconversion are higher than the nucleoside analogs. But again, there should be a careful patient selection. We cannot use this in patients who have a very high transaminitis in patients who have cirrhosis, be it compensated or decompensated cirrhosis. So only in patients who have chronic hepatitis B with these parameters, it can be used. There is another way in which this interferon is used which is called a sequential regime. And in the sequential regime, the patient is first given tenofovir or any other nucleotide analog for 12 weeks, then combined tenofovir and interferon is used for 24 weeks and then again, a lone tenofovir is used till the end of one year and it has found in various studies that there is a very good response in such patients. Even the patient can have HBSHE conversion also. Now, the next is who should be treated? Now, this is a very confusing and topic because there are various guidelines from American Association, from the European Association and the Asia Pacific Association. All these three agree on this that a patient have a very high DNA level and a high ALT level. In E positive patients should be treated and in E negative patient who have more than 10 for four log DNA and high ALT should be treated. But in practical this scenario, majority of the patients do not fall in this category. So again, how to monitor this patients on treatment for hepatitis B DNA? So HVB DNA should be detected every three months until it is undetectable and every three to six months thereafter. ALT similarly should be monitored every three months until normalization and every three to six months thereafter. For E positive patients, HBE antigen should be monitored every six months until it is negative and NTHBE is achieved. And in E negative patients once sustained suppression of HVB DNA is achieved, HBS AG is monitored every 12 months. We call the treatment response by virological response. If there is a definition of non-responses, primary non-response, when there is a less than one log reduction of DNA at 12 weeks. Passion virological response when there is more than one log reduction but still it is detectable. And virological breakthrough when there is a confirmed increase of one log DNA from the NADIR on treatment. And similarly for the pegging interferon, virological response is when the DNA level is less than 2000 and evaluated at six months and at the end of therapy. And sustained off therapy virological response is when the DNA level is less than 2000 for at least 12 months after the end of therapy. The response again are divided into biochemical, histological and serological. Biochemical response is the minimal follow up of at least one year post-treatment with ALT determined every three months to confirm sustained off treatment biochemical response. Histological response is decreased in the necro-inflammatory activity by more than two points without worsening in fibrosis. And serological response is E-antigen loss and seroconversion and HBase HG loss and seroconversion. Usually HBase HG losses are the goal, the endpoint which we seek but there are very less chances of HBase HG loss. So what is the significance of the estimation of this quantitative HBase HG? We all know this HBVDNA is a marker of HVV replication. But what does HBase HG detect? They are various viral particles which indicates HBV replication. So this HBase HG is a marker of transcriptionally active CCCDNA which is the core of this HBase HG. So it may be that the DNA is negative but this virus still remains inside the DNA in the form of active CCCDNA. And it's very difficult to detect this CCCDNA so we detect this quantitative HBase HG for this. So another significance is that this HBase HG level provides the complementary information of triple CDNA. The true inactive carriers are those who have HBase HG have less than 1,000 HBV DNA, less than 2,000 a normal serum AFD. In the immune tolerance phase, HBase HG can be more than 1,000. An annual rate of HBase HG loss is approximately 0.4 to 2.3%. And HBase HG loss rate is lowest in E-positive patients followed by E-negative with the loss rate being highest in inactive carriers. So baseline HBase HG is usually a predictor of HBase HG loss. Both DNA and HBase HG levels positively correlate with HCC development. But in E-negative patients, HBase HG level more than 1,000 is an independent predictor for HCC development. Thus it's very important to measure this. And HBase HG level of more than 1,000 was noted to be consistently associated with a higher risk of E-negative hepatitis and cirrhosis. And thus combining both DNA and HBase HG level could be used to define minimal risk hepatitis with chronic HBV infection. So what are the rules for stopping this nucleotide after confirmed HBase HG loss with or without NPHBase seroconversion? This is the desired endpoint. But in non-serotic E-positive chronic hepatitis patients, even those who achieve E-seroconversion, that means conversion of HBE antigen into NPHBE and undetectable DNA and who complete at least 12 months of consolidation therapy. This consolidation therapy means followup after HBV DNA negative. That there also we can think of stopping. But again, there is a chance of recurrence in these patients. In HBE antigen negative patients, in selected non-serotic E-negative who have achieved long-term virological, at least three years of HBV DNA negative under a nucleotide envelope, we may consider of stopping it. But still we perhaps it is indefinite therapy that is usually given in E-negative chronic hepatitis B patients because it is considered unsafe to stop nucleotide analogs until we achieve HBase AG negativity. And recent evidence have shown, especially from Asian countries, that nucleotide envelope can be discontinued in E-negative chronic hepatitis B patients who achieve DNA undetectability on three separate occasions, six months apart. So either of the three we think, but the best of course, is when the HBase AG is negative and NPHBase is present. But it's very less chances of these. So this we have discussed that in E-negative, another thing to remember in serotic patients, we usually continue the antiviral treatment for life. So a word about HCC surveillance, the surveillance is done by AFP and by abdominal ultrasound. It should be done every six months. There are certain high risk patients like those who are serotic and there's a family history of HCC and low to moderate risk like in inactive carriers, immune tolerant patients, HBase AG positive means less than 40 and female less than 50 and patients with HBase AG loss. These are low risk. So let's see first to quickly the guideline. There are various guidelines, but what we follow usually is the Asian Pacific guidelines. The, there were another nice guidelines. In the nice guideline, they have divided according to the fibro scan, which we commonly use the fibro scan. There is a LSM value. If the LSM value is less than 11, that means it is either F1, F2, or F3 fibrosis. The patient has a low DNA. We monitor and measure the ALT and DNA level every 24 to 48 weeks. If the DNA is very high, that is more than 10 to the power five dog, we usually treat. And if the DNA is between 2000 to 20,000, then if the ALT is normal, we can monitor. The ALTs have normal and the patient age is more than 30, we treat. If the patient's age is less than 30, we go for biopsy. The biopsy is normal. Again, we monitor, but in the biopsy, which shows F2, F3 fibrosis or evidence of necro inflammation, we have to treat. If the fibrosis more than 11, which is usually indicative of cirrhosis and the DNA is detected, we have to treat. This is the nice guideline. The other appasal guidelines is for E positive and E negative. E positive patients, if the DNA is less than 2000 and ALTs less than upper limit of normal, we monitor the patient. If the patient has a 2000 to 20,000 DNA level in E positive, ALTs more than upper limit of normal, we monitor three to six months, assess fibrosis. If there is F2, F3 fibrosis or moderate to severe inflammation biopsy, we have to treat. And if the DNA is more than 20,000 and ALTs one to two times upper limit of normal, again, we monitor for three to six months by means of either fibroscan or apri. We assess the fibrosis and or we do a liver biopsy. If the ALT is persistently one to two times, age is more than 35, family history of HCCR cirrhosis, we should treat these patients. Or if the ALTs more than two times upper limit of normal, we should directly treat these patients. In case of E negative chronic hepatitis B infection patients, well, there are only two things. One is less than 2000, one is more than 2000. In less than 2000, if the ALT is normal, we assess the fibrosis noninvasively, monitor ALT and DNA individualized liver biopsy and treat if there is more to severe inflammation or significant fibrosis. Significant fibrosis means F2, F3 fibrosis. If the ALT is more than upper limit of normal, if elevated ALT, we have to exclude the other causes. We have to assess the fibrosis noninvasively and we have to monitor three monthly and individualized liver biopsy, like if the patient who has persistently elevated ALT aged more than 35 or family history of cirrhosis or HCC, we should do directly a liver biopsy and in case of moderate to severe inflammation or significant fibrosis, we have to treat. The DNA is more than 2000 and ALT is one to two times upper limit of normal or normal, again, the similar things we have to assess, individualized liver biopsy and treat if there is moderate to severe inflammation or significant fibrosis. If the ALT is more than two times upper limit of normal, we should treat these patients and we may initially observe for three months, but again, we have to individualize and we have to, we should have low threshold for treating, starting the treatment of these patients. For again, the chronic HVB infected, for the decompensated cirrhosis, any HVB DNA injectability we should treat and we should consider liver transplantation and there is no stabilization. For compensated cirrhosis, if there is a normal ALT, DNA more than 2000 or if elevated ALT, DNA detectable, we should treat. And if there is a reactivation, we should immediately treat. Now, let's see few case business. The first case is of a 45 years old male with HBCG positive in 2014, E-negative, anti-positive, ALT was 44, DNA was not detected. But now in 2020, again, the ALT is 100, AST is 88, E-negative, anti-positive. Serum albumin and total bilirubin still are normal and patient has overweight with BMI of 26.4. So what should we do? Should we, patient has most likely developed HCC or the patient has an E-negative immune reactivation chronic hepatitis B, which could be presentably diagnosed by obtaining a serum DNA level? Or do you think that the patient is likely infected with a pre-core mutant HPV or the patient's liver enzyme elevation is undetected to hepatitis B? So of this, the answer is that patient has an E-negative immune reactivation chronic hepatitis B and which could be diagnosed by obtaining a serum DNA level. The patient in 2004, he was in the inactive phase of chronic hepatitis B. 20% of these patients in the inactive phase will transition to the E-negative immune reactivation. This we have discussed in the previous slides. And this usually is by the mutation of pre-core or core promoter gene. So in this patient, obtaining a DNA level would provide valuable information and one would expect the DNA level to be elevated, which would be low in the inactive phase. Now the second case is a 34 years old injection drug users with HBCG DNA of N plus seven E positive and time negative. ELT is 135 and 96, three months apart. LSM is 12.5, which is indicative of F3, F4 fibrosis. NT-HCV-HIV is negative and liver ultrasound is normal. So what should we do in these cases? Should we do a liver biopsy or should we start directly with the treatment or we should continue to monitoring as ELT appears to be settling like in three months apart, it has come down or we should do a repeat E-antigen to check for clearance. So for this, we should see this algorithm proposed by ASLD, that is American Association. And this is very much similar to our appasal guideline which we have just discussed. So in this patient, the patient who has more than two times upper limit of normal to both all the three societies recommend that in patients with a high DNA level, with high ELT level, we should monitor for three to six months and we should treat if there is no spontaneous E-antigen loss. So we should do this in E-negative patients. Again, if there's a high DNA ELT more than two times, all the three societies recommend that treatment is required. And liver biopsy rather is optional in these cases. The third case is of a 55-year-old main with diabetes, BMI at 22, old history of blood transfusion in 1990, presented with jaundice followed by acitis in three weeks. His DNA is 10 to the power seven, E-positive and D-negative, AFP is 211 which is high, AST is 786, ELT is 822, and ITM and THB core is positive, which is of the range of one is to 200. So what is the diagnosis in this patient? Do we think because the patient has a high AFP, whether he has developed HCC or the patient has a HBV reactivation or the patient has acute hepatitis B or he should be advised directly liver transplantation. So I would say that the patient has a HBV reactivation and he should be started directly on antivirus. The reason for this is that how do we differentiate between acute hepatitis B and reactivation? In acute hepatitis B, the patient will have a very high IgM anti-coated, that is more than one is to 1,000. The HBV DNA is less than 10 to the power five. There is absence of an imitation. There's a recent history of exposure in this patient, the history of exposure over is 1990. And when treated as reactivation, 95% will show HBV sagy loss. Whereas in reactivation, this IgM anti-HBV tartar is low. These are very high HBV DNA more than 10 to the power of four, like in this patient, it is 10 to the power seven. There are presence of mutations. There's a previous history of hepatitis B in patient or in family members. And the patient is unlikely to clear HBV sagy even after therapy. Another case as of 45 years old businessman, prior policies tech to me a year ago, the patient will present with a fatigue and a routine health checkup shows HBV sagy positive, VMI is 28.6, E-positive, anti-negative, ALT is 45 and 48. DNA is 10 to the power seven docs. Fibro scan shows LSM of 8.9, which corresponds to F2 fibrosis. ASG, USG shows a mildly coarse and liver ecotexture. So what should we do in these patients? Important thing to remember is the age of this patient. Now, liver biopsy should be done in this patient. Why? Because the nasal guideline, easel guideline and American and a puzzle guideline all says that treatment is not required on the immune tolerance phase. But because there's a likelihood of response to available treatment is low. But liver biopsy should be considered in persistently borderline normal or slightly increased reality level like in this patient, particularly those older than age 40. And according to easel guideline that is your open guidelines age 30. And treatment should be recommended if the biopsy shows F2, F3 fibrosis or moderate to severe inflammation. Another case is of a pregnant lady, 32 years old with 24 weeks of pregnancy. HBase G is found positive. Patient has a normal ALT, but DNA is 10 to the power 5. So what should we do in this patient? Should the patient we ask to abort or we should ask to take nucleotide nods? So now the current guidelines says the patient should be given 10 off of it, which is safe, which is category B. And it can be done in all the three trimesters, but at least in the third trimester, that is after 28 weeks of pregnancy, irrespective of the DNA level. And the patient when a child is born, HBIC2 is to be given and three doses of vaccination will be given. And after the patient can, then after delivery, the nucleotide and lock can be stopped depending on the case to case. And then the breastfeeding can continue. And last case I think is the 28 years female. This is an interesting case. The patient presented with a history of being married 11 months back and the husband lived in Dubai. And four months back he consulted some infertility center in view of not being able to conceive in the first six months. And incidentally was found to have HBICG positive. She was complaining of weakness, easy fatigability and shortness of breath. And the patient's lab was done which showed a very low hemoglobin level. LFT was more or less okay and DNA was 10 to the power 5 log, E negative and USG was also normal. Our endoscopy was done which showed many erosions in the stomach. And a biopsy was taken from this which showed evidence of vesculitis. Our PNK was positive. So we thought what to do next because liver was normal, DNA was 10 to the power 5, but E negative, ALT is normal, no family history of CLB or HCC. So should hepatitis B treatment be started? Now these are the extra hepatic manifestations of hepatitis B, that is vesculitis. Skin manifestations, polyacroitis, neurosa, peripheral neuropathy and luminal fractus. And it is seen that this HBICG positive with extra hepatic manifestations and active HBV replication, they may respond to antiviral therapy. And in these patients, second typhanone should not be used. And we started on this treatment and it all the lesions improved within one month. There's one more case. This is 65 years old main patient diabetic on oral hypoglycemic. This is a known case of CLL, that is lymphoma on chemotherapy. The patient was diagnosed in 2014 and all the workup was done and patient received say five cycles of chemotherapy. And last cycle was in September 2014. And the baseline investigation showed a normal LFT. But in October, the patient developed jaundice, decreased appetite, generalized weakness. He was evaluated, found to have HBICG positive. Patient was then started on entechovir. His bilirubin, which on 17 was one, increased to 21 on 26th. ASTLT was very high. And his LFT started showing and his CT was done which showed neurosis and acitis and patient expired after a few months. So any patient undergoing chemotherapy or immunosuppressive therapy should be tested for HBV markers prior to immunosuppression and all HBV positive should receive the entechovir or tenofovir as treatment or profile access. And HBV negative patients should also be checked for co-total and positive subjects should receive anti-HBV profile access if they are at high risk of HBV reactivation. So I'll skip this one. So to summarize, in India, majority of chronic hepatitis patients are unaware of their infections. The clinical course of chronic hepatitis B consists of immune tolerant, immune clearance, inactive carrier reactivation and resolution phase. Not all patients will go through every phase of infections. However, chronic hepatitis B patients are at risk for severe liver damage. And HBV screening is important to identify chronically infected persons who may need treatment and to allow for interventions to reduce transmission to others. HBV screening consists of simple blood tests for physiological markers of infection. Screening vaccination and appropriate management of persons with chronic hepatitis B are important steps to help prevent hepatitis B and its liver complications. So gentlemen, hepatitis B is a treatable disease, but we need to know hepatitis B to prevent that. Thank you. Now I'll request Dr. Suflap to discuss of our new... Thank you, Dr. Lavkesh. So after a wonderful presentation by Dr. Lavkesh on hepatitis B, I'm going to speak through on the topic of immunative polystasis. Although it is a very elaborated topic, but I have tried to make it a bit concise with clinical pointers for easy diagnosis in day-to-day practice. So this is the most common cause of conjugated hypervillipinemia that you see in your practice. So I'm going to start with some cases that you see in your practice and how we should deal through with them. So usually these are the kind of cases that you see in your practice.  The jaundice was noticed since her week of life with dark urine and intermittent clay-coloured stool. The birth rate of the child was normal, and he's gaining weight appropriately with all normal development signs and symptoms. There was no history of any consignments marriage with one healthy female sibling. And another, they could be in history of another male sibling who's expired with jaundice a couple months ago. So on examination, it's a well-looking active child with interest over the body and eyes with a discontented abdomen and a palpable liver and spleen. There was no murmur and all the other systemic examination is normal. So the pointers here are this was the colour of the stool initially and later on the stool colour changed to nearly clay-coloured. So it was a little bit pigmented initially to begin with and then it lost the pigment. So this is a very clear-cut pointer towards one of the possible diagnoses that is the lary trachea that you most commonly see. Then another presentation that could be a four-month-old child with a term baby born by cesarean, non-consignments marriage, no other sibling. Jaundice noticed since one month. The child is on examination and could be mildly intrigued with a pitocidino megalee. Rest of the systemic examination is normal. There's no itching marks on the body, no papyrus, no bruising. On investigation, you may see a raised enzyme with a normal gamma-GT level. So this level is very, very important whenever you are dealing with a child with conjugated hyperbilalobinemia. The child may have mildly raised serum-bilalobin levels with the range combination profile. A high-dose scan done was normal. So these are the kind of presentation that we get in clinical practice and then we have to decide about whether the neonatal polystasis is because of the intrahepatic causes or the extrahepatic causes. So let's proceed and see how we can diagnose and go about this truth. See, objective of my talk is when cholestatic liver disease should be suspected, how do we evaluate these infants with conjugated hyperbilalobinemia? What are the differential diagnosis and how do we manage them? So if you look by definition, there is a diminished bio-formation or extrusion in cholestasis. And Aspegan has given clear definition that neonates who are jaundiced beyond two weeks of age with a direct bilirubin of more than one milligram per deciliter, if the total bilirubin is less than five and if the total bilirubin is more than five, then it should be more than 20%. The IAP has given the guideline that the conjugated bilirubin of more than 1.5 or two milligram in a newborn infant with a high color duty with or without a colic stool. If you look at the incidence, cholestatic jaundice is fairly common. So in the Western world, one in every 2,500 line birth suffers from cholestatic jaundice. Biliriatrasia is one in 10,000 to 15,000 infants and idiopathic neonatal hepatitis is again fairly common, one in 5,000 to 10,000 line births. In India, however, neonatal cholestasis constitute around 19 to 30% of all the chronic liver disease in century. So it is quite common. If you look at the etiology, we just to simplify it, we divide it into two causes. So either it is liver related causes or it is violet or extra hepatic related causes. So it's very important when a child present whether on based on the presentation, then clinical findings and investigation you have to divide whether the child has got extra hepatic disease that is like biliriatrasia or polydopocyst or if it is an intra-hepatic disease, then because is it because of hepatocyte injury or bile duct injury? The hepatocyte injury can be because of multiple causes. They are roughly divided into metabolic, viral and adiopathy, whereas bile duct injury can be because of bile duct capacity. Now, if you look at the Western world literature, the most common causes of neonatal hepatitis and polystasis is extra hepatic biliriatrasia, which is around 25% followed by idiopathic neonatal hepatitis. Then they have the infectious causes followed by parental nutrition associated, then metabolic and then the rare syndromic causes that includes PFIC as well. If you look at the Indian data, which has been given by IP, again, the most common causes are from the hepatocellular causes, the neonatal hepatitis. The idiopathic one is the most common, whereas we cannot find out the cause of this disease, followed by torch infectious causes in which there is torch infections, sepsis, other causes. Then there are obstructive causes are quite common. So they are around 28% out of which 34% constitute is constituted by biliriatrasia. And then there are other causes which are metabolic miscellaneous and collidopal cysts in which they are bile salt transport disorder, bile acid synthetic disorders are also there, but they are quite rare. So if you look, this is the explanation for all the different causes and they're being categorized. So in extra hepatic biliria obstruction, it can be caused by biliriatrasia, collidopal cysts, insipid bile or mucus plug. It could be cause of polylithiasis or tumor or masses or neonatal sclerosis or meningitis. These are quite rare as compared to biliriatrasia. Then there are various infection, like viral infections, which is much more common. Then bacterial infection, sepsis, protozoal infection. Followed by this, there are metabolic and genetic causes which have been divided again into disorders of carbohydrate metabolism, amino acid metabolism and lipid metabolism. So you see, this is quite common, like galactosemia and fructosemia, tyrosinemia. Then you see a nemenpic disease in lipid metabolism. Then there are rare disorders which are quite rare in which there is disorders of bile acid synthesis because of deficiency of certain enzymes which are responsible for synthesis of bile. In that also we cover the Zellpeger syndrome and Slipp-Lemeli-Optin syndrome. Then there are inherited polystatic disorder which are much more common in the western world as compared to our side of the world. So there are allergies, there are ARC, there is cystic fibrosis. Then there is PFIC, which is quite common in India as well. Then there are mitochondrial disorders. And then again, other metabolic disorders in which there is alpha-1 antithesis and certain deficiency. Then it is also important to rule out endocrine disorders, hyperpetitism, and then the hepatitis or polystasis caused by drugs or parental nutrition. So children, especially preterm babies who are on parental nutrition on long time are quite prone to develop neonatal polystasis. They get better also once the parental nutrition has stopped. Then there are alloimmune disorders and miscellaneous disorders. So we have seen that idiopathic neonatal hepatitis in which no cause has been found of neonatal hepatitis is quite common as well. So let's see what are the pointers in the history. Usually in the obstructive parts, it is a rough type but it is not the rule of the book. Usually you will see a history of full-term baby with a normal birth rate, a calling stool growing well, feeding well with an uneventful antinatal history or there will be no family history. This is the pointer towards beliery atrasia or polytopansis or any other obstructive disease. And in non-obstructive causes or the hepatocellular causes, the baby is usually preterm or full-term with a low birth rate failure to thrive. Important thing is the baby will have pigmented stool with poor feeding. There could be other pointers in the diagnosis. For example, if it is a viral neonatal polystasis, then there could be history of fever, rash or lymphedinopathy. They may have family history of another sibling affected by the same. If the child on examination is dysmorphic in appearance, think of eligible or trisomers. Cataract is quite common in babies who have got galactosine. Similarly, in energies, you look up for posterior ambiotoxin in the lens. Then in torch anomalies or septuoptic dysplasia, retinal examination is very common because we know chorionetinitis is very, very common in torch infection. Sometimes beliery atrasia is associated with cytosine versus as well. Again, cardiac murmurs are seen in LHL and beliery atrasia. There could be a mass when there will be a presence of polygobal cyst. And then again, in septuoptic dysplasia, look out for microbinus. So these are rough clinical pointers which you can see on clinical examination and general examination of the child, which can points toward a certain diagnosis. Most of timely evaluation. The reason we want to timely evaluate these child is so that we can treat any medical or life-threatening condition. You know that the liver can get compromised very quickly. They can go into cirrhosis and acute liver failure. So they need to be diagnosed and treated on time. Obviously, we know that there is a crucial window for the surgery for beliery atrasia. So such disorders which are treatable by surgery should be diagnosed and treated in appropriate time frame. And very, very important, a lot of intrahepatic disease are referred for surgical intervention without knowing the underlying cause. So such errors should be avoided by doing the right diagnosis. So let's see what all can be helped in terms of investigations to diagnosis disorder. So if you look at the liver function test, I discussed earlier as well that gamma GT levels are very, very important. Usually you see a raised gamma GT levels in extrahepatic beliery atrasia or PFIC-3. That is primary familial intrahepatic polystasis type G, not in one and two. In the primary sclerosing colonitis and energy. So the GGT along with the other liver function test is a good pointer towards diagnosis of what kind of disorder it could be. In PFIC-2 and 1, it is usually normal, especially in biotubbed disorders and biosynthetic disorders as well, biosynthetic disorders, gamma GT could be normal. PT and ILR is severely, if it is severely abnormal, think about tyrosinemia, galactosinemia because it's hugely associated with sepsis. Then look out for urine for reducing substance, especially galactosinia, tors cleaning, thyroid status, cortisol screening. If there is evidence of hyperglycemia, think about galactosinia or hyperglycemia. AFP levels are very, very high in tyrosinemia. But for the conformation, it is very important that you do a urinary succinyl acetone levels because AFP can be high in enter condition as well. So that's why confirmatory diagnosis is always warranted before starting the treatment. So again, I'll go for the gamma GT levels. If it is normal or low, think about neonatal hepatitis could be associated with idiopathic or hypotheticalism or biosynthetic disorder or PFIC 1 and 2. But if it is high, then think about either obstructive disorders or neonatal hepatitis. So usually in related atresia, colidococyst, PFIC 3, allergis, and it can be high in alpha 1, and even alpha 1, anti-truxine deficiency as well. So let's see the ultrasound scan. Usually in all the babies, it is being told that you should do a fasting ultrasound scan followed by a post-perennial ultrasound scan. And this is the triangle, classical triangular chord sign that you see near the bifurcation of portal vein for conformation of diagnosis of really atresia. Now why it is done? Why it is very, very important? A good sonologist and a fasting scan, it can confirm if there is any other surgical treatable condition like colidococyst or insipid bilbacrisis. Triangular chord sign, as I said, is diagnostic. Then abnormal gallbladder morphology. For example, the gallbladder is not visualized on a fasting scan or the length is less than 1.9 centimeter or the lining is not complete or it's not smooth. The other thing is that no contraction of gallbladder happens after oral bleeding. So that's why it's very important that you do a fasting scan first and followed by that you do a post-perennial scan to look for the contraction of gallbladder and also non-visualization of the common bilbacrisis. So these are all the diagnostic signs for diagnosing bilader atresia. Now, afterwards, after this, we have to do the Hyda scan on the hepato- biladeris integrative scan. It has certain disadvantages. Although to confirm the diagnosis of bilader atresia, we always look for the excretion of the dye. So we give the child technician-labeled dyes. It depends on the hepatocellular function and patency of the biladerie trap. So if the child has got neonatal hepatitis, there will be delayed uptake, but there will be excretion. Whereas in bilader atresia, there will be a normal uptake, but there will be absent excretion. So it is 97% sensitive, but it is not specific for bilader atresia. It is very important to remember whenever you do a scintigraphy scan, you have to prime the baby for five days with pinovacetone. So as I was saying, that there are certain disadvantages of Hyda scan, especially when we have a time lag or we don't have enough time for the baby to wait for the surgery. So always, it's always better to go for a liver biopsy rather than waiting for five days to do a Hyda scan to confirm the diagnosis of bilader atresia. So because there is a new delay because of the priming and 40% cases of neonatal hepatitis will not show any excretion. And it has been shown that 20% cases, even with show excretion on Hyda scan, later provoked to be bilader atresia. So it's not a very specific test. So this is the clinical picture. The positive finding is when you give the dye, there is uptake in the liver and then there is excretion in the bald data in the early phase. And later on, you can see the tracer activity in the geodinum as well. Whereas when there is biladeria atresia, there will be no uptake and no excretion. And ultimately the dye will be seen in the bladder. There will be normal uptake in the liver, but there will be no excretion in the bowel. You can't visualize the biladerie tree and then you will see it in the bladder. So this is for biladerie atresia. So now we come to the next step of investigation which is liver biopsy and it is the gold standard and it is very, very useful, especially in defining the etiology in up to 95% of cases. You can also find out the extent of fibrosis. And it also gives a clue to the diagnosis. So you can avoid unnecessary surgery if the child is not suspected to have biladeria atresia then putting the child in the life is unnecessary. So it is very, very important in differentiating neonatal hepatitis and biladeria atresia. Acuracy is around 83% to 97%. The mandatory requirement is that the pro-common time should be normal. There should be no acytis or any other contraindication and the platelet count should be normal. Sometimes complication may occur, but it is extremely rare. It can lead to bleeding if adequate precautions are not being taken or peritonitis or pneumothonics. So this is the histological appearance. You can see biladuct proliferation in extraepatic biladerie atresia with bioplux. This is another picture in which you can see biladuct proliferation in biladeria atresia. Now in paucity of intraepatic biladucts, you can see that there are only few biladucts because of lack of it. This is the histological picture. This is giant cell formation in neonatal hepatitis. In PFIC, again, you can see that there is not only biladuct proliferation, but there is also fibrosis. So following all this, if we still don't get the diagnosis, then we go ahead and do the genetic and enzymatic study. It is very important to remember sometimes when you are investigating this child, you will get multiple diagnosis that you will find some amino acid to be raised in our DMS level. You will find that some of the IgM, especially the rubella IgM antibodies are raised. So you are always in a fix whether the child has got metabolic condition or viral condition or which treatment to start. So whenever you get this multiple kind of factors, it is always important to remember that for viral etiologies, the PCR should be done for confirmation in the diagnosis, unless clinically the child has got all the clinical condition which fits into a viral induced polystasis. Other than that, for genetic, you can do genetic and enzymatic studies which do take time to come to confirm the diagnosis of the cause. So alpha 190 trypsin deficiency, you have the PISZ gene, which is responsible. Then you can do the CFPR gene for CAF gallatin enzyme study for galactosemia. Then there are glycogen storage disorders. Then for hemopromatosis, usually you do the iron studies and then you look at the deposition of iron in the pancreas and iron. Then nemenpig disease, you do the nemenpig genetic studies. In citrin deficiency, you look for citrulline and raised alpha pitotopy with ferritin. Then in allergens, you see jag and non-chain. And then in PFI C123, you see the ABCB4 and ABCB1180P8B1 genes. These are very, very common. That's why I'm discussing because all these genetic and enzymatic studies are easily available and down nowadays to conclude the diagnosis of neonatal polystasis. So let's look at the diagnostic algorithm.  If the septic spleen is negative, then look out for other viral illness, like CMVHSV, to a ferritin level, a urinary succinyl acetone level to exclude tyrosinemia, valve level as well. If it is normal, then biopsy is optional. Sorry. If the child is not sick, look for pale stool. If there is pale stool, then do a fasting ultrasound scan and for gallbladder contractility. If it is normal, then biopsy is optional. If there is small gallbladder that you see on an ultrasound scan or epsom gallbladder, it's important to exclude biliary atresia. For that, you need to go ahead with either with the liver biopsy or do an introop cholangiogram. And if there is evidence of political cysts on ultrasound, then you have to do a surgery. If the stools are pigmented, then you do a sonography, look for any surgical cause. If there are not, then do not for metabolic cause as well. In biliary atresia, if the age is less than six weeks, do a Hyda scan after three days of priming. You look out for excretion. If there is no excretion, obviously you have to go ahead with the surgery. Again, no excretion, liver biopsy. If it is inconclusive, then introop cholangiogram with the site. If the age is more than six weeks, then directly go for liver biopsy. Don't wait for Hyda scan. If the child with biliary atresia present to you after three months of age with the site is, or maybe more than six months of age, then it should directly be delivered to the transplants and the child has developed cirrhosis in a site and it's a transplant. Now comes to the management. So we all know that liver needs a lot of nutrition and this is of prime importance in any child who has got chronic liver disease. So it's very important to ensure that the child gets adequate nutrition. It could be breastfeeding with supplemental feeds or you can give them a supplementary formula as well, but make sure that you provide all the adequate amount of carbohydrate, fats and protein. The energy intake should be adequate. With all the vitamins, fat-soluble vitamins, these are the recommended doses of ADEK, which needs to be given along with other minerals, calcium, phosphorus, vitamin zinc and iron. Now puritis is very, very common in polystasis so and it is very difficult to treat as well, especially in infants sometimes. Initially we start with the urso. If it doesn't get better, you can add the 1% of inobarbitone and if it doesn't get better, then you can give polystyramine as well in the dose of 428 gram per day. All these are good to be given in divided doses. So let's look, if there are associated common condition, then you need to treat. For example, if the child has got hyperthyroidism or hyperbacterialism, then you have to do hormone replacement. If the baby has got polystasis because of galactosinia, then obviously elimination of dietary galactose, elimination of dietary fructose for the fructose intolerance, tyrosine-free formula for tyrosinemia, and for bile acid synthetic defects, you have to supplement all your bile salts. Now finally, if the child doesn't get better with all this and the child has got progressive or chronic liver disease, then the child should be referred for liver transplantation. The indication is decompensated liver disease, psitis or encephalopathy, or failed auto-entry storming. Now, the survival rate for liver transplantation is very, very good. The one year survival rate is approximately 85 to 90%. Five to eight year survival rate is around 75 to 80%. And mostly the most common reason in child who undergo liver transplantation, half of them belong to biliretrizia. So, if the age of, I'm just going to skip this slide, it's not, so this was the study which was done in 1999, but the results are much better. Earlier the survivors used to be around 30 to 50% and 10 year survival was around 23 to 43%. This is now gone up to about, the five year survival has gone up to around 85 to 90% in the recent times. So, if you look at the long term outcome, the mean survival of biliretrizia patient who are untreated is around 90 months or maybe lesser. Three year survival is less than 10%. But all this kids' life can be saved if they are referred for an early liver transplant. Similarly, in neonatal hepatitis, 60% of the patient with idiopathic neonatal hepatitis will recover without any specific therapy. 10% die quickly because of bleeding or pulmonary hepatic failure and 30% of them can progress to progressive liver disease. So the key message I would like to give from my presentation is early diagnosis is the key to save the child with or maybe with chronic liver disease. Congenital infection is the most common cause of polystatic jaundice. Parputaneous liver biopsy is safe and most useful tool for diagnosing of any kind of chronic liver disease in babies. And surgery for biliretrizia and the CES should be done before two months of age. With that, I thank you for your patient listening and we're gonna take the questions from you.


for the potential of any civil unrest over the next few days. But while reassuring our public that it is our expectation, that any demonstrations will remain peaceful. With that said, I'm going to hand off to our Mayor, Stephen K. Benjamin, as well as our Chair of Richland County Council, Paul Livingston, for some opening remarks. And then I'll come back up and we'll proceed through the agenda with any information that we're able to share at this time. Thank you. Thank you all for taking some time to be with us today. I want to thank, obviously, all of our program participants to hear from our law enforcement leaders, and Sheriff Lottin, Chief Holbrook, who I want to terribly want to, obviously, thank our amazing public policy leaders, our city manager, her great team, Chief Jenkins and Director Tensley, and certainly our newest members of County Council here with Chairman Livingston, Derek Pugh, and Gretchen Baron, and my colleague, Tamika Devine, and of course, Sam Davis. We have other members of City Council who will be joining us probably before we wrap for today. But thank you, all members of the media, for being here with us today. This is a unique opportunity where, just as guardians of the public trust that we are elected to these roles, I've always believed and stated, some of you have known for years, that you are the fourth estate as well. And while we may not always be on the same page, the role and responsibility of keeping the public informed, particularly as we emerge from, notice that, in terms of optimism, the greatest pandemic since 1918 and the greatest economic disruption, certainly election year since 1932, and the greatest social illness that we've seen in America cities since 1968, your role in getting good news out to the public is crucial. Probably no more crucial than it is today. Many of us, all of us, witnessed last week probably one of the most challenging days that we could have imagined as a space crucial sacrosanct to our history as a republic. So actions that were intolerable. There's been, as we all know, continued messaging that the threats of similar actions in capital cities. And that's why we thought it'd be prudent for us to have some opportunity to make sure that we were all on the same page as we prepare for this weekend, as well as for inauguration day. While we have every reason to give credibility to any threat, whether it be clear and direct or if it's simply articulated on social media, it was important for us, as we respect the honor and sanctity and safety of our public and our public institutions and our citizens, that we step up as one unified voice and help all of us understand that as leaders, we are always prepared for the worst what we hope and pray for the best. So we gathered here today this afternoon to assure all citizens in Columbia and Richmond County across the region that every preparation is being made to ensure the safety of our citizens and their property as concerns of planned protests continue in this country and the state and certainly in this capital city as we see protests often as the home of our state house, we understand that First Amendment rights are sacred. They are sacrosanct to who we are as a country and they will always be protected. But acts of violence will not and never will be tolerated. It's important, again, that First Amendment rights not only protect the rights of citizens, the lawfully protest, but it also extends to each and every one of you as members of the media. And we will continue to work closely with all of you to ensure your safety as well. Chief Holbrook is going to detail how his department is working very closely with every available law enforcement agency to protect our citizens and our public institutions, as will Sheriff Leon Lott. I am so thankful for the team of men and women that these two gentlemen lead, I believe, that combined. We have the very best law enforcement leadership in the country. Again, we will continue to be communicative and transparent in ensuring that information that you need, that our public needs to ensure that we're all safe and secure, enjoying the peaceful enjoyment of our homes and our property, that it's clear. And obviously every tool that we have in our toolbox to make sure that happens, we will not hesitate to use. Before I pass the microphone, I do want to say this, I do want to emphasize to our citizens, we're preparing for anything, but we are optimistic that citizens will exercise a thoughtful discretion to make their views known, but to do with respecting each of us, our individual property, and certainly public property. But unless there's a need this weekend, and certainly on inauguration day, to be downtown, if you have no need to be downtown, I encourage you to stay home. There's no need to add to the mix. So that is a word for each and every one of you. So I'm going to step aside and give the microphone to my friend, our chairman of Richland County Council, Paul Livingston. Thank you. Thank you, Mr. Mayor. One thing, Steve, you make my job easy when I follow you because you cover it all, and I just have a feeling a few little blanks in there. Appreciate that. On behalf of Richland County Council and all the citizens you represent, let me first start out by just simply thanking our law enforcement and first responders. Those at individuals are going to be at the front line and make the difference if there need to be a difference made coming of this upcoming event. Now, but let me say I'm extremely confident that we're in good hands when I think about last year's protests and the challenges and how well we handled that relative to many, many situations across our country. So as a matter of fact, some individuals saw us as a model. That's how it was handed. So we have to thank individuals for that. Now, it's still a question about the function our community had to have urgent opinions and beliefs about the presidential election. But at the same time, we should all agree that everyone has a right to exercise their first amendment right. But keep in mind, we expect for you to do that peacefully. And if not, is our intent to make sure we hold citizens accountable. I'm confident that we're prepared for that based on the feedback and comments I've gotten from our law enforcement, as well as past experience of our law enforcement. I want to urge our citizens, too, to if you can still wait for the core of the city on the inauguration of the day, please plan to do so so you can help us with our safety and our community. And let me also, too, Mr. Mayor did it. But I'd be remiss if I didn't make sure I, again, recognize my colleagues who are here, Ms. Gresham Barron, as well as Mr. Derek Kuehl. And I want to do that again because there are new county council members. I want to make sure they get recognized and noticed as often as they can. So you can know who you talk to when you meet and see them. Steve, don't give the secret away. But again, on behalf of Mr. County Council, we represent, I'm honored for this opportunity. And again, help us keep our community safe. Do your part, and I think we'll be in good hands. Thank you. So at this time, we will get into the actual law enforcement related updates as well as any operational updates for city center that I will give following Chief Holbrook and Sheriff Lott's comments. I'll also recognize my colleague who will also come up and give any Richland County operational updates. Thank you. Good afternoon. Thank you, Ms. Wilson, Mayor.  We often talk about the value of relationships and partnerships, and that is an investment that pays dividends for us time and time again. And this is another example of that. Really, the purpose for my remarks is to provide reassurance to our citizens, to have confidence in our preparation and planning. It's been extraordinary. It's a pleasure to, and really a privilege to lead the police department, but participate in planning or have any responsibility for planning of an event of this magnitude or events of this magnitude with the support of manager and mayor and our elected officials. They have never once been impediments. They clear the path and provide all the support and resources that we need to not only plan but have everything at our disposal to protect our city, our citizens, our facilities, infrastructure, and that's exactly what we've done today. Lots of lessons learned. Without a doubt, lots of lessons learned from May. We have a situation that's a little bit different. The primary operational area for us is supporting efforts on state property with the state capital. We are a capital city. Our state capital sits in the business district of our city. And we also know that as they heighten security on capital grounds and place restrictions in place that that tends to push people out into the city and oftentimes that's a burden on us that's a consequence of the heightened security that's at the state capital grounds. So we have to plan accordingly. It's always one phone call for me without debate or deliberation with our sheriff. It's not what do you need, where do you need us? And it's seamless and that's what makes this a very effective partnership. We have worked very closely with our state and federal partners along with the sheriff's department as we gather information, that information and intelligence so we can make decisions. But I can tell you that we have an extraordinary in-depth plan in place with, as we often say, all hands on deck. Our goal is to have high visibility to again provide that reassurance to our business community. Our operational picture really begins Saturday and we'll go through Wednesday. And of course we'll make any adjustments beyond that as necessary. We, I know there's always questions about numbers. We're not gonna talk about numbers. But again as we've released in some of our preliminary information we obviously have a strong uniform presence, field force options, tactical options, as well as our EOD, K9s, aviation units and really everything that we have to, and the technical assistance we have to monitor our crowds and make decisions. We've worked hand in glove with our emergency management division of the city and our fire department. As always they will work closely with us as we move a lot of people around the city in the next few days. This message has to be clear. We're gonna be there to support and protect those that choose to exercise their first amendment rights but we will not tolerate any lawlessness, civil unrest. The response will be immediate, swift and certain. We want everybody to be safe. And again what you can count on from your law enforcement is professional, ethical, constitutional policing always. You see Chief Hobock and I are standing up here together and that's because we do work so close together. Our team is one team. It's not the Sheriff's Department, it's not the Columbia Police Department. It is one team of public safety in the city of Columbia and Richland County and it works closely together and we are capable of addressing any kind of issue that arises. Terrorist, one of the tools of terrorism is to create fear and that's what we're seeing right now is people that are trying to make all of us scared, make our citizens scared. There's emails and Facebook posts and flyers going out now that are saying all kinds of things that are not true. That is fake, they're not true and we need to reassure our citizens that what you see on the internet or what you may get on an email is not true. And we're trying to address that as much as we can. We do not have any credible threats that anything's gonna happen here in Columbia. But if it does, we're ready for it. Since this past summer we've trained, we've equipped our people better and we're better prepared. And so if something does happen you're gonna see us address it very quickly and very effectively. As Chief Holbrook said and the mayor said, peace will protest, that's your right. We're gonna be there to make sure that you're able to peacefully protest. But rioting is something different. We're not gonna allow rioting. So live your life citizens, live your life, don't live in fear, go about your normal daily activities that you would do any other time. Don't let those who are trying to disrupt our way of life win. And you'll do that if you live in fear and you change your activity. So just be assured that we're here to protect you. And I'm gonna echo what Chief Holbrook just said just a second ago. If you come to Columbia and think you're gonna riot, you'd better think twice because between both of us, we've got a force that's gonna deal with that and we're gonna deal with it the way it needs to be done. So to compliment what you have heard from both Chief Holbrook and Sheriff Lott, I'd ask Administrator Leonardo Brown also to join me if he has any additional updates regarding the operational plan for the city and the county. From the city center perspective, due to COVID, all of our public-facing facilities in the city remain closed anyway to the public. Operations and services continue and have been seamless since the beginning of the pandemic, but they're for the most part being handled remotely. And so for any of our staff that do continue to work in those facilities right now, we are going to ask that they too will be working remotely on Wednesday, January 20th. So again, the citizens won't see any difference really with public-facing facilities. They're already closed due to COVID. Our staff that may be working in those facilities on staggered schedules, et cetera, we are gonna ask that they work from home or work remotely on Wednesday, January 20th. We've also been in communication with many of our major property managers in the city, center, downtown corridor, the major business complexes, and they too on their own have made operational plans for next week, Tuesday and Wednesday. Many of them have determined to restrict public access to many of those major business facilities downtown and add additional security measures out of an abundance of precaution. In general terms, and I think you've heard now, this probably for the third time, I know Mayor Benjamin stated it, Councilman Livingston stated it, and then both the chief and the sheriff have reiterated that while we are not wanting anyone to live in fear, we are also wanting and urging you to use common sense approach to your day to day activities over the next few days. And so out of an abundance of caution, we do advise citizens to be in, that may have to be in the vicinity of the state house and the city center on Wednesday, January 20th to only do so if it's just absolutely necessary. Finally, from parking, a parking perspective downtown, the parking services division will modify its operations on Sunday, January 17th and Wednesday, January 20th. Public visitor parking will not be available at the following locations on again, Sunday, January 17th and Wednesday, January 20th. And those locations are the Lady Street Deck, the Park Street Deck, Lincoln Street Deck and the Washington Street Deck Facility. Those addresses of those parking decks will be widely shared on all of our social media platforms and the city's website. We will ask monthly permanent holders to be able to continue to have in-grass and egress access as normal because they have access cards to do that. But to the public, there'll be restricted access on January 17th and January 20th. Two of our parking facilities will offer one access point, the Assembly Street access point at our Lady Deck will be closed. Monthly parkers are advised to use the Lady Street access point and the Park Street access point at the Park Street Deck, which it will be closed. So monthly parkers and hotel guests downtown are advised to use the Pendleton Street access point. And again, all of this, we will have widely shared on our social media platforms and the city's website at columbiasc.gov. The parking services division will communicate the same information via their parking services website and further press releases. If you have further questions about this parking plan, you can contact our parking director, y'all matinee at<PHONE_NUMBER> or parking services. The general office line is<PHONE_NUMBER>. And we will share all of this information widely on all of our platforms. Again, we just reiterate that we are taking an abundance of precaution to protect the public. We want to make sure that everyone who wants to, if they choose to protest, they do it in a peaceful manner. That indeed is the expectation. Leonardo? Yes, ma'am, thank you. So good afternoon, everyone. My name is Leonardo Brown, Richardson County Administrator. Again, on behalf of the Wilson County Council, while we have some of our members present, the limited physical presence of our council does not represent the immense support that they have for law enforcement as they have combined together to represent this community in a way to keep the safety of the public paramount. In saying that, one of the things I want to echo is that, Richardson County's model last year was safety over everything. And I think what you see here, working along with the city manager and the members of city council, is that all of our combined forces represent our commitment to a unified approach to serve this public. Myself as the Richardson County Administrator, want to speak to our specific folks who are out and about who may not be necessarily in the city center. I have spoken with the Sheriff's Department. Sheriff Lott is here. We want to make sure that you are aware that even though the city may be the center, that the Sheriff's Department will continue to have its forces available for any of our county facilities spread throughout Richardson County. So no one should be under the impression that Richardson County would not have the necessary coverage that it needs. So I've been informed by the Sheriff's Department that everyone should continue to, as the Sheriff's had said himself, live your life. So whether you're at the city center or throughout Richardson County and one of our governmental facilities, you will be protected as necessary. Also want to remind everyone that our Emergency Services Operations Center is at an enhanced awareness level, which simply means that our EMS responders will be available to respond as necessary should the need arise, as well as our fire marshals in coordination with the Columbia Richland Fire Department. So again, that just echoes that our joint commitment to serving the citizens of Richardson County and those who are represented within the city limits. The last thing I'll say is, again, on behalf of Richland County, that if you are an employee of Richland County, please look at Richland County's website, monitor our social media pages. If there is any changes to any status of our facilities, we will post those. So that's where you need to get your information from. If you are an employee of Richland County, as well as a citizen who may be entering to a Richland County facility. Again, thank you on behalf of Richland County, City Manager Wilson, for the opportunity to speak to the citizens. Thank you, Mr. Mayor. Thank you, Chairman Livingston. At this time, I think all recognitions have been made by Mayor Benjamin and Chairman Livingston. But again, I know I speak on behalf of Administrator Brown, that we're very thankful for the elected leadership and the priority that all of these elected members here and those who couldn't be here, place on the safety of our city and our county. So thank you again, Mayor Benjamin, Chairman Livingston, Mr. Davis, Mr. Vine, Mr. Pew and Ms. Barron, looking forward to meeting you more and working with you more. I'll be remiss and they asked me to say on their behalf that Councilman Duvall and McDowell are in the line waiting and being proactive as they are getting their COVID vaccine today. And it's a long line over there and we're happy about that. So they couldn't quite get here, but they wanted me to give their regrets for not being here. At this time, Mayor Benjamin will close with some remarks and then I'll come back up in between any of us. We'll answer any questions you may have. No, just summarize all the comments you've received We're prepared for anything and we're hoping for the best. After we are done with question and answer, some of you may have heard we've made some significant improvements as a region and certainly as a city continuing to invest in emergency management. You've seen literally the same team come together when we're preparing for inclement weather, storms, floods, hurricanes. And I dare say that no one responds the way that we do in those challenging events. We've made some of those investments certainly directed across the street in our emergency operations center. And I believe there'll be limited access for some of you who may want a more hands-on idea of some of the significant investments made. We limited access, great leadership of Director Tinsley working in concert with Chief Hogue, Work Chief Jenkins, the sheriff and the direction of our city manager. We've made the right moves on behalf of the people. So thank you all for being with us. Happy to field as many questions as we possibly can. You've seen that with us. I mean, the, does General speaking? This is, it's a little bit different. And now I defer to the chief and the sheriff that they want to add in. I mean, I think it's fair to say that what we saw in our nation's capital last week shocked the conscience of America and it shocked the conscience of Democrats and Republicans and independents and people who don't like politics at all. That this is indeed, some people think it a fallacy or a dream. This country is meant to be a shining city on the hill to countries all across the globe and there's certain things that we hold dear and true. So the events of last week certainly have each and every one of us, I think that much more focused, that much more diligent, that much more focused on our individual collective responsibilities to do our jobs and do them well. We are optimistic that there will be a non-event. But the important part of preparation, particularly in public leadership is that you prepare for everything. And that's what we're in fact doing. A key piece of any type of emergency preparation and responses is clear and complete and transparent communication. And that's what we're just making sure we do here today. We're communicating those who might want to cause problems, but more importantly, we're speaking to the mom and dad at the kitchen table who are concerned from what they're reading or hearing or seeing on social media. We're speaking to our citizens who care about this city and care about this country and just making sure that we're working to reassure them. And again, you can only do that, Ms. Wilson and others, you know, these things you learn over the course of time that I remember, many of you remember are constant press conferences in the wake of the storms in 2015 and we learn very quickly that constant communication is pushing it out and being fully transparent when you can do so and do it responsibly. It helps the soul. As he asked about a sense, it helps the soul of body politic and that's what this is about. And Ms. Wilson touched on some of that, but there has been open and constant communication. We, as you all know, we don't have a shy business community here. They stay engaged and involved and I think the message is quite clear and I think, you know, you don't do what we say, you do what we do unless there's a need to be downtown as everyone up here said, then let's all stay home. And we will not have our employees in the offices, many of them have been working remotely already, but there's been constant communication. We'll continue to do so. We want everyone to be thoughtful and judicious, recognizing again that we are hoping to see an emergence from some real economic challenges that have affected businesses all across this country over the last several months. So we recognize that need and that's how we're having that constant communication with them that has been open and constant communication. Let's go here first and then here. And you all feel free to jump in at any point. Well, as the sheriff mentioned, there hasn't been a specific threat. There's been general threats nationally directing certain groups or ideologies to target certain facilities specifically state capitals and we're a state capital city. So the FBI immediately shares information that they receive and quite frankly, they've made a national call out for information to be pushed up to them. Oftentimes, especially domestic terrorism, history has shown that typically that case is solved or a critical breaking point is from that local police or sheriff's deputy on the road to make that traffic stop or that citizen contact. So there's a tremendous mutual respect up and down all of law enforcement and that information sharing is we all know through history is more important now than ever. So we're aware of certain groups and the history of certain groups and their ideologies and we've certainly witnessed what happened last week. And again, we've locally had lessons learned on just how quickly emotionally charged crowd can go from lawful and peaceful assembly with people expressing themselves to civil unrest, property destruction and injury. And again, the question was asked about the downtown businesses. There's been lots of communication but our message is that we're not gonna let property get damaged and we're not gonna let people get hurt. Not with the city of Columbia. Yes ma'am, I mentioned earlier that our operational picture really begins Saturday runs through the 20th but we do have specific information of groups that plan to protest on the state capital grounds on the 17th Sunday and then specifically on the 20th. That's why the 17th, fortunately, is a non-business day, it's Sunday. We don't feel like there'll be as much activity downtown. Wednesday definitely is a day that we're concerned. And that's why we've expressed that if you don't need to be downtown, we would ask that you not be downtown because you may be inconvenienced. Out of an abundance of caution, we may have to close the road briefly or for a period of time that will create inconvenience. Our downtown is unique. We have entertainment area restaurants but business is high rises and we also have residential areas. So in a school that all sits contiguous to one another and those are areas that we're very focused on we have personnel that are prepared to again have high visibility and respond immediately to anything that may be unlawful or concerning. Let's see if you can use that, this is more appropriate. I have that authority on our state law and if the situation presents itself, I won't hesitate to use that as one of the important tools in our toolbox. Under our state law, many of you know I have the authority to establish a career for you but our city council must meet within 24 hours to confirm it, to extend it. We have no plans to do so right now but based on information and any intelligence we receive as you all know from experience, we don't hesitate to use that tool. So again, the city has not received any permits, requests for permits for any kind of protests, marches or anything of that nature. You'd have to speak with the BPS to specifically address whether any permits have been requested on their property and what was your second question? It's true. What are the streams groups that you're monitoring about the state right now and especially since we asked you to choose groups out of the state house as recently as last week? Yeah, well I won't get into what groups specifically we're monitoring other than to tell you that obviously we are monitoring several groups. Many of them have been talked about openly in public but we're doing a tremendous amount of intelligence gathering and intelligence sharing to the extent we can. This, we've seen some, I guess, a different approach from some of these groups that may not be as vocal on social media platforms as we have seen with other groups. So, it's oftentimes difficult to anticipate numbers like maybe we would be able to do in the past. So again, that's what we plan for, what are our experiences, we plan from what our experiences have been in the past, plan for the worst and expect the best. If we have no other questions, we do want to still make cognizant of the fact we're working away through a great pandemic. I want to thank everyone for showing up and wearing your mask.  So be fully prepared, he did tell me that. I think Desuma has one in his back pocket too, a ticket book. So thank you all. Thank you for what you're doing. Thank you for what you continue to do. We'll be heading across the street, just catty corner to the EOC if you want to come say some things. 1800 Main Street, it's catty corner. If you can't get there, you're in bad shape. God bless you. God bless this country, this state, and God bless the city of Columbia. Thank you to all these amazing men and women who do their part every single day to make this place a special place to live.


That's crazy. There's so many people here. Who's the leader? Who's the Merlach leader? Where is she? This is the leader of the Merlachs. Okay, let's run back because we gotta move quick. Alright, we'll see you later. That was great. To be honest, you're just here for the K-pop finale. That is not true. Okay, now I see an S-man. There you go. Cool. Of course. To me, it's S-man. What are the chances? What are the chances that she called me S-man? I have no idea. Hey, how's it going? Doing good. You're good. Super good. Awesome. Awesome. Okay, got it. Awesome. Thank you so much. Let's go. We're about to meet you, man. It's been a long time, man. I watched the whole thing. It was so fun. How's your voice? It sounds like it's shot. Okay. Classic plus likes. Classic plus beta. Beta, yeah. I know what they're doing. Could you sign my flag? Just anywhere that's, like, meaningful to you. Anywhere that's meaningful, let's go here. We're going to go smack dab. Or stormwind. There we go. Stormwind right here. There we go. Oh my God. I can't believe I made it to here. The line is out of the blue spot. Really? That's crazy, man. Thank you so much. I thought I'd be enjoying it. Hey, how's it going? Nice. I saw you earlier. I don't know why you're so excited to be here. I don't know. I'm glad I'm glad I came here. Long time ago. Yeah. Oh, sick. Nice. I'm a survivor. Isn't that sick? Can I see that? Nice. That's cool. Yeah, okay. We're telling this line to have 45 seconds total. Oh my God. They're going to be super pissed if you're talking, because I feel that they don't have time. To be fair, there's so many people. That's how it is. What's up, Ice Man? I'm standing out down here. Annie. How about the short hair? I'm sorry. Nice to meet you. Sorry, hot dog man, by the way. I never meant anything like real estate. It was entirely like in good school. You know, I wake up at like 5 a.m. when I got my Twitter phone.  Jazz and Old Tweet, where it was, this guy attacked me, it was him, and he's like, he attacked me. He was like, we murder Esfand's group. We always push us to travel. So I saw this. Which he did a couple of times, but of course you admitted it. And then afterwards, I screen shot it, I was like, what the hell? Wait, I remember this guy, and we played 5 games. We burst like 5 or 6 times, and if you lose at Blacksmith, you just throw the game. You just throw the game, so you can open another queue. I just wanted to, I'm just going to address it, okay, I appreciate it. It was very fun playing against you. Can I get a selfie real quick? Yeah, of course, man. We are here with Esfand. The Esfand. I feel like there's probably video proof. Well, okay, I believe the second one. Nice. Staying on your perch. Hey, shout out to Asmigold, Emeru, and Tectone. Best podcast every week. I love to see it. They do a great thing. I wish they were here though. What happened? You're the only representative. I have to stop this. Having a leisurely time. But you're out here with the fans. That's something that's really, really cool. Not everybody has the time or whatever to do that, but I really appreciate you're out here meeting people, just being a cool dude. One thing that you do that is really incredible is your green screen. When you're in that tournament and you're just standing on the field interviewing the people, that was hilarious. I want to see you in Seasonate Discovery in front of those new raid bosses giving a pep talk to your raid. Just like the old days. Yeah, just like you're there in the raid. I used to be like 6 years old, real on YouTube. Nice. Do like a Leroy Jenkins type where you're like explaining it and then somebody just runs in and you're like wait, I wasn't done yet. It's just chaos. That would be hilarious. Scam Guild, we are recruiting. Sorry to take up so much of your time. That was fun. Thank you. Hi. Yeah, she's here. She is? Yeah, she's here somewhere. Oh my god, yeah. You like it? I actually really like it. Everybody said it's boring. I thought the football game was sick though. It is. But it's like all I have. Did you do any nails? Oh no, no. If that's your hometown everybody hates where they're from. Everybody thinks where they're from is boring. That's because you grew up there. Yeah, but I think if that was the truth I wouldn't have fun either. I had them scream snipe you because I was like I'm so did you look at everybody and you actually were talking with one of our friends yesterday and they're like oh as fun as you are I absolutely love watching your screams. My life is super chaotic and like... I met some of my guild members last night. Yeah, I was like 20 people growing guild members. That's awesome. And there are people like other guild people like oh I know you from this and everything too and then just like it's so cool just to see everybody. Yeah, I watched it last night. Did you double everybody? Yeah, I tried using like the same thing you did over all the judges. It's okay. I like shield twisting more but it's okay. It's not bad. Oh yeah. It's a classic for the first time with these new abilities. I appreciate it. You always cosplay? Yeah, I do. You literally just made it. So you literally... That's hilarious actually. But I quit for a lot of years. There was like a middle chunk after Rath that I just like was back for a while. That was literally me too. And then I came back during I think Warlords and then Legion. I came back for Warlords and I was like what am I doing? It's so funny. I put a lot of league in there in the middle. Oh my gosh. I started playing league at one point and I got into that and then like after I think certain champions came out I was like I just can't get into this anymore. I got to toxic. I remember like it was like I think it was like season 4-ish that's when I fell off. It was like 120 or something like that. Almost. Oh my goodness. Oh my gosh, well thank you for your time. I really appreciate it. Yeah, of course. They did ride them again. American shopper made them on this GoPro channel. Wait, really? Oh, so they're a good company. Yeah. Well this is like if you could like actually turn the end on. Okay, sounds good. We're slowly walking away. I think in on this soon as fun is flying after. Why did you tell him to do that? It's not my fault. Yeah, it's your fault. You should know better.