It is no doubt that acute hepatitis is an inflammatory process leading to hepatocyte death by inducing necrosis or apoptosis (programmed cell death). A wide variety of clinical entities can cause global hepatocellular injury of sudden sunset. Acute hepatitis worldwide is most commonly caused by infecting one of several types of viruses.
These viral agents can be distinguished by serological examination according to their antigenic properties, but all cause clinically similar diseases. Other less common infectious pathogens can cause liver damage. Acute hepatitis is sometimes caused by application to pharmaceuticals (eg, isoniazid) or poisons (eg, ethanol).
The severity of the disease in acute hepatitis ranges from asymptomatic to clinically invisible to fulminant and fatal. The development of acute hepatitis can change very much. Some patients are quite asymptomatic and abnormalities are indicated only by laboratory tests.
There are various symptoms and signs such as anorexia, fatigue, weight loss, nausea, vomiting, abdominal abdominal pain, jaundice, fever, splenomegaly, ascites. The extent of hepatic dysfunction may be significantly different, approximately correlated with the severity of liver injury. The relative degree of cholestasis and liver cell necrosis is also very variable.
Viral hepatitis: Acute hepatitis is caused by one of the five major viruses: hepatitis A (hepatitis B, hepatitis B, hepatitis B, hepatitis C, Trojan horse).
Viral drugs that may develop acute hepatitis are less common, but Epstein-Barr (the reason for infectious mononucleosis), cytomegalovirus, varicella virus, measles virus, herpes simplex virus, rubella virus And yellow fever Trojans.
The newly discovered DNA virus SEN Trojan horse may be associated with infusion-related acute hepatitis not attributable to other viruses. For HAV, liver disease, a few RNA trojans due to direct killing of hepatocytes and host immune response to infected hepatocytes, respectively. It is spread by fecal - oral route from contaminated persons.
Even though most cases are mild, hepatitis A causes liver failure and hepatocellular necrosis and can lead to death. Regardless of severity, patients recovering completely are, do not show evidence of remaining liver disease, and have antibodies that protect them from reinfection. HBV is a DNA trojan that infects by contact with sexual contact or infected blood or other body fluids.
This Trojan horse does not kill infected cells. Rather, the infected hepatocytes are rarely the result of an attack by the immune system after recognizing viral antigens on the hepatocyte surface. Most cases of hepatitis B infection are asymptomatic or cause only mild disease before clearance from virus, but excessive immune response can cause dramatic liver failure.
In a small number of patients with mild acute disease, the immune response is not sufficient to completely clear the Trojan horse and there is no onset of continuous hepatitis. Approximately 1,250,000 Americans are contaminated with HBV and it is estimated that 70,000 new infections will occur every 12 months.
In addition, complications of HBV-induced liver disease result in 5000 deaths every 12 months in the United States. HCV is actually an RNA virus that is also transmitted by blood and body fluids for hepatitis of a type similar to HBV infection, but the proportion of cases progressing to continuous hepatitis (60-85%) is much higher.
Approximately 4 million Americans are infected with HCV and about 30,000 new infections occur every 12 months. End-stage liver disease of HCV causes 8,000 to 10,000 deaths each year. End-stage liver disease caused by HCV may be the most common indication for liver transplantation in the United States. HDV, also known as delta agent, is actually an RNA RNA Trojan that requires helper function of HBV to cause infection.
Therefore, those who are chronically contaminated with HBV have a higher chance of HDV virus, but rarely people who received immunization against HBV. HDV infection occurs as either coinfection with HBV or superinfection in setting up chronