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Kembara Xtra - Medicine - Hepatitis B infections brought on by the hepatitis B virus (HBV), a member of the Hepadnaviridae family of DNA viruses. From acute hepatitis to chronic disorders like cirrhosis or hepatocellular carcinoma (HCC), HBV can cause a variety of liver diseases. Incidence 80% of instances affect people between the ages of 30 and 59, however it can affect individuals of any age. Males outnumber females (2:1) in fulminant HBV cases. White, non-Hispanic people had the greatest risk of acute HBV infection in the US, with 3,200 cases reported in 2019. Since 1991, the overall rate of new infections has decreased by almost 80% (as a result of a countrywide vaccination program). Since 2014, there has been a modest rise in new infections (linked to increased IV drug use). 72% of Americans have received their first dose of vaccination. 1.59 million people in the US have chronic HBV, ranging from 1.25 to 2.49 million. The largest populations at risk for HBV include those living in Asia, the Pacific Islands, and African-born individuals. The second most significant carcinogen (after cigarettes) is chronic HBV, which affects 350 to 400 million people globally and causes 1 million deaths yearly. Of chronic carriers with active illness, 25% pass away from cirrhosis or HCC complications. Seventy-five percent of chronic carriers are Asian. Pathophysiology and Etiology Hepadnaviridae family DNA virus HBV is extremely contagious through blood and secretions. Genetics history of HCC or HBV in the family Risk Factors: Screen for HBV using HBsAg/sAb in the following high-risk populations, and vaccinate if seronegative. - People born in endemic areas (45% of the world's population) - Dialysis for end-stage renal disease - Past or present IV drug users (IVDUs) - Men who have sex with men (MSM) - People who are HIV- and HCV-positive - People with chronic liver illness - Family members of HBsAg carriers - Sexual partners of HBsAg carriers - Prison inmates - People with persistently increased AST/ALT levels - Other risk factors: - Needle stick injuries/workplace exposure - Blood/product recipients; organ transplants - Inhaling drugs; getting body piercings or tattoos - Sexual assault victims Child Safety Considerations Less complications and a shorter acute course 90% of perinatal/vertical infections progress to chronic disease. pregnant women's issues Check for HBsAg in all patients who are pregnant. Obtain HBV DNA if HBsAG is positive. Consider administering oral nucleos(t)ides to patients with high viral loads at 28 weeks or a history of prior HBV (+) infants to minimize perinatal transmission. Hepatitis B immune globulin (HBIg) (0.5 mL) and the HBV vaccine must be administered to newborns of HBV-infected mothers within 12 hours of birth. If the HBIg and HBV vaccines are given and the areolar complex is free of fissures or open sores, breastfeeding is safe. During lactation, oral nucleoside medicines are not advised. HIV raises the possibility of vertical transmission. To avoid an acute flare, keep taking your meds if you become pregnant while receiving oral antiviral therapy. Prevention All infants should have three IM vaccinations at birth and twice more at the age of one and six months for healthy people or infants. - All patients who are at risk (see "Risk Factors") - Personnel in public safety and health Proper sanitation and hygiene practices by medical professionals, IVDUs, and tattoo/piercing artists - Barrier precautions, needle disposal, sanitize equipment, and cover open cuts in HBsAg carriers' homes - Sexual encounters with HBsAg carriers Avoid sharing personal goods with blood exposure, such as toothbrushes, razors, and nail clippers. Use of condoms is a safe sexual practice. Blood and tissue cannot be donated by HBsAg carriers. Postexposure (such as a needle stick): - HBIg 0.06 mL/kg in less than 24 hours in addition to vaccination (within no more than 7 days of exposure) - A second HBIg dose needs to be given 30 days following exposure. HIV and hepatitis C coinfection is associated with extrahepatic symptoms such serum sickness-like syndrome (fever, erythematous skin rash, myalgias, arthralgias, and exhaustion). Glomerulonephritis (IgA-mediated nephropathy, membranous or membranoproliferative glomerulonephritis) - Polyarteritis nodosa, which causes a primary systemic necrotizing vasculitis and is characterized by a high fever, weakness, malaise, and hunger and weight loss. - Dermatologic diseases (such as lichen planus, bullous pemphigoid, and Gianotti-Crosti syndrome) - Cryoglobulinemia (Arthritis, Sicca Syndrome, Raynaud's phenomenon) - Neurologic or psychological disorder (e.g., depression, psychosis, impaired mental status, Guillain-Barré syndrome) Exposure: thorough family history, including HBV infection and liver illness, as well as social history, which includes alcohol and drug use as well as sexual history Acute HBV - Fever, malaise, lethargy, arthralgias, and myalgias - Jaundice, scleral icterus; dark urine; pale stools; anorexia; nausea; and vomiting - Abdominal pain in the right upper quadrant (RUQ) - Chronic HBV: usually asymptomatic clinical assessment Anorexia, jaundice/scleral icterus, RUQ tenderness, hepatomegaly are examples of acute diseases. Differential diagnosis: drug-induced, alcoholic, or autoimmune hepatitis; Epstein-Barr virus (EBV); cytomegalovirus (CMV); hepatitis A, C, or E Hemochromatosis and Wilson disease Initial test results from the laboratory and imaging AST/ALT: Acute HBV is markedly raised, and ALT is often greater than AST. - Chronic HBV may have normal or modestly increased transaminases: Transaminases increase prior to bilirubin. Bilirubin (conjugated/unconjugated): acute HBV: normal to noticeably raised - Final test to return to normal when acute infection subsides Alkaline phosphatase: slight increase The sole early discovery (the "window period," before HBsAg turns positive) might be HBcAb IgM. - PT/INR, albumin, electrolytes, glucose, and CBC for acute hepatitis - If acute HBV is severe, look for hepatitis D superinfection (HDV Ag and HDV Ab). - Serologic markers for hepatitis B strong HBV DNA levels (105 copies/mL) and the hepatitis B e-antigen (HBeAg+) suggest strong replication and infectivity; these conditions are treatable with medication. Check for the presence of HDV, HIV, HCV, and hepatitis A virus immunity (HAV Ab total/IgG). - An acute HBV infection alone is usually not as severe as an acute HBV + HDV coinfection. The use of ultrasound to detect hepatic or portal blockage, ascites, organomegaly, symptoms of portal hypertension, and to screen for HCC. Tests in the Future & Special Considerations Chronic HBV is defined as having an HBsAg+ persistence of >6 months. - Check ALT and HBV DNA levels every 3-6 months. Consider a liver biopsy if you are older than 40 and your ALT level is borderline or slightly raised. - Calculate AFP at baseline. Follow HBeAg for elimination every 6 to 12 months. - Continuous monitoring of progress HCC screening (number 5): - HCC surveillance is advised for all patients with viral loads greater than 100,000 copies per milliliter. - Screening for HCC can be done every six months using abdominal ultrasonography alone; adding AFP enhances the sensitivity for early identification. Other/Diagnostic Procedures Liver biopsy Elastography (FibroScan) or non-invasive procedures (Hepascore, FibroTest) to evaluate fibrosis Interpretation of Tests In patients with chronic HBV, liver biopsy results may reveal necrosis, cholestasis, fibrosis, cirrhosis, or chronic active hepatitis. Management If seronegative, get a HAV vaccination. Be sure to keep an eye on your CBC, coagulation, electrolytes, glucose, renal function, and phosphate levels. Track ALT and HBV DNA levels; rising ALT and falling DNA indicate a positive response to treatment. If HBsAg+, check for HCC. First Line of Medicine Supportive care for acute HBV; spontaneous resolution occurs in 95% of immunocompetent individuals; antiviral therapy is not recommended unless a patient has fulminant liver failure or is immunosuppressed. – Those