Viral Hepatitis: Viral Hepatitis: Hepatitis B and D

0:00Welcome to Board Pearls. This is episode two of three of the Viral Hepatitis chapter, in the Liver Disease module. This episode is hepatitis B, with hepatitis D at the end. A woman with a positive screen shows what each marker means and how the phases of chronic infection are told apart, and a man with an isolated core antibody shows the pattern that has four explanations. A man with cirrhosis shows who qualifies for treatment, which of the three drugs to use, and when it's ever safe to stop. A woman starting rituximab shows who's at risk of reactivation under immunosuppression and why prophylaxis beats rescue. A pregnant woman with a high viral load shows newborn prophylaxis, when the mother needs tenofovir, and the flare after delivery. And a man whose liver tests rise while his hepatitis B stays quiet shows why hepatitis D needs hepatitis B, how coinfection and superinfection differ, and what treats it now.

0:55Here's the first patient. A forty-two-year-old woman who emigrated from Vietnam has a positive hepatitis B surface antigen on screening. Her mother has hepatitis B. Her core antibody is positive with a negative immunoglobulin M, IgM, and her surface antibody is negative. Her e antigen is negative and her e antibody positive. Her hepatitis B virus, HBV, deoxyribonucleic acid, DNA, is one thousand two hundred international units per milliliter, and her alanine aminotransferase, ALT, is nineteen on two checks. Her FibroScan is normal. She asks whether she needs treatment.

1:33She has chronic hepatitis B, and whether she needs treatment comes from reading her markers and placing her in a phase. Each marker has one meaning. Surface antigen, HBsAg, is the envelope protein, produced in excess during active infection, acute or chronic. Surface antibody, anti-HBs, neutralizes the envelope and marks immunity from recovery or vaccination. Core antibody, anti-HBc, is made only after natural infection, because the vaccine contains surface antigen alone, so it separates exposure from vaccination and persists for life. Its IgM form appears in acute infection and during flares of chronic infection, while the total core antibody, mostly immunoglobulin G, IgG, marks remote exposure.

2:20The last two markers measure replication. The e antigen, HBeAg, is a secreted protein that marks high replication and infectivity, and e antibody appears with seroconversion. But precore mutants replicate without making e antigen, so a negative e antigen doesn't guarantee low replication. HBV DNA measures the viremia directly and settles ambiguous serology.

2:46The three main markers are read together. All three negative means uninfected and unvaccinated, so the patient is vaccinated. Surface antibody alone is vaccine immunity. Surface antibody with core antibody is resolved natural infection, which matters for reactivation under immunosuppression. Surface antigen with core antibody and no surface antibody is active infection, acute with a positive core IgM, and chronic with a negative IgM and a positive total core antibody. Her surface antigen with total core antibody and no IgM confirms chronic infection.

3:22Her treatment depends on her phase, which is defined by e antigen, HBV DNA, and ALT, set against the histology. For these decisions, the upper limits of the ALT are thirty-five in men and twenty-five in women. The immune-tolerant phase has a positive e antigen, a DNA above one million, a normal ALT, and minimal histologic change, the typical picture in a young person infected at birth in an endemic country. The e antigen-positive immune-active phase has a DNA above twenty thousand and a raised ALT, with moderate to severe inflammation and fibrosis, and it's a treatment indication.

3:59The e antigen-negative phases come next. The inactive carrier phase, e antigen-negative chronic infection, has e antibody, a DNA below two thousand, a normal ALT, and minimal histology. The e antigen-negative immune-active phase, often from precore or basal core promoter mutants, has a DNA above two thousand and a raised or fluctuating ALT, and it's a treatment indication. Resolved infection is a negative surface antigen with a positive core antibody, with or without surface antibody, and an undetectable DNA. The active phases are treated because, untreated, they progress to cirrhosis at roughly two to ten percent a year.

4:47A negative e antigen is shared by the inactive carrier and by immune-active disease from a precore mutant, so the DNA and ALT have to be read with it. She's e antigen negative, with a DNA under two thousand, an ALT that's normal even by the stricter limit, and a normal FibroScan. Significant fibrosis, stage two or more, would be a treatment indication on its own. She's an inactive carrier and doesn't need treatment now.

