Hepatitis is an inflammation of the liver tissue. Some people have no symptoms while others develop yellow discoloration of the skin and white of the eyes, poor appetite, vomiting, fatigue, stomachache, or diarrhea. Hepatitis can be temporary (acute) or long-term (chronic) depending on whether it lasts for less than or more than six months. Acute hepatitis can sometimes heal itself, develop into chronic hepatitis, or rarely cause acute liver failure. Over time, chronic forms can develop into scarring of the liver, liver failure, or liver cancer.
The most common cause worldwide is virus. Other causes include heavy alcohol use, certain drugs, toxins, other infections, autoimmune diseases, and non-alcoholic steatohepatitis (NASH). There are five main types of viral hepatitis: type A, B, C, D, and E. Hepatitis A and E are mainly spread by contaminated food and water. Hepatitis B is mainly sexually transmitted, but can also be transmitted from mother to baby during pregnancy or childbirth. Both hepatitis B and hepatitis C are commonly spread through infected blood as may occur during the sharing of needles by injecting drug users. Hepatitis D can only infect people who are already infected with hepatitis B.
Hepatitis A, B, and D can be prevented by immunization. Drugs can be used to treat chronic viral hepatitis cases. No special treatment for NASH; However, a healthy lifestyle, including physical activity, a healthy diet, and weight loss, is important. Autoimmune hepatitis can be treated with drugs to suppress the immune system. Liver transplantation can also be an option in certain cases.
Around the world by 2015, hepatitis A occurs in about 114 million people, chronic hepatitis B affects about 343 million people and chronic hepatitis C is about 142 million people. In the United States, NASH affects about 11 million people and alcohol hepatitis affects about 5 million people. Hepatitis produces more than one million deaths per year, mostly indirectly from scarring of liver or liver cancer. In the United States, hepatitis A is estimated to occur in about 2,500 people per year and result in about 75 deaths. This word is derived from the Greek hÃÆ'ªpar ( ???? ), meaning "heart", and -itis ( - ???? ), which means "inflammation".
Video Hepatitis
Signs and symptoms
Hepatitis has a wide spectrum of presentation that ranges from lack of symptoms to severe liver failure. The acute form of hepatitis, commonly caused by viral infections, is characterized by constitutional symptoms that are usually self-limiting. Chronic hepatitis arises in the same way, but may reveal specific signs and symptoms for liver dysfunction with long-lasting inflammation and organ damage.
Acute hepatitis
Acute viral hepatitis follows three distinct phases:
- The initial prodromal phase (previous symptoms) involves non-specific and flu-like symptoms that are common in many acute viral infections. These include fatigue, nausea, vomiting, poor appetite, joint pain, and headaches. Fever, currently, is most common in cases of hepatitis A and E. Late in this phase, people may experience liver-specific symptoms, including coluria (dark urine) and purple stools.
- Yellowing of the skin and whites of eyes follows prodrome after about 1-2 weeks and can last up to 4 weeks. The non-specific symptoms seen on prodromal are usually lost at this time, but people will develop an enlarged heart and upper right abdominal pain or discomfort. 10-20% of people will also experience an enlarged spleen, while some people will also experience light weight that is not accidental.
- The recovery phase is characterized by resolution of clinical symptoms of hepatitis with persistent elevations in hepatic and potentially enlarged liver labor values. All cases of hepatitis A and E are expected to heal completely after 1-2 months. Most cases of hepatitis B also heal itself and will recover within 3-4 months. Some cases of hepatitis C will heal completely.
Both drug-induced hepatitis and autoimmune hepatitis may present very similar to acute viral hepatitis, with slight variation in symptoms depending on the cause. Drug-induced hepatitis cases can manifest by systemic signs of an allergic reaction including rash, fever, serositis (inflammation of the lining of the lining of a particular organ), increased eosinophils (a type of white blood cell), and suppression of bone marrow activity.
Fulminant hepatitis
Fulminant hepatitis, or very large liver cell death, is a rare and life-threatening acute hepatitis complication that can occur in cases of hepatitis B, D, and E, in addition to drug-induced and autoimmune hepatitis. This complication is more common in cases of hepatitis B and D co-infection at 2-20% and in pregnant women with hepatitis E at 15-20% of cases. In addition to signs of acute hepatitis, people may also show signs of coagulopathy (abnormal coagulation studies with easy bruising and bleeding) and encephalopathy (confusion, disorientation, and drowsiness). Mortality due to fulminant hepatitis is usually the result of various complications including cerebral edema, gastrointestinal bleeding, sepsis, respiratory failure, or renal failure.
Chronic hepatitis
Acute cases of hepatitis appear to be resolved well within six months. When hepatitis is continued for more than six months, this is called chronic hepatitis. Chronic hepatitis is often asymptomatic early in its course and is only detected by liver laboratory studies for screening purposes or for evaluating non-specific symptoms. As inflammation develops, patients may develop constitutional symptoms similar to acute hepatitis, including fatigue, nausea, vomiting, poor appetite, and joint pain. Jaundice can also occur, but much later in the disease process and is usually a sign of advanced disease. Chronic hepatitis interferes with hormonal functions of the liver that can cause acne, hirsutism (abnormal hair growth), and amenorrhea (lack of menstrual periods) in women. The extensive damage and scarring of the liver over time defines cirrhosis, a condition in which the ability of the liver to function is permanently inhibited. This causes jaundice, weight loss, coagulopathy, ascites (abdominal fluid removal), and peripheral edema (leg swelling). Cirrhosis can lead to other life-threatening complications such as hepatic encephalopathy, esophageal varices, hepatorenal syndrome, and liver cancer.
Maps Hepatitis
Cause
The causes of hepatitis can be divided into the following major categories: infection, metabolic, ischemic, autoimmune, genetic, and others. Transmission agents include viruses, bacteria, and parasites. Toxins, drugs, alcohol, and non-alcoholic fatty liver diseases are the metabolic causes of liver injury and inflammation. The causes of autoimmune and genetic hepatitis involve genetic predisposition and tend to affect population characteristics.
Contagious
Viral hepatitis
Viral hepatitis is the most common type of hepatitis worldwide. Viral hepatitis is caused by five different viruses (hepatitis A, B, C, D, and E). Hepatitis A and hepatitis E behave similarly: both are transmitted by the fecal-oral route, more common in developing countries, and are self-limiting diseases that do not lead to chronic hepatitis.