with acute liver failure and individuals with severe or extended conditions should be treated. Tenofovir or entecavir monotherapy are available as treatments. Treatment for chronic HBV depends on the presence of HBeAg - Medication that is FDA-approved: pegylated interferon (peg-IFN) 2a, 2b SC weekly; lamivudine 100 mg, adefovir 10 mg, entecavir 0.5 to 1.0 mg, telbivudine 600 mg, or tenofovir alafenamide 25 mg. Extended oral regimens should be used: - If HBeAg+, start treatment 6 to 12 months after HBeAg disappears and HBeAb increases. - If HBeAg, treat for as long as necessary or until HBsAg is cleared and HBsAb is developed. Modify/add a medicine in response to resistance: - Verify medication compliance before presuming drug resistance. Modify the dosage based on renal function. Peg-IFN is recommended over conventional interferon: Goals of treatment include undetectable HBV DNA, normal ALT, loss of HBeAg and gain of HBeAb as well as loss of HBsAg and gain of HBsAb. - Weekly peg-IFN (Pegasys) injections for 48 weeks. Safety measures: - Peg-IFN: coagulopathy, myelosuppression, depression/suicidal ideation - Oral medications: renal insufficiency Next Line It is advised to transition to tenofovir in patients who have antiviral resistance that has been verified or suspected, which is defined as a history of past exposure or primary nonresponse to lamivudine, entecavir, adefovir, or telbivudine. Referral All HBsAg+ persistent patients should be referred. Immediate referral for a liver transplant if the patient has HCC, end-stage liver disease, or fulminant acute hepatitis Chronic Hepatitis B Therapy HBeAg HBV DNA Viral Load ALT* Recommend + ≥20,000 IU/mL Elevated Treat with antiviral or interferon. − ≥2,000 IU/mL Elevated Consider biopsy or serum fibrosis marker and treatment. + ≤20,000 IU/mL Any Monitor q6–12mo. − ≥2,000 IU/mL Normal Biopsy; treat if disease. + ≥20,000 IU/mL Normal Observe, consider treatment if ALT elevated. Biopsy if age >40 y or ALT is high normal to mild elevation. − ≤2,000 IU/mL Any Monitor q6–12mo. Cirrhosis Any Any Treat with mono or combination treatment. Liver failure Any Any Treat and refer for transplant. *ALT elevated if >2 × ULN; ULN for male = 30 IU/mL and for female = 19 IU/mL Surgical Techniques surgical resection, radiofrequency ablation, and liver transplantation for HCC Admission Hepatic failure (high PT, encephalopathy), worsening course (marked increase in bilirubin, transaminases, or symptoms) Patient Follow-Up Monitoring Serial ALT analysis and HBV DNA: CBC for WBC and platelets if on interferon therapy - High ALT + low HBV DNA correlated with positive response to therapy - Monitor HBV DNA q3-6mo during therapy - Watch for consequences (ascites, encephalopathy, variceal bleed) in cirrhosis if undetectable DNA at week 24 of oral drug therapy is associated with low resistance at year 2. vaccinate intimate partners and members of the household. Starting at age 40 for males and 50 for women, ultrasound is used to screen for HCC every 6–12 months (5). DIET Alcohol raises the risk of developing HCC or cirrhosis. Education of Patients Review transmission safety measures for acute HBV. Chronic HBV, alcoholism, and cigarette use speed up development. - To avoid flares, place an emphasis on medication compliance. Inform chronic HBV carriers about the dangers of spreading the disease. Immunizations, particularly those for hepatitis A Chronic hepatitis B prognosis: In those with untreated chronic HBV, the cumulative 5-year incidence of developing cirrhosis is between 8 and 20 percent once HBV is detected. 2-5% of individuals with persistent HBV will develop HCC, whether or not they have cirrhosis. Complications Cirrhosis, hepatic necrosis, and liver failure Reactivation of infection if immunosuppressed HCC (all chronic HBV patients are at risk) Severe flare of chronic HBV with corticosteroids and other immunosuppressants. If receiving systemic chemotherapy and testing positive for HBsAg or HBcAb, use preventative medication.
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