We can eliminate and protect ourselves against hepatitis B with the help of excellent vaccines available in market. Three injections at regular intervals of time i.e., at 0, 1 and 6 months gives around 90-95% protection against hepatitis. For an effective management apart from vaccination, patients should be checked if they are protected after the vaccination. Hence, it is wise to check one antibody-titer (anti-HBs) after vaccination; a level of more than 10 reflects adequate protection against hepatitis B.
For hepatitis C, unfortunately, there isn’t any vaccine. As both hepatitis B and C are transmitted through blood borne infections, general precautions need to be taken. IV drug abusers are usually prone to hepatitis C. It is important to educate the masses about the dangers of sharing needles or razors with infected individuals.
Another important route of transmission of hepatitis B, and to a lesser extent hepatitis C, is from mother to child. Hence, it is necessary to thoroughly examine expectant mothers during pregnancy. HBV DNA levels should be checked for in the third trimester, and if they are very high (above 108), the expectant mother should undergo treatment. In case the mother is not treated during pregnancy, the newborn baby should be vaccinated within 12 hours of birth, administering both active (vaccine) and passive (immunoglobulin) immunization.
Hepatitis B is a viral infection caused from a small, circular, double stranded DNA virus which predominantly infects the liver in the human body. The most common modes of infection are blood borne or sexual.. Vaginal and seminal secretions contain a large amount of the hepatitis B virus. The most important mode of transmission is the vertical transmission, where the baby gets it from the mother.
Hepatitis B affects the liver, and can either be acute or chronic in nature. Acute infections are self-limiting, i.e., ≥ the disease is healed on its own in 95% of patients due to their strong immune system. Chronic infections have two forms - Chronic active hepatitis and Carrier state hepatitis, which can last for life. In some patients, it can even progress to decompensated liver disease, i.e., cirrhosis, with the end stage being hepatocellular carcinoma. Therefore, it has got a varied presentation, it can be acute/chronic, from where it can advance to form cirrhosis and liver cancer.
Hence, precautionary measures should be adhered to avoid hepatitis B. As a universal health protocol, vaccination of hepatitis B should be administered to every newborn in India. Along with vaccinations, safe sexual practices, avoiding promiscuity and not having multiple sexual partners, avoiding sharing of injections or razors can also help in preventing Hepatitis B infection.
Before investigations, we need to know from the person if there is any history of fever, anorexia, vomiting, joint pain, or any exposure to toxins like alcohol, or drugs like hormonal preparations/alternative medicines and also if there is any family history of liver disease. These questions will also help us identify if the condition is acute or chronic. Lab investigation plays an important role in diagnosing hepatitis. For instance, hepatitis A and E are most common causes of acute hepatitis and can be diagnosed with blood investigations. Similarly, Hepatitis B and C can also be diagnosed with blood investigations. Alcoholic hepatitis is indicated by the history of alcohol intake over a long period of time. Once these common causes are ruled out, we move to rare causes like autoimmune hepatitis, which also need blood investigations.
It appears that the patient is in a chronic inactive carrier state. Chronic hepatitis B can be active or inactive. Treatment should be initiated based on HBV DNA levels results as per the guidelines. If the HBV DNA levels are very high, E antigen +ve is more than 20,000 or E antigen -ve is more 2000, and SGPT is more than 1.5 times the normal level, the patient doesn’t require immediate treatment. As per the protocol, the patient has to undergo a few tests every 6 months, like checking the DNA levels, the LFT and ultrasound of upper abdomen just to look at the liver. We also check alpha fetoprotein. Hepatitis B is a carcinogenic virus which can sometimes lead to tumor in the liver without causing cirrhosis.
The family members (wife, children, parents, etc.) of the infected patients should also be checked for Hepatitis B virus. If the close family members are not found to be hepatitis B positive, then they should be vaccinated.
Liver diseases can be categorized into acute infection and chronic infection. Most of the acute infections, in the sub-continents, are hepatitis A and E. Hepatitis A and E are not blood borne infections, but are caused due to fecal-oral route through contaminated water and food. So, safe hygienic practices need to be advocated to avoid this.
For hepatitis B, vaccination is the only precaution.
For hepatitis C, unfortunately, we don’t have any vaccine available.
For alcohol liver diseases causing liver cirrhosis, alcohol is a substance abuse which has the potential to cause permanent liver damage. Avoid drinking alcohol up to a carcinogenic dose. In India, the carcinogenic cut-off level is about 40-80gms/day of alcohol for men and 20-40gms/day for women. In the absence of history of any liver disease, this should not be a potential danger. There are inherited liver diseases where are acquired through genes. One could be hemochromatosis, where the pregnant mother can undergo genetic screening. Lastly, the most common are drug induced liver injuries causing permanent hepatic failure. A proper treatment is needed for control and cure of the disease.
Yes, definitely. In 2016, we have got drugs called as directly acting antiviral agents. These are expensive in western countries but in India, we get them at a reduced cost. These drugs have got the potential to cure and eradicate hepatitis C from the body. Hence, hepatitis C is curable. Cirrhosis is an irreversible process in which the liver undergoes permanent damage. So, cirrhosis is not curable but in such patients, liver transplantation can be done.
The viral load is high but the patient’s E-antigen status is unknown. The treatment depends on E-antigen status, but if the viral load is very high then the patient requires treatment. There is slight variance in the drugs we choose if it is E-antigen positive. There are 2 oral drugs available, Tenofovir and Entecavir; either of them can be prescribed. There is no definite guideline for drug selection. Prescription can depend on the side effect profile, e.g., Tenofovir is slightly renal toxic. However, Entecavir is costlier than Tenofovir.