Hepatitis B, hepatitis C and hepatitis D are transmitted when blood or mucous membranes are exposed to infected blood and body fluids, such as semen and vaginal discharge. Viral particles have also been found in saliva and breast milk. However, kissing, sharing equipment, and breastfeeding does not cause transmission unless this fluid is inserted into an open wound or wound.
Hepatitis B and C may appear acutely or chronically. Hepatitis D is a flawed virus that requires hepatitis B to replicate and is only found with hepatitis B coinfection. In adults, hepatitis B infection is the most commonly self-limited, with less than 5% developing into a chronic condition, and 20 to 30% of those who are chronically infected with cirrhosis or liver cancer. However, infections in infants and children often cause chronic infections.
Unlike hepatitis B, most cases of hepatitis C cause chronic infection. Hepatitis C is the second most common cause of cirrhosis in the US (second for alcoholic hepatitis). In the 1970s and 1980s, blood transfusion was a major factor in the spread of hepatitis C virus. Since extensive screening of blood products for hepatitis C began in 1992, the risk of acquiring hepatitis C from blood transfusion has decreased from about 10% in 1970 to 1 out of 2 million today.
Parasitic hepatitis
The parasite can also infect the liver and activate the immune response, producing acute hepatitis symptoms with elevated serum IgE (although chronic hepatitis may occur with chronic infection). From protozoa, Trypanosoma cruzi, Leishmania species, and Plasmodium species causing malaria all can cause inflammation of the liver. Another protozoa, Entamoeba histolytica, causes hepatitis with different liver abscesses.
From the worms, the Echinococcus granulosus cestode, also known as dog tapeworm, infects the liver and forms the characteristics of a liver hydatid cyst. Heart beat Fasciola hepatica and Clonorchis sinensis live in the bile ducts and cause progressive hepatitis and liver fibrosis.
Hepatitis Bacteria
Bacterial infections of the liver usually result in pyogenic liver abscess, acute hepatitis, or granulomatous (or chronic) liver disease. Pituogenic abscesses generally involve enteric bacteria such as Escherichia coli and Klebsiella pneumoniae and consist of several bacteria up to 50% of the time. Acute hepatitis is caused by Neisseria meningitidis , Neisseria gonorrhoeae , Bartonella henselae , Borrelia burgdorferi , salmonella species, brucella species and campylobacter species. Chronic or granulomatous hepatitis is seen with infections from mycobacteria species, Tropheryma whipplei, Treponema pallidum, Coxiella burneti and rickettsia species.
Metabolic
Alcoholic hepatitis
Excessive alcohol consumption is a significant cause of hepatitis and is the most common cause of cirrhosis in the US. Alcoholic hepatitis is in the spectrum of alcoholic liver disease. It revolves around the order of severity and reversibility of alcoholic steatosis (most severe, most reversible), alcoholic hepatitis, cirrhosis, and liver cancer (most severe, least reversible). Hepatitis typically develops over many years of exposure to alcohol, occurring in 10 to 20% alcoholics. The most important risk factors for the development of alcoholic hepatitis are the quantity and duration of alcohol intake. Long-term alcohol intake of more than 80 grams of alcohol a day in men and 40 grams a day in women is associated with the development of alcohol hepatitis (1 beer or 4 ounces of wine equivalent to 12g of alcohol). Alcoholic hepatitis may vary from asymptomatic hepatomegaly (enlarged liver) to acute or chronic hepatitis symptoms to liver failure.
Drug-induced and drug-induced hepatitis
Many chemicals, including drugs, industrial toxins, and herbal and dietary supplements, can cause hepatitis. The spectrum of drug-induced liver damage varies from acute hepatitis to chronic hepatitis to acute liver failure. Toxins and drugs can cause liver damage through various mechanisms, including direct cell damage, cell metabolic disorders, and causing structural changes. Some drugs such as paracetamol show liver damage dependent predictable doses while others such as isoniazid cause idiosyncratic and unpredictable reactions that vary among individuals. There are many variations in the mechanism of liver damage and latency periods of exposure to clinical disease progression.
Many types of drugs can cause liver damage, including analgesic paracetamol; antibiotics such as isoniazid, nitrofurantoin, amoxicillin-clavulanate, erythromycin, and trimethoprim-sulfamethoxazole; anticonvulsants such as valproate and phenytoin; cholesterol-lowering statins; steroids such as oral contraceptives and anabolic steroids; and highly active anti retroviral therapy used in the treatment of HIV/AIDS. Of these, amoxicillin-clavulanate is the most common cause of drug induced liver damage, and paracetamol toxicity is the most common cause of acute liver failure in the United States and Europe.
Herbal remedies and dietary supplements are another important cause of hepatitis; this is the most common cause of drug-induced hepatitis in Korea. The United States-US Reduced Infectious Disease Chain connects over 16% of cases of hepatotoxicity to herbal and dietary supplements. In the United States, herbal and dietary supplements - unlike pharmaceutical drugs - are not regulated by the Food and Drug Administration. However, the National Institutes of Health maintains a LiverTox database for consumers to track all prescribed and non-prescribed compounds that are associated with liver injury.
Exposure to other hepatotoxins may occur accidentally or intentionally through ingestion, inhalation, and skin resorption. Carbon Toxin Industries Tetrachloride and Wild Mushrooms Amanita phalloides is another known hepatotoxin.
Non-alcoholic fatty liver
Non-alcoholic hepatitis resides in the spectrum of non-alcoholic liver disease (NALD), which ranges in severity and reversibility of non-alcoholic fatty liver disease (NAFLD) to non-alcoholic steatohepatitis (NASH) to cirrhosis to liver cancer, similar to the disease spectrum alcoholic heart.
Non-alcohol liver disease occurs in people with little or no history of alcohol use, and is strongly associated with metabolic syndrome, obesity, insulin resistance and diabetes, and hypertriglyceridemia. Over time, nonalcoholic fatty liver disease can progress to non-alcoholic steatohepatitis, which also involves the death of liver cells, liver inflammation and possible fibrosis. The accelerated development factors of NAFLD to NASH are obesity, older age, non-African American ethnicity, female gender, diabetes mellitus, hypertension, higher ALT or AST levels, higher AST/ALT ratios, platelet count low, and ultrasound steatosis score.
In the early stages (such as NAFLD and early NASH), most patients had no symptoms or mild upper right quadrant pain, and the diagnosis was suspected based on abnormal liver function tests. As the disease progresses, typical symptoms of chronic hepatitis can develop. While imaging may show fatty liver, only liver biopsy can show inflammation and fibrosis characteristics of NASH. 9 to 25% of patients with NASH develop cirrhosis. NASH is recognized as the third most common cause of liver disease in the United States.
Autoimmune
Autoimmune hepatitis is a chronic disease caused by an abnormal immune response to liver cells. The disease is thought to have a genetic predisposition because it is associated with certain human leukocyte antigens involved in the immune response. As with other autoimmune diseases, circulating auto-antibodies can be present and assist in diagnosis. Auto-antibodies found in patients with autoimmune hepatitis include sensitive but less specific antibody (ANA) antibodies, smooth muscle antibodies (SMA), and atypical perinuclear antineutrophil cytoplasmic antibodies (p-ANCA). Other less common but more specific autoantibodies for autoimmune hepatitis are antibodies to liver kidney microsome 1 (LKM1) and dissolved liver antigen (SLA). Autoimmune hepatitis can also be triggered by drugs (such as nitrofurantoin, hydralazine, and methyldopa), after liver transplantation, or by viruses (such as hepatitis A, Epstein-Barr virus, or measles).
Autoimmune hepatitis can be present anywhere in the spectrum from asymptomatic to acute or chronic hepatitis for fulminant liver failure. Asymptomatic patients are 25-34% of the time, and diagnosis is suspected based on abnormal liver function tests. Up to 40% of cases present with signs and symptoms of acute hepatitis. Like other autoimmune diseases, autoimmune hepatitis usually affects young women (although it can affect patients with any gender), and patients can show classic signs and symptoms of autoimmunity such as fatigue, anemia, anorexia, amenorrhea, acne, arthritis, pleuritis, thyroiditis , ulcerative colitis, nephritis, and maculopapular rash. Autoimmune hepatitis increases the risk of cirrhosis, and the risk for liver cancer increases by about 1% for every year of disease.
Many people with autoimmune hepatitis have other autoimmune diseases. Autoimmune hepatitis is different from other autoimmune diseases of the liver: primary biliary cirrhosis and primary sclerosing cholangitis. However, all of these diseases can cause scarring, fibrosis, and liver cirrhosis.
Genetic
The genetic causes of hepatitis include alpha-1-antitrypsin deficiency, hemochromatosis, and Wilson's disease. In alpha-1-antitrypsin deficiency, a co-dominant mutation in the gene for alpha-1-antitrypsin results in the abnormal accumulation of proteins in the liver cells, leading to liver disease. Haemochromatosis and Wilson's disease are autosomal recessive diseases involving abnormal mineral storage. In hemochromatosis, the amount of excess iron accumulates in some body sites, including the liver, which can cause cirrhosis. In Wilson's disease, excess amounts of copper accumulate in the liver and brain, causing cirrhosis and dementia.
When the liver is involved, alpha-1-antitrypsin deficiency and Wilson's disease tend to appear as hepatitis in the neonatal period or in childhood. Hemochromatosis usually occurs in adulthood, with the onset of clinical disease usually after the age of 50 years.
Ischemic hepatitis
Ischemic hepatitis (also known as liver shock) results from reduced blood flow to the liver, such as in shock, heart failure, or vascular insufficiency. This condition is most commonly associated with heart failure but can also be caused by shock or sepsis. Blood tests in a person with ischemic hepatitis will show very high levels of transaminase enzyme (AST and ALT). This condition is usually lost if the underlying cause is successfully treated. Ischemic hepatitis rarely causes permanent liver damage.
More
Hepatitis can also occur in neonates and is caused by various causes, some of which are not seen in adults. Congenital or perinatal infections with viral hepatitis, toxoplasma, rubella, cytomegalovirus, and syphilis can cause neonatal hepatitis. Structural abnormalities such as biliary atresia and choledochal cysts can cause cholestatic liver damage that causes neonatal hepatitis. Metabolic diseases such as glycogen storage disorders and impaired lysosomal storage are also involved. Neonatal hepatitis may be idiopathic, and in such cases, biopsy often shows large multinucleated cells in the liver tissue. This disease is called giant cell hepatitis and may be associated with viral infections, autoimmune disorders, and drug toxicity.
Mechanism
Specific mechanisms vary and depend on the cause of hepatitis. Generally, there is an initial insult that causes liver damage and activation of an inflammatory response, which can become chronic, leading to progressive fibrosis and cirrhosis.
Viral hepatitis
The pathway in which the liver virus causes viral hepatitis is best understood in the case of hepatitis B and C. The virus does not directly cause apoptosis (cell death). In contrast, infection of the liver cells activates the innate and adaptive immune system arms leading to an inflammatory response that causes cellular damage and death. Depending on the strength of the immune response, the type of immune cells involved and the ability of the virus to evade the body's defenses, the infection can lead to cleaning (acute illness) or persistence (chronic disease) of the virus. The chronic presence of viruses inside the liver cells produces a double wave of inflammation, injury and wound healing that overtime causes scarring or fibrosis and leads to hepatocellular carcinoma. Individuals with impaired immune responses are at greater risk of chronic infection. Natural killer cells are a major driver of early innate response and create an environment of cytokines that result in the recruitment of CD4 T-helper and cyto- toxic CD8 T-cells. Type I interferon is a cytokine that promotes an antiviral response. In chronic hepatitis B and C, natural killer cell function is impaired.