5:13Her label isn't permanent. Patients drift between the inactive and the e antigen-negative active phases, so a single normal ALT doesn't lock in the label, and inactive carriers can have a DNA up to twenty thousand without histologic hepatitis. She's followed with an ALT and DNA every three to six months, and her liver cancer surveillance is decided separately by her age, sex, origin, and family history, as chapter twenty-four covers. And because she's surface antigen positive, any future meaningful immunosuppression needs antiviral prophylaxis, so her status belongs where every prescriber will see it.

5:50Her follow-up also depends on what counts as cure. E antigen seroconversion isn't cure, because the disease can continue as e antigen-negative immune-active hepatitis. Functional cure is loss of surface antigen with an undetectable DNA, and it's achieved in fewer than ten percent of patients on current oral antivirals. Virologic cure, eradicating the covalently closed circular DNA, the cccDNA reservoir in hepatocyte nuclei, isn't achievable. That's why treatment is usually indefinite, and why a patient who looks recovered can reactivate.

6:23The second patient shows a pattern with four explanations. A thirty-eight-year-old man has an isolated core antibody, with negative surface antigen and surface antibody. That can mean a window period in acute infection, after the surface antigen has cleared and before surface antibody appears; a remote resolved infection with waned surface antibody; occult chronic hepatitis B with low-level replication detectable only by DNA; or a false positive. His HBV DNA is undetectable on a repeat panel, so occult replicating infection is excluded. He's offered vaccination, and his core antibody still matters before any intense immunosuppression.

7:02Not every chronic carrier needs treatment, and the third patient shows who does. A fifty-five-year-old man has chronic hepatitis B, e antigen negative, with an HBV DNA of eight thousand and an ALT of seventy-two on two checks. His FibroScan stiffness is fourteen kilopascals and his platelets are one hundred twenty thousand, which is compensated cirrhosis, without ascites, bleeding, or encephalopathy. His creatinine is normal, and he has osteoporosis from years of steroids for asthma. He's never been treated.

7:34He has e antigen-negative chronic hepatitis B with compensated cirrhosis, and the treatment criteria show why he qualifies twice over. The criteria combine DNA, ALT, fibrosis, and context. The immune-active phases qualify: e antigen positive with a DNA above twenty thousand and a raised ALT, or e antigen negative with a DNA above two thousand and a raised ALT. Significant histology qualifies, meaning at least stage two inflammation or fibrosis, whatever the DNA and ALT. Compensated cirrhosis with any detectable DNA qualifies, even below two thousand. Decompensated cirrhosis with a positive surface antigen qualifies regardless of DNA, e antigen, or ALT, because a failing liver can't tolerate a flare.

8:24Two more groups qualify for other reasons. High-risk contexts, meaning immunosuppression, pregnancy, and vasculitis, qualify because of what's about to happen, not because of the liver numbers. And acute hepatitis B is treated in the minority with fulminant or protracted severe disease.

8:41He meets two of the criteria. He has e antigen-negative immune-active disease, a DNA above two thousand with an ALT above thirty-five, and compensated cirrhosis with detectable DNA, and either alone is an indication, so the cirrhosis means he'd be treated even with a DNA of three hundred. Without cirrhosis, a DNA of eight thousand with a normal ALT would sit in a gray zone where fibrosis decides: stage two or more means treatment, and no fibrosis means follow-up every three to six months. Hepatitis D testing is indicated at a new hepatitis B diagnosis, with origin from an endemic region, with high-risk exposures, and with an ALT flare and a low DNA, and his cirrhosis makes it worth checking once.

9:25His osteoporosis decides among the three first-line drugs: entecavir, tenofovir disoproxil fumarate, and tenofovir alafenamide. Entecavir is given at zero point five milligrams daily in treatment-naive patients and at one milligram after prior lamivudine, because of cross-resistance. The two tenofovir prodrugs deliver the same active drug, tenofovir diphosphate, but alafenamide reaches higher concentrations inside liver cells with lower blood levels. In head-to-head trials over ninety-six weeks, the two suppressed the virus equally well, but alafenamide caused smaller declines in kidney function and bone density. So alafenamide is preferred with renal or bone risk, and disoproxil in pregnancy, where its data are more robust.

10:09Peginterferon is a niche option, with side effects and a fixed duration, and it's contraindicated in cirrhosis because it can precipitate decompensation. His osteoporosis rules out disoproxil, he has no lamivudine history, and he starts tenofovir alafenamide.

10:25He needs to know what treatment achieves and why it won't stop. Entecavir suppresses the DNA in most patients at one year, more often in e antigen-negative disease, e antigen seroconversion occurs in about twenty percent, and surface antigen loss occurs in only one to five percent over years. Success means an undetectable DNA and a normal ALT on treatment, and treatment is generally indefinite. The only acceptable stopping points are confirmed surface antigen loss with surface antibody seroconversion, or sustained e antigen seroconversion with prolonged suppression in a patient without cirrhosis.

11:01Patients with cirrhosis and transplant recipients continue indefinitely, and he's told that at the start, because a flare in a cirrhotic liver is exactly what treatment prevents. A year later his DNA is undetectable and his ALT is normal, and he needs liver cancer surveillance for his cirrhosis.

11:18The drug rules shift with circumstances. A thirty-two-year-old woman with e antigen-positive immune-active disease who's planning a pregnancy within the year is treated with tenofovir disoproxil, and a patient on another antiviral is switched to it when planning to conceive. A sixty-eight-year-old man with decompensated cirrhosis, ascites, a positive surface antigen, a DNA of three hundred, and a normal ALT is treated anyway, with entecavir, because his liver can't tolerate a flare, and peginterferon would be dangerous for him.

11:51Treatment isn't only for active liver disease, and the fourth patient shows the most important exception. A sixty-seven-year-old woman with diffuse large B-cell lymphoma is about to start rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone, CHOP, chemotherapy. Her surface antigen is negative, her core antibody positive, and her surface antibody positive. Her HBV DNA is undetectable and her liver tests are normal. She never knew she'd had hepatitis B. Her oncologist asks whether it matters.

12:24It does. She has resolved hepatitis B, and rituximab puts her at high risk of reactivation. Even after apparent recovery, the virus persists as cccDNA in hepatocyte nuclei, held in check by the immune system, and immunosuppression removes that control. Reactivation is the abrupt reappearance or rise of HBV DNA, with or without the return of e antigen and surface antigen. As the immune system reconstitutes, the ALT rises and hepatitis follows, so the liver injury often comes after immune recovery. The spectrum runs from subclinical to fulminant failure, and severe cases carry a mortality of twenty to forty percent even with rescue therapy, so reactivation is prevented with prophylaxis rather than rescued.

13:11Her old infection was found only because she was tested properly. Everyone is tested for surface antigen and core antibody before immunosuppression, and surface antigen alone would have missed her. Risk combines serology with the intensity of the drug. Patients positive for surface antigen have the higher risk, and those negative for surface antigen but positive for core antibody have a lower but real risk, especially with B-cell depletion.

13:36The drugs set the level of risk. The highest-risk drugs are the anti-CD20 antibodies, rituximab and obinutuzumab, and stem cell transplant conditioning, which are high risk in both serologic groups. Prednisone above ten milligrams daily for more than four weeks, anthracyclines such as doxorubicin, and Janus kinase, JAK, inhibitors and certain biologics are high risk in patients positive for surface antigen. Tumor necrosis factor, TNF, inhibitors and other biologics carry a moderate risk with a positive surface antigen and a lower but nonzero risk in resolved infection. On rituximab, her risk approaches that of a patient positive for surface antigen. Her positive surface antibody doesn't change that, because the antibody doesn't touch the cccDNA, and rituximab removes the B cells that make it.

14:28So she gets prophylaxis, and the rules set which drug, when, and for how long. Every patient positive for surface antigen on meaningful immunosuppression, and every patient negative for surface antigen but positive for core antibody on rituximab, obinutuzumab, or stem cell transplant, gets entecavir, tenofovir disoproxil, or tenofovir alafenamide, chosen by the same kidney, bone, and lamivudine rules. It starts ideally a week before immunosuppression, or with it, so the virus is suppressed before control is lost. It continues six months after standard immunosuppression ends, and twelve to eighteen months after B-cell depletion or transplant, because B cells take months to recover and reactivation can occur late.

15:15The evidence is strong. In randomized lymphoma trials of patients positive for surface antigen on CHOP, preemptive antiviral therapy sharply reduced reactivation, jaundice, severe flares, and deaths compared with treating reactivation when it appeared. She starts entecavir a week before her first rituximab dose and continues it for eighteen months past her last, and her DNA stays undetectable.

15:41Without prophylaxis, the sequence is predictable. The HBV DNA reappears first, while she's suppressed, and then weeks later the ALT rises as her immunity recovers, and core IgM can reappear, mimicking new acute hepatitis B. So a lymphoma patient whose liver tests rise months after rituximab with a positive core IgM may have reactivated an old infection. The workup is the acute panel plus HBV DNA and hepatitis D testing, and the treatment is an antiviral at once. Reactivation has also been reported during direct-acting antiviral therapy for hepatitis C in patients positive for surface antigen, which is why hepatitis B serology comes before hepatitis C treatment.

16:26Monitoring can sometimes replace prophylaxis, but only when it's reliable. A forty-five-year-old man with Crohn disease and the serology of resolved infection is starting an anti-TNF drug. He's at lower risk, so he could be monitored with a monthly ALT and an HBV DNA every three months, treating on demand. But monitoring only protects if it happens, and he lives two hours away and has missed lab visits, so he gets entecavir instead. A fifty-one-year-old woman with a positive surface antigen and rheumatoid arthritis, starting prednisone twenty milligrams daily for two months, gets tenofovir alafenamide before the prednisone and for six months after it stops.

17:05Pregnancy is the other context where treatment follows what's about to happen, and the fifth patient shows it. A twenty-nine-year-old woman at ten weeks has a positive surface antigen on her first prenatal screen. Her e antigen is positive, her HBV DNA fifty million, her ALT normal, and her FibroScan normal. She's never been treated and asks whether her baby will get it.

17:27She has chronic hepatitis B in pregnancy with a very high viral load, and her baby's risk is the main concern, because infection at birth usually becomes lifelong. About ninety percent of newborns infected at birth become chronic carriers, far more than children infected between one and five years or immunocompetent adults. Transmission is mainly through exposure to maternal blood and fluids at delivery, with a smaller transplacental share, and the risk tracks the mother's viral load. Below two hundred thousand international units per milliliter, newborn immunoprophylaxis is highly effective. Above it, newborn prophylaxis alone fails in seven to nine percent.

18:06Her care has three parts, and the first two apply to every exposed pregnancy. Every pregnant woman is tested for surface antigen at the first visit, and positive women get an HBV DNA, an ALT, and a baseline assessment of fibrosis and liver cancer risk, early enough to act. And every infant of a mother positive for surface antigen gets hepatitis B immune globulin plus the first vaccine dose within twelve hours of birth, whatever the maternal viral load, with the series completed at one and six months. That reduces transmission to under five percent overall, and the infant's surface antibody is checked at nine to twelve months.

18:43The third part is the mother's antiviral. With a DNA above two hundred thousand, she gets tenofovir disoproxil from twenty-eight to thirty-two weeks, or as early as the first trimester with a baseline above seven logs, so that her DNA falls below two hundred thousand by delivery. Lamivudine and telbivudine are no longer used because of resistance, and tenofovir alafenamide isn't yet recommended in pregnancy. At about seven point seven logs, she starts tenofovir disoproxil in the second trimester, and by delivery her DNA is eighteen thousand.

19:15Her delivery needs no changes for hepatitis B. Cesarean delivery hasn't been shown to reduce transmission and isn't indicated for hepatitis B alone. Amniocentesis carries a theoretical risk and is avoided when possible. Breastfeeding is allowed once the infant has had immune globulin and vaccine, even with cracked or bleeding nipples. She delivers vaginally, her son gets immune globulin and the first vaccine dose two hours after birth, and she breastfeeds.

19:42After delivery, her tenofovir has to be stopped carefully. Without another indication, the antiviral can stop at delivery or up to six weeks postpartum. But a postpartum flare occurs in three and a half to twenty-five percent of women within three months, occasionally with clinical hepatitis or decompensation, so the ALT and DNA are monitored for six months, and a mother with advanced fibrosis continues therapy. Her own pattern before pregnancy was immune-tolerant with a normal FibroScan, so she stops at six weeks.

20:12Two months after delivery her ALT rises to one hundred ten, and the flare settles without treatment by four months. A persistently high ALT with a high DNA would have meant reassessing her for immune-active disease, and a rising international normalized ratio, INR, or jaundice would have meant treating at once. Her son's surface antibody at nine months is protective.

20:34A lower viral load changes only part of the plan. A pregnant woman with chronic hepatitis B and a DNA of nine thousand doesn't need an antiviral for her baby's sake, but her baby still gets immune globulin and vaccine within twelve hours. Her own need for treatment is decided by her phase, as outside pregnancy, with tenofovir disoproxil if she's immune active. Acute hepatitis B early in pregnancy carries about a ten percent perinatal transmission rate, rising sharply near term, and the infant gets the same prophylaxis.

21:08The last patient shows a rising ALT that hepatitis B can't explain. A forty-eight-year-old man who moved from Romania twelve years ago has chronic hepatitis B, followed as an inactive carrier. Over six months his ALT has risen to one hundred sixty while his HBV DNA is only four hundred. His platelets have drifted to one hundred thirty thousand. He feels well, and his doctor wonders whether he's become immune active.

21:36A rising ALT with a low HBV DNA, in a man from Romania, suggests hepatitis D superinfection rather than immune-active hepatitis B. Hepatitis D is a defective, negative-stranded ribonucleic acid, RNA, virus that uses hepatitis B surface antigen as its envelope, so it exists only with hepatitis B. Immune-active hepatitis B would have raised his DNA above two thousand along with the ALT. An ALT flare with a low HBV DNA is the classic clue to hepatitis D, which drives injury using the surface antigen already circulating, without active hepatitis B replication.

22:07He meets two of the testing indications. Testing is done at a new hepatitis B diagnosis, with an ALT flare and a low DNA, in anyone from an endemic area, and with high-risk behaviors such as injection drug use, multiple partners, and human immunodeficiency virus, HIV, coinfection. The endemic regions are the Mediterranean basin, the Middle East, central and west Africa, the Amazon basin, central and eastern Europe, especially Romania, Mongolia, and parts of Asia. European guidance from twenty twenty-three recommends testing every patient positive for surface antigen at least once, while United States guidance is risk-based, plus testing whenever there's uncertainty.

22:49The tests come in order. Hepatitis D antibody comes first, and hepatitis D virus, HDV, RNA confirms active infection. Patients positive for antibody but negative for RNA aren't actively infected and don't need hepatitis D treatment, though their liver cancer risk is slightly raised. His antibody is positive and his RNA is detectable.

23:12How he acquired it matters, because coinfection and superinfection behave differently. In coinfection, hepatitis B and D are acquired together, with a biphasic course: a peak in aminotransferases from hepatitis B, then a second peak from hepatitis D days to weeks later, with a high risk of acute liver failure. The serology shows hepatitis D antibody IgM and HDV RNA with core IgM, and most survivors clear both viruses. In superinfection, hepatitis D infects a chronic carrier and looks like a flare, with hepatitis D markers and total core antibody but a negative core IgM. More than ninety percent become chronic, with faster progression to cirrhosis. The core IgM separates the two, and his is negative, so he has superinfection.

24:00Hepatitis D is the most aggressive chronic viral hepatitis, with more cirrhosis, earlier decompensation, and a higher liver cancer risk than hepatitis B alone. His falling platelets prompt fibrosis staging now. The twenty twenty-three guidance of the American Association for the Study of Liver Diseases, AASLD, lists hepatitis D positivity as an indication for liver cancer surveillance even without cirrhosis.

24:26His active infection needs treatment. The historic option for active infection, a detectable RNA with a raised ALT, is pegylated interferon alfa, one hundred eighty micrograms weekly for twelve months or longer. It gives sustained suppression in about twenty-five to thirty percent, relapse is common, and so many centers extend therapy, adding a hepatitis B antiviral when the HBV DNA is high.

24:53Bulevirtide has changed that. It's a synthetic lipopeptide that mimics the preS1 region of surface antigen and blocks NTCP, the sodium taurocholate cotransporting polypeptide that both viruses use to enter hepatocytes. It's given subcutaneously once daily, at eight point five milligrams on the United States label and two milligrams in most European trials. About half of patients on monotherapy have a fall in HDV RNA with a normal ALT, more when it's combined with peginterferon, and sustained response after stopping is uncommon, so treatment generally continues. It's long been available in the European Union, and it received Food and Drug Administration, FDA, accelerated approval in May twenty twenty-six for chronic hepatitis D without cirrhosis or with compensated cirrhosis, the first approved hepatitis D therapy in the United States.