We should also know the patient’s LFT and also the stage of hepatitis B, if it is acute or chronic. If it is acute, even with viral load of 4 lakh we won’t treat. If it is chronic, we have to treat. To know if it is acute or chronic, the patient must undergo the IgM anti core antibody (IgM anti-HBc) test. If that antibody is positive, it is acute hepatitis B or it could be the immune response of the body where the DNA is so high that the condition cannot be treated; the patient has to be monitored and the investigations have to be repeated. But, if chronic, it needs to be treated.
Chronic hepatitis B is incurable, so HBs-Ag in most of the cases remain positive. The aim of treatment in chronic hepatitis B is to reduce the HBV DNA level and detectable level. If a patient is E-antigen positive before the treatment starts and his HBV DNA is undetectable and anti HBe antibody is positive and HBe antigen is negative, then we can try to stop the medicine. But in most cases it is not possible. You need to continue antiviral therapy for at least 3-4yrs. There is one guideline which suggests that when the DNA level is undetectable, we can stop medicine after one year of undetectable DNA, but there is risk of relapse in one third of patients.
Diagnosis is by serology, where you have anti HCV antibody positivity. There are 1-6 genotypes in hepatitis C, but in sub continents including Bangladesh and Pakistan, genotype 1 and 3 are more common; 2 and 4 are common in the western world. We need to know the genotype first and then the HCV RNA viral load, which is quantitative assessment of the viral load. After we know the genotype and viral load, we can treat them. Depending on the genotype and viral load, we have directly acting antivirals. Sofosbuvir has revolutionized the treatment of hepatitis C throughout the world. We also have other drugs like ledipasvir and daclatasvir. We treat them for 12 weeks, and the duration can increase up to 24 weeks if not compensated. At the end of four weeks, we do an EVR to assess the viral load and then reassess the viral load at the end of 12 weeks. If required, we continue the treatment for 24 weeks.
Before directly acting antivirals were available, we had interferon and we used to add ribavirin. These used to suppress the immune system. The adverse effects are less with the new agents, including cirrhotic, who take these drugs well and have a very good cure rate.
The patient has transaminases where the SGOT and SGPT levels are high. There are a lot of other causes than hepatitis B and C which can increase these levels. Increase in these levels means that hepatocytes are getting destroyed in the liver. These enzymes remain inside hepatocytes and when they are destroyed, the enzymes are released into the blood. The most common etiology other than viral etiology (as viral is negative) is the fatty liver disease. Almost 30-40% of the population has non-alcoholic fatty liver disease. If the patient drinks alcohol, SGOT and SGPT increase. If the patient is non-alcoholic, the cause can be non-alcoholic fatty liver disease, which is usually associated with metabolic syndrome. If features of non-alcoholic fatty liver disease are absent, other investigations are done. If the patient is young, we should check the copper levels to check for Wilson’s disease. To diagnose Wilson’s disease, we perform the Serum Ceruloplasmin Test and 24hrs urinary copper level test. Another rare cause is hemochromatosis. Most common causes are viral etiology, Wilson’s disease, non-alcoholic fatty liver disease, alcoholic liver disease and drug induced diseases. If the person is taking alternative medicines or drugs to build his body (most contain anabolic steroids) or anti tubercular drugs, the history must be noted.
The most common cause is developmental anomaly of biliary tract. Choledochal cysts, and long standing biliary obstruction can cause cirrhosis. Other than developmental anomaly, metabolic liver diseases like glycogen storage disorders, Autoimmune hepatitis type 2, Wilson’s disease, Mitochondrial Hepatopathies, Hepatopulmonary Syndrome and familial progressive intrahepatic cholestasis are a few rare causes. If the child is known to have any liver disease, the most important symptom would be failure to thrive. More importance should be given to nutrition because during childhood and adolescence where development and growth takes place, nutritional abnormalities should be given more importance. Liver transplantation can give a good life to such children.
Hepatitis B is blood borne infection and it can spread through percutaneous, ocular and mucous membrane exposure to contaminated body fluids. These fluids include contaminated blood, blood products like plasma, semen, saliva, etc. Hepatitis B is 100 times more infectious than HIV and 10 times more infectious than HCV. The causes can be perinatal transmission of HBV from mother to child, unprotected sexual intercourse, sex with same gender; healthcare workers exposed to infected body fluids and hemodialysis patients are in the high risk group.
Hepatitis virus can survive for at least seven days outside the body.
Nowadays obesity is epidemic. Non-alcoholic fatty liver disease is a metabolic problem. It is associated with hypertension, diabetes, hyperuricemia and obesity. Check other risk factors like obesity or dyslipidemia (treat cholesterol). Studies show that atorvastatin can be given to such patients to decrease LDL and total cholesterol level. Increased triglyceride, which is common in such patients, can be treated with Fenofibrate group of drugs. For the treatment of fatty liver, the most important strategy is physical exercise and weight loss. Even 5-10% of weight loss has shown histological improvement in liver. If SGOT and SGPT levels are high, drugs are prescribed. For a diabetic patient with high SGPT level, the drug of choice is pioglitazone. For non-diabetics, we give antioxidants like vitamin E which is a very powerful antioxidant. No matter the cause, the end point of liver injury is free radical mediated injury to liver. The SGPT and SGOT levels improve with vitamin E, in practice, but whether it causes histological improvement in liver is not proven, and can only be achieved through physical exercise and weight loss. New drugs in the pipeline line like Obeticholic acid, which is in phase 2 or 3 of trial, is very promising and much awaited. Non-alcoholic fatty liver disease is now the most common cause of cirrhosis and a few such patients also develop hepatocellular carcinoma.