Steatohepatitis
Steatohepatitis is seen in both alcoholic and non-alcoholic liver disease and is the culmination of a cascade of events beginning with injury. In the case of non-alcoholic steatohepatitis, this cascade is initiated by changes in metabolism associated with obesity, insulin resistance, and lipid dysregulation. In alcoholic hepatitis, chronic excessive use of alcohol is the cause. Although inciting events may differ, the development of similar events begins with the accumulation of free fatty acids (FFAs) and their breakdown products in liver cells in a process called steatosis. This reversible process initially controls the ability of hepatocytes to maintain a lipid homeostasis that leads to a toxic effect when fatty molecules accumulate and are broken down in the regulation of the oxidative stress response. Overtime, this abnormal lipid deposition triggers the immune system through the fool 4 receptors (TLR4) that results in the production of inflammatory cytokines such as TNF that cause cell liver injury and death. These events mark the transition to steatohepatitis and in the setting of chronic injury, fibrosis eventually develops the setting of events that cause cirrhosis and hepatocellular carcinoma. Microscopically, visible changes include steatosis with large hepatocytes and swollen (balloon), evidence of cellular injury and cell death (apoptosis, necrosis), evidence of inflammation in particular in the 3 liver zone, the degree of fibrosis variable and Mallory's body..
Diagnosis
The diagnosis of hepatitis is made on the basis of some or all of the following: patient signs and symptoms, medical history including history of sexual and substantial use, blood tests, imaging, and liver biopsy. In general, for viral hepatitis and other acute causes of hepatitis, patient blood tests and clinical features are sufficient for diagnosis. For other causes of hepatitis, especially chronic causes, blood tests may be useless. In this case, a liver biopsy is the gold standard for diagnosis because histopathologic analysis is able to reveal appropriate levels and patterns of inflammation and fibrosis. However, liver biopsy is usually not an early invasive diagnostic test and is associated with a small but significant increased risk of bleeding in patients with liver injury and cirrhosis.
Blood tests include liver enzymes, serologies (ie for autoantibodies), nucleic acid testing (ie for hepatitis/RNA virus DNA), blood chemistry, and full blood count. Pattern characteristics of liver enzyme abnormalities may indicate a particular cause or stage of hepatitis. Generally, AST and ALT increase in most cases of hepatitis regardless of whether the patient shows any symptoms. However, elevation levels (ie levels within hundreds vs. in thousands), dominance for AST vs. ALT elevation, and the ratio between AST and ALT informative diagnosis.
Ultrasound, CT, and MRI all can identify steatosis (fat changes) of the liver tissue and nodularity of the liver surface suggestive of cirrhosis. CT and especially MRI are able to provide a higher level of detail, allowing visualization and structural features such as blood vessels and tumors in the liver. Unlike steatosis and cirrhosis, no imaging tests are capable of detecting inflammation of the liver (ie hepatitis) or fibrosis. Liver biopsy is the only definitive diagnostic test capable of assessing inflammation and liver fibrosis.
Viral hepatitis
Viral hepatitis is primarily diagnosed through blood tests for viral antigen levels (such as hepatitis B surface or core antigen), anti-viral antibodies (such as anti-hepatitis B antibodies or anti-hepatitis A antibodies), or viral DNA./RNA. In the initial infection (ie within 1 week), IgM antibodies are found in the blood. In advanced infections and after recovery, IgG antibodies are present and remain in the body for many years. Therefore, when a patient is positive for IgG antibodies but negative for IgM antibodies, he is considered immune from the virus through previous infections and previous recovery or vaccinations.
In the case of hepatitis B, blood tests exist for some viral antigens (which are distinct components of virion particles) and antibodies. Combinations of antigens and antibodies can positively inform the stage of infection (acute or chronic), viral replication rate, and viral infectivity.
Alcoholic versus non-alcohol
The most obvious distinguishing factor between alcohol steatohepatitis (ASH) and non-alcoholic steatohepatitis (NASH) is a history of alcohol use or abuse. Thus, in patients who do not use alcohol or not, the diagnosis is unlikely to be alcohol hepatitis. However, in those who use alcohol, the diagnosis may be the same as alcoholic or nonalcoholic hepatitis especially if there is obesity, diabetes, and metabolic syndrome at the same time. In this case, alcoholic and nonalcoholic hepatitis can be distinguished by a pattern of liver enzyme abnormalities; specifically, in AST steatohepatitis & gt; ALT alcohol with AST ratio: ALT & gt; 2: 1 while in nonalcoholic steatohepatitis ALT & gt; AST with ALT: AST & gt; 1.5: 1.
Of note, a liver biopsy showed identical findings in patients with ASH and NASH, in particular, the presence of polymorphonuclear infiltration, hepatocyte necrosis and apoptosis in the form of balloon degeneration, Mallory's body, and fibrosis around the veins and sinuses.
Screening
Viral hepatitis
The purpose of screening for viral hepatitis is to identify people infected with the disease as early as possible. This allows for early treatment, which can prevent disease progression, and reduce transmission to others.
Hepatitis A
Hepatitis A causes an acute illness that does not develop into chronic liver disease. Therefore, the role of screening is to assess the status of immunity in people at high risk of contracting the virus, as well as in people with known liver disease for whom hepatitis A infection can lead to liver failure. People in these non-immune groups can receive the hepatitis A vaccine.
Those who are at high risk and require checks include:
- People with poor sanitary habits such as not washing their hands after using the restroom or changing diapers
- People who do not have access to clean water
- People who are in close contact (either living with or having sex) with someone with hepatitis A
- Illicit drug users
- People with liver disease
- People traveling to an area with hepatitis A endemic
The presence of anti-hepatitis A IgG in blood suggests past infections with previous viruses or vaccinations.
Hepatitis B
CDC, WHO, USPSTF, and ACOG recommend routine hepatitis B screening for certain high-risk populations. Specifically, this population includes people who:
- Born in countries where the prevalence of high hepatitis B (defined as> = 2% of the population), whether they have been vaccinated
- Born in the United States whose parents are from countries where the prevalence of hepatitis B is very high (defined as> = 8% of the population), and unvaccinated
- HIV positive
- Intravenous drug users
- Men who have sex with men
- Closely related to (ie living or having sex) people with known hepatitis B
- Pregnant
- Start immunosuppressive or cytotoxic therapy
- Found elevated liver enzymes without known cause
- Blood donor, organ, or tissue
- Jailed
- In hemodialysis
Screening consists of blood tests that detect hepatitis B surface antigen (HBsAg). If HBsAg is present, a second test - usually done on the same blood sample - that detects antibodies to the hepatitis B core antigen (anti-HBcAg) can distinguish between acute and chronic infections. High-risk people whose blood tests are negative for HBsAg may receive hepatitis B vaccine to prevent future infections.
Hepatitis C
CDC, WHO, USPSTF, AASLD, and ACOG recommend screening people at high risk for hepatitis C infection. These populations include people who:
- Intravenous drug users (past or present)
- Illegal intranasal drug user
- HIV-positive
- Men who have sex with men
- Jailed, or ever in the past
- In long-term hemodialysis, or that had existed in the past
- Tattoo recipient in "unregulated settings"
- Recipient of blood or organ products before 1992 in the United States
- Adults in the United States were born between 1945-1965
- Born from a positive HCV mother
- Pregnant, and engage in high-risk behavior
- Workers in health care settings with needlestick injuries
- Blood or organ donation.
- Sex worker
For people in the above group whose presentation is ongoing, screening should be "periodic," although according to the USPSTF, studies have not determined optimal screening intervals. AASLD recommends screening men who have sex with HIV-positive men each year. People born in the US between 1945-1965 should be screened once (unless they have other exposure risks).
Screening consists of blood tests that detect anti-hepatitis C virus antibodies. If hepatitis C anti-viral antibodies are present, confirmatory tests to detect HCV RNA suggest chronic disease.
Prevention
Vaccines
Hepatitis A
CDC recommends hepatitis A vaccine for all children from one year of age, as well as for those who have not been previously immunized and are at high risk of contracting the disease.
For children age 12 months or older, vaccination is given as a shot to the muscle in two doses of 6-18 months and should begin before the age of 24 months. Dosing is slightly different for adults depending on the type of vaccine. Ã, If the vaccine is only for hepatitis A, two doses are given 6-18 months depending on the manufacturer. Ã, If the vaccine is combined with hepatitis A and hepatitis B, up to 4 doses may be required.
Hepatitis B
CDC recommends routine vaccination for all children under the age of 19 with hepatitis B vaccine. They also recommend it for those who want it or are at high risk.
Regular vaccination for hepatitis B starts with the first dose administered as an injection to the muscle before the newborn is discharged from the hospital. Two additional doses should be given before the child is 18 months old.
For infants born to mothers with hepatitis B, the positive surface of the antigen, the first dose is unique - in addition to the vaccine, immune hepatitis globulin should also be given, both within 12 hours after birth. These newborns should also be tested regularly for infections at least during the first year of life.
There is also a combination formulation that includes hepatitis A and B vaccine.
More
There is currently no vaccine available in the United States for hepatitis C or E.
Behavior change
Hepatitis A
Because hepatitis A is transmitted primarily through oral-fecal routes, primary prevention in addition to vaccination is good hygiene, access to clean water and appropriate waste handling.
Hepatitis B and C
Because hepatitis B and C are transmitted through blood and lots of body fluids, prevention is aimed at filtering blood before transfusion, avoiding the use of injection drugs, safe needles and sharps practices in health care settings, and safe sex practices.
Hepatitis D
Hepatitis D virus requires that a person first be infected with hepatitis B virus, so prevention efforts should focus on limiting the spread of hepatitis B. In people who have chronic hepatitis B infection and are at risk for superinfection with hepatitis D virus, prevention strategies are the same as for hepatitis B.
Hepatitis E
Hepatitis E spreads primarily through the mouth-to-mouth route but can also be transmitted by the blood and from the mother to the fetus. The prevention of hepatitis E is similar to hepatitis A (ie, good hygiene and clean water practices).
Alcoholic hepatitis
Due to excessive alcohol intake can cause hepatitis and cirrhosis, the following is the maximum recommendation for alcohol consumption:
- Women - <= 3 drinks on certain days and <= 7 drinks per week
- Men - <= 4 drinks on a certain day and <= 14 drinks per week
Success
Hepatitis A
In the United States, universal immunization has resulted in two-thirds reduction in hospital admissions and medical expenses due to hepatitis A.
Hepatitis B
In the United States, new cases of hepatitis B decreased 75% from 1990-2004. The groups that saw the greatest decline were children and adolescents, possibly reflecting the implementation of the 1999 guidelines.
Hepatitis C
Hepatitis C infection has declined annually since the 1980s, but began to increase again in 2006. The data is unclear as to whether the decline can be attributed to needle exchange programs.
Alcoholic hepatitis
Because people with alcoholic hepatitis may have no symptoms, it can be difficult to diagnose and the number of people with this disease may be higher than many estimates. Programs such as Alcoholics Anonymous have been successful in reducing deaths due to cirrhosis, but it is difficult to evaluate their efficacy in reducing the incidence of alcoholic hepatitis.
Treatment
Hepatitis treatment varies based on the form (acute versus chronic), the severity of the disease, and the cause
Hepatitis A
Hepatitis A generally does not progress to a chronic state and rarely requires hospitalization. Treatment is supportive and includes measures such as providing intravenous (IV) hydration and maintaining adequate nutrition.
Rarely, people with hepatitis A virus can rapidly develop liver failure, called fulminant liver failure , especially elderly and those with pre-existing liver disease, particularly hepatitis C. Risk factors include age greater than. and chronic hepatitis C. In this case, more aggressive supportive therapy and liver transplantation may be necessary.
Hepatitis B
Acute
In healthy patients, 95-99% recover without long-term effects, and antiviral treatment is not necessary. Age and comorbid conditions can lead to longer and more severe disease. Certain patients require hospitalization, especially those who come with ascites clinical signs, peripheral edema, and hepatic encephalopathy, and laboratory signs of hypoglycemia, prolonged prothrombin time, low serum albumin, and very high serum bilirubin.
In this rare and severe acute case, patients have been successfully treated with antiviral therapy similar to those used in cases of chronic hepatitis B, with nucleoside analogues such as entecavir or tenofovir. Because there is a scarcity of clinical trials data and medications used to treat susceptible to developing resistance, experts recommend booking treatment for severe acute cases, not mild to moderate.
Chronic
Chronic hepatitis B management aims to control viral replication, which correlates with disease progression. There are 7 approved drug treatments to date in the United States:
- Interferon alpha injection is the first approved therapy for chronic hepatitis B. It has several side effects, most of which can be eliminated by the removal of therapy, but has been replaced by newer treatments for these indications. These include long-acting interferon bonded to polyethylene glycol (pegylated interferon) and oral nucleoside analogues.
- Pegylated interferon (PEG IFN) is administered only once a week as a subcutaneous injection and is more convenient and effective than standard interferon. Although it does not develop resistance like many oral antivirals, it is not well tolerated and requires close monitoring. PEG IFN is estimated to cost around $ 18,000 per year in the United States, compared to $ 2,500-8,700 for oral medicines; However, the duration of treatment is 48 weeks compared with oral antiviral, which requires unlimited treatment for the majority of patients (at least 1 year). PEG IFN is not effective in patients with high levels of viral activity and can not be used in patients with immunosuppression or those with cirrhosis.
- Lamivudine is the first approved oral nucleoside analogue. Although effective and efficacious, lamivudine has been replaced by a new, stronger treatment in the Western world and is no longer recommended as first-line treatment. However, it is still used in areas where new agents have not been approved or are too expensive. Generally, treatment is a minimum of one year with a minimum of six additional months of "consolidation therapy." Based on viral responses, longer therapy may be needed, and certain patients require unlimited long-term therapy. Due to a less robust response in Asian patients, consolidation therapy is recommended to be extended to at least one year. All patients should be monitored for viral reactivation, which, if identified, requires re-treatment. Lamivudine is generally safe and well tolerated. Many patients develop resistance, which correlates with longer treatment durations. If this happens, additional antivirus is added. Lamivudine as a single treatment is contraindicated in HIV co-infected patients, as resistance develops rapidly, but can be used as part of a multidrug regimen.
- Adefovir dipivoxil, a nucleotide analogue, has been used to supplement lamivudine in patients who develop resistance, but is no longer recommended as first-line therapy.
- Entecavir is safe, well tolerated, less susceptible to developing resistance, and the strongest of existing hepatitis B antivirals; this is a first-line treatment option. Not recommended for patients who are resistant to 3TC or as monotherapy in HIV-positive patients.
- Telbivudine is effective but not recommended as first-line treatment; compared with entecavir, both are less powerful and more vulnerable.
- Tenofovir is a nucleotide analogue and an antiretroviral drug that is also used to treat HIV infection. Preferably for adefovir is good in patients who are resistant to 3TC and as an early treatment because they are both more potent and less likely to develop resistance.
The first-line treatments currently used include PEG IFN, entecavir, and tenofovir, depending on patient and physician preferences. Treatment initiation is guided by recommendations issued by the American Association for the Study of Liver Diseases (AASLD) and the European Association for Liver Studies (EASL) and is based on detectable HBeAg virus levels or negative status, ALT levels, and in certain cases, family history of HCC and liver biopsy. In patients with compensated cirrhosis, treatment is recommended regardless of HBeAg status or ALT level, but different recommendations on HBV DNA levels; AASLD recommends care at detectable DNA levels above 2x10 3 IU/mL; EASL and WHO recommend treatments when HBV DNA levels are detected at any level. In patients with decompensated cirrhosis, treatment and evaluation for liver transplantation is recommended in all cases if HBV DNA is detected. Currently, multidrug treatment is not recommended in the treatment of chronic HBV because it is not more effective in the long term than individual treatment with entecavir or tenofovir.
Hepatitis C
In contrast to hepatitis A and B, progression to chronic hepatitis C is much more common. The ultimate goal of hepatitis C treatment is the prevention of hepatocellular carcinoma (HCC). The best way to reduce the long-term risk of HCC is to achieve a sustained virological response (SVR). SVR was defined as an undetectable viral load at 12 weeks after treatment was completed and showed healing. Currently available treatments include indirect and direct antiviral drugs. Indirect work antivirals include pegylated interferon (PEG IFN) and ribavirin (RBV), which in combination has historically been the basis of therapy for HCV. The duration and response to these treatments vary by genotype. These agencies are poorly tolerated but are still used in some resource-poor areas. In high-resource countries, they have been replaced by direct-acting antiviral agents, which first appeared in 2011; these agents target the proteins responsible for viral replication and include the following three classes:
- NS3/4A protease inhibitors, including telaprevir, boceprevir, simeprevir, etc.
- NS5A inhibitors, including ledipasvir, daclatasvir, and others
- NS5B polymerase inhibitors, including sofosbuvir, dasabuvir, and more
These drugs are used in various combinations, sometimes in combination with ribavirin, based on the patient's genotype (described as genotypes 1-6). Genotype 1 (GT1), which is the most common genotype in the United States and around the world, can now be cured with a direct antiviral regimen. First-line therapy for GT1 is a 12-week combination of sofosbuvir and ledipasvir (SOF/LDV) for most patients, including those with advanced fibrosis or cirrhosis. Certain patients with early disease require only 8 weeks of treatment while those with advanced fibrosis or cirrhosis who have not responded to previous care require 24 weeks. Fixed costs are a major factor limiting access to these drugs, especially in low-resource countries; the cost of a 12-week GT1 regimen (SOF/LDV) is estimated at US $ 94,500.
The American Association for the Study of Liver Diseases and the Infectious Diseases Society of America (AASLD-IDSA) recommends antiviral treatment for all patients with chronic hepatitis C infection unless they are with additional chronic medical conditions that limit their life expectancy.
Hepatitis D
Hepatitis D is difficult to treat, and effective treatment is lacking. Interferon alfa has been shown to be effective in inhibiting viral activity but only temporarily.
Hepatitis E
Similar to hepatitis A, hepatitis E treatment supports and includes rest and ensures adequate nutrition and hydration. Hospitalization may be necessary for very severe cases or for pregnant women.
Alcoholic hepatitis
The first-line treatment of alcoholic hepatitis is the treatment of alcoholism. For those who alienate completely from alcohol, reversal of liver disease and longer life is possible; patients at every stage of the disease have been shown to be beneficial with the prevention of additional liver injuries. In addition to referrals to psychotherapy and other treatment programs, care should include nutritional and psychosocial evaluation and treatment. Patients should also be treated appropriately for related signs and symptoms, such as ascites, liver encephalopathy, and infection.