25:48His elastography shows advanced fibrosis without cirrhosis, so he's eligible. A hepatitis B antiviral isn't needed for the hepatitis D, since his HBV DNA is low, but his advanced fibrosis is a hepatitis B treatment indication on its own. He starts bulevirtide with tenofovir alafenamide and begins liver cancer surveillance. Six months later his HDV RNA has fallen and his ALT is normal. Treating him for immune-active hepatitis B alone would have missed the virus driving his injury.

26:22Coinfection shows the other danger. A twenty-six-year-old woman who injects drugs develops acute hepatitis, with an ALT peak, partial improvement, and then two weeks later a second, larger peak with a rising INR. Her serology shows core IgM, hepatitis D antibody, and HDV RNA. That's coinfection with the classic biphasic course, and the second peak is the danger. Treatment of acute hepatitis D is supportive, so she's watched closely, with transfer ready if her INR keeps rising, as chapter nineteen describes. She recovers and clears both viruses.

26:59Here are the traps the boards set in these patients. Core antibody isn't a sign of vaccination. Surface antigen with total core antibody isn't acute infection. Immune-tolerant patients and inactive carriers aren't treated, and a patient isn't labeled inactive from one normal ALT or a DNA alone. The ALT limits are thirty-five in men and twenty-five in women. A negative e antigen doesn't mean low replication. E antigen seroconversion isn't cure. And an isolated core antibody needs an HBV DNA.

27:31The treatment traps follow. Compensated cirrhosis is treated without waiting for a DNA over two thousand, and decompensated cirrhosis is treated regardless of DNA. Peginterferon isn't used in cirrhosis. Entecavir after lamivudine is the one-milligram dose. Disoproxil is avoided with kidney or bone disease, and alafenamide isn't used in pregnancy. And treatment doesn't stop in cirrhosis.

27:56The reactivation traps come next. Testing before immunosuppression includes core antibody, not only surface antigen. Surface antibody doesn't protect a patient on rituximab. Reactivation is prevented, not rescued, prophylaxis starts before immunosuppression, and it doesn't stop when chemotherapy ends.

28:16The pregnancy traps are about the newborn and the mother. Every exposed newborn gets immune globulin and vaccine within twelve hours, whatever the mother's viral load. A DNA over two hundred thousand calls for tenofovir. Cesarean delivery isn't indicated, and breastfeeding is allowed. And tenofovir isn't stopped postpartum without six months of monitoring, or at all with advanced fibrosis.

28:39The hepatitis D traps close the list. A flare with a low HBV DNA isn't hepatitis B. A positive hepatitis D antibody isn't treated without checking the RNA. Coinfection and superinfection are separated by the core IgM. And hepatitis D needs cancer surveillance even without cirrhosis.

29:00So, start to finish. Surface antigen means infection, surface antibody alone means vaccination, and core antibody means natural exposure. Stage chronic infection by e antigen, DNA, and ALT, with ALT limits of thirty-five and twenty-five, and follow immune-tolerant and inactive patients every three to six months. Treat immune-active disease, significant fibrosis, any cirrhosis with detectable DNA, decompensated cirrhosis regardless of DNA, and high-risk contexts. Use entecavir, tenofovir disoproxil, or tenofovir alafenamide, never peginterferon in cirrhosis, and expect indefinite treatment.

29:42Test everyone for surface antigen and core antibody before immunosuppression. Give prophylaxis to patients positive for surface antigen on meaningful immunosuppression and to patients positive for core antibody on rituximab, obinutuzumab, or transplant, starting before and continuing for six months, or twelve to eighteen months after B-cell depletion.

30:04In pregnancy, every exposed newborn gets immune globulin and vaccine within twelve hours, mothers with a DNA over two hundred thousand get tenofovir disoproxil from twenty-eight to thirty-two weeks, and stopping it postpartum needs six months of monitoring.

30:20Hepatitis D needs hepatitis B. Suspect it with a flare and a low HBV DNA, confirm it with RNA, separate coinfection from superinfection by the core IgM, survey for cancer even without cirrhosis, and treat with bulevirtide or peginterferon long term.

30:37Episode three, the last of the chapter, is hepatitis C: universal screening, the test sequence, the regimens that cure almost everyone, and the special populations.

30:49For the full chapter, the practice vignettes, and the topic-tagged question bank, head to board pearls dot com. You'll find the rest of the series on Apple Podcasts, Spotify, or wherever you listen to podcasts. That brings us to the end of episode two of three of chapter eighteen, and I'll see you in the next one.