Severe alcohol hepatitis has a poor prognosis and is very difficult to treat. Without treatment, 20-50% of patients may die within a month, but evidence suggests treatment may prolong life beyond one month (ie, reduce short-term mortality). Available treatment options include pentoxifylline (PTX), which is a nonspecific TNF inhibitor, corticosteroids, such as prednisone or prednisolone (CS), corticosteroids with N -acetylcysteine ​​(CS with NAC) and corticosteroids with pentoxifylline (CS with PTX). Data show that CS alone or CS with NAC is most effective in reducing short-term mortality. Unfortunately, corticosteroids are contraindicated in some patients, such as those with active gastrointestinal bleeding, infection, renal failure, or pancreatitis. In this case PTX may be considered on a case-by-case basis as a substitute for CS; some evidence suggests PTX is better than no treatment at all and may be comparable to CS while other data show no evidence of more benefit than placebo. Unfortunately, there is currently no drug treatment that reduces the risk of patients dying in the long term, at 3-12 months and so on.
Weak evidence suggests that milk thistle extract may increase survival in alcoholic liver disease and improve certain liver tests (serum bilirubin and GGT) without side-effects, but strong recommendations can not be made for or against milk thistle without further study.
Recommendations
Many people with hepatitis will prefer to rest in bed, although it is not necessary to avoid all physical activity during recovery. High calorie diets are recommended. Many people develop nausea and can not tolerate food later in life, so most intake can be concentrated in the early part of the day. In the acute phase of the disease, intravenous feeding may be necessary if the patient is unable to tolerate food and has poor mouth intake after nausea and vomiting.
People with hepatitis should avoid taking drugs that are metabolized by the liver. Glucocorticoids are not recommended as treatment options for acute viral hepatitis and may even cause harm, such as the development of chronic hepatitis.
Universal precautions must be observed, but isolation is not really necessary; isolation may be required in cases of fecal incontinence in hepatitis A and E and uncontrolled bleeding in hepatitis B and C.
Prognosis
Acute hepatitis
Almost all patients with hepatitis A infection recover completely without complications if they are healthy before the infection. Similarly, acute hepatitis B infection has a beneficial course leading to a complete recovery in 95-99% of patients. However, certain factors may indicate a worse outcome, such as a co-morbid medical condition or early symptoms of ascites, edema, or encephalopathy. Overall, the mortality rate for acute hepatitis is low: ~ 0.1% of total for hepatitis A and B cases, but the rate may be higher in certain populations (super infection with hepatitis B and D, pregnant women, etc.).
In contrast to hepatitis A & amp; B, hepatitis C has a higher risk of developing into chronic hepatitis, approaching 85-90%. Cirrhosis has been reported to develop in 20-50% of patients with chronic hepatitis C.
Other rare complications of acute hepatitis include pancreatitis, aplastic anemia, peripheral neuropathy, and myocarditis.
fulminant hepatitis
Although most cases of hepatitis are viral, fulminant hepatitis represents a rare but feared complication. Fulminant hepatitis is most common in hepatitis B, D, and E. Approximately 1-2% of cases of hepatitis E can cause fulminant hepatitis, but pregnant women are particularly vulnerable, occurring in up to 20% of cases. The mortality rate in fulminant hepatitis cases increases by more than 80%, but survivors often experience total recovery. Liver transplant can save lives in patients with fulminant liver failure.
Hepatitis D infection can change the case of hepatitis B to progressive severe hepatitis, a phenomenon known as superinfection.
Chronic hepatitis
Acute hepatitis B infection becomes less likely to develop into a chronic form as the patient's age increases, with development rates approaching 90% in cases of vertically transmitted infants compared to 1% risk in young adults. Overall, the 5-year survival rate for chronic hepatitis B ranges from 97% in mild cases to 55% in severe cases with cirrhosis.
Most patients suffering from hepatitis D at the same time as hepatitis B (co-infection) recover without developing a chronic infection; However, in people with hepatitis B who subsequently acquire hepatitis D (superinfection), chronic infection is much more common in 80-90%, and liver disease progression is accelerated.
Chronic hepatitis C progresses to cirrhosis, with an estimated 16% cirrhosis prevalence at 20 years after infection. While the main cause of death in hepatitis C is end-stage liver disease, hepatocellular carcinoma is an important additional long-term complication and cause of death in chronic hepatitis.
The mortality rate increases with the progression of underlying liver disease. A series of patients with compensated cirrhosis due to HCV has shown 3.5, and a 10-year survival rate of 96, 91, and 79% respectively. The 5-year survival rate drops to 50% if cirrhosis becomes decompensated.
Epidemiology
Viral hepatitis
Hepatitis A
Hepatitis A is found worldwide and manifests as a major outbreak and epidemic associated with contamination of water and food stools. Hepatitis A viral infection is very dominant in children aged 5-14 years with infant infections are scarce. Infected children have little or no clear clinical disease, unlike adults who are greater than 80% symptomatic if infected. The highest rates of infection in low-resource countries with inadequate public sanitation and large concentrated populations. In such areas, as many as 90% of children younger than 10 years old have been infected and immune, appropriate to lower rates of clinical illness and outbreak disease. The availability of childhood vaccines has significantly reduced infection in the United States, with incidents declining by more than 95% by 2013. Paradoxically, the highest rates of new infections are now occurring in young adults and adults who come with worse clinical disease. Specific populations with the greatest risk include: travelers to endemic areas, men who have sex with men, those exposed in the workplace to non-human primates, individuals with clotting disorders who have received clotting factors, individuals with a history of liver disease chronic infection where hepatitis A infection can cause fulminant hepatitis, and intravenous drug users (rare).
Hepatitis B
Hepatitis B is the most common cause of viral hepatitis in the world with over 240 million chronic viral people, 1 million of whom are in the United States. In about two-thirds of patients with acute hepatitis B infection, no identifiable exposure is present. Of those who are acutely infected, 25% become carriers of the virus for life. The risk of infection is highest among injecting drug users, individuals with high-risk sexual behavior, health care workers, individuals with multiple transfusion histories, organ transplant patients, dialysis patients, and infant newborns who are infected during labor. Nearly 780,000 deaths worldwide are associated with hepatitis B. The most endemic areas are in sub-Saharan Africa and East Asia where as many as 10% of adults are chronically ill. Transport rates in developed countries are much lower, covering less than 1% of the population. In endemic areas, transmission is thought to be associated with exposure during birth and close contact between young infants.
Hepatitis C
Chronic hepatitis C is the leading cause of cirrhosis of the liver and hepatocellular carcinoma. This is a common medical reason for liver transplantation due to severe complications. It is estimated that 130-180 million people worldwide are affected by this disease which represents a little over 3% of the world's population. In developing regions of Africa, Asia and South America, the prevalence can be as high as 10% of the population. In Egypt, a high rate of hepatitis C infection of 20% has been documented and associated with iatrogenic contamination associated with schistosomiasis treatment in the 1950s 1980s. Currently in the United States, approximately 3.5 million adults are estimated to be infected. Hepatitis C is very common among people born between 1945-1965, a group of about 800,000 people, with a prevalence as high as 3.2% compared to 1.6% in the general US population. Most chronic hepatitis C carriers do not know the status of their infection. The most common mode of transmission of hepatitis C virus is exposure to blood products through blood transfusion (before 1992) and intravenous drug injection. The history of intravenous drug injections is the most important risk factor for chronic hepatitis C. Other vulnerable populations include individuals with high-risk sexual behavior, infants of infected mothers, and health care workers.
Hepatitis D
Hepatitis D virus causes chronic and fulminant hepatitis in the context of co-infection with hepatitis B virus. It is primarily transmitted through non-sexual contact and through needles. The susceptibility to hepatitis D differs by geographic area. In the United States and Northern Europe, the at-risk populations are intravenous drug users and individuals who receive multiple transfusions. In the Mediterranean, hepatitis D is predominant among individuals coinfected with hepatitis B virus.
Hepatitis E
Similar to Hepatitis A, hepatitis E manifests as a major outbreak and epidemic associated with faecal contamination of water sources. It accounts for more than 55,000 deaths annually with about 20 million people worldwide suspected of being infected with the virus. It affects mainly young adults, causing acute hepatitis. In an infected pregnant woman, Hepatitis E infection can cause fulminant hepatitis with a third trimester mortality rate as high as 30%. Individuals with weakened immune systems, such as organ transplant recipients, are also susceptible. Infection is rare in the United States but is high in developing countries (Africa, Asia, Central America, Middle East). Many genotypes exist and are distributed differently throughout the world. There is some evidence of hepatitis E infection in animals, serving as a reservoir for human infection.
Alcoholic hepatitis
Alcoholic hepatitis (AH) in its severe form has a one month mortality as high as 50%. Most people who develop AH are men but women are at higher risk of developing AH and its complications are likely secondary to high body fat and differences in alcohol metabolism. Other contributing factors include younger age & lt; 60, binge drinking patterns, malnutrition status, obesity and hepatitis C coinfection. It is estimated that as many as 20% of people with AH are also infected with hepatitis C. In this population, the presence of hepatitis C virus causes more severe disease with faster development of cirrhosis, hepatocellular carcinoma and increased mortality. Obesity increases the likelihood of developing into cirrhosis in individuals with alcoholic hepatitis. It is estimated that a high proportion of individuals (70%) who have AH will develop into cirrhosis.
Non-alcoholic steatohepatitis
Non-alcoholic steatohepatitis (NASH) is projected to be the main reason for liver transplantation in the United States by 2020, replacing chronic liver disease due to hepatitis C. About 20-45% of the US population has NAFLD and 6% have NASH. Estimated prevalence of NASH in the world is 3-5%. Of NASH patients who develop cirrhosis, about 2% per year will likely develop into hepatocellular carcinoma. Worldwide, the estimated prevalence of hepatocellular carcinoma associated with NAFLD is 15-30%. NASH is considered the leading cause of cirrhosis in approximately 25% of patients in the United States, representing 1-2% of the general population.
History
Initial thoughts
The initial account of the syndrome we now think is likely is hepatitis beginning to occur around 3000 BC. The clay tablet that serves as a medical handbook for the ancient Sumerians illustrates the first observation of jaundice. The Sumerians believe that the heart is the home of the soul, and correlates the finding of jaundice with a person's heart attack by a demon named Ahhazu. Around 400 BC, Hippocrates recorded the first documentation of the epidemic jaundice, specifically noting the unique nature of a group of patients who all died within two weeks. He wrote, "The bile contained in the liver is full of sputum and blood, and eruption... After such an eruption, the patient immediately becomes angry, becomes angry, speaks nonsense and barks like a dog." The recommended treatment is a mixture of honey and water called melicrates .
Given the poor sanitary conditions of warfare, infectious jaundice played a major role as the leading cause of death among troops in the Napoleonic Wars, the American Revolutionary War, and both World Wars. During World War II, the estimated army affected by hepatitis was over 10 million. Soldiers receive vaccines against diseases such as yellow fever, but this vaccine is stabilized with human serum and often creates an epidemic of hepatitis. British researchers Findlay and MacCallum suspect the epidemic is caused by a separate infectious agent and not because of the yellow fever virus itself after it recorded 89 cases of jaundice in the months following the vaccination of a total of 3,100 patients they vaccinated. After changing the virus strain of the seeds, they observed no cases of jaundice at the next 8,000 vaccinations.
Willowbrook State School Trial
A New York University researcher named Saul Krugman continued this research into the 1950s and 1960s, the worst with his experiments on mentally disabled children at Willowbrook State School in New York, a dense urban facility where hepatitis infections are highly endemic to student body. Krugman injects students with gamma globulin, a type of antibody. After observing the temporary protection against infection given this antibody, he then tried to inject the hepatitis virus directly to the students. Krugman also controversially picks up dirt from infected students, mixes them into milkshakes, and gives them to newly-received children.
His research was received with much controversy, as people protested the questionable ethics surrounding the target population chosen. Henry Beecher was one of the foremost critics of an article in the New England Journal of Medicine in 1966, arguing that parents were unaware of the risk of consent and that the research was conducted to benefit others at the expense of children. In addition, he argues that poor families with mentally handicapped children often feel pressured to join a research project to get into school, with all the educational resources and upcoming support with him. Others in the medical community are talking to support Krugman's research in terms of the benefits and broad understanding of viral hepatitis, and Willowbrook continues to be a frequently cited example in the debate on medical ethics.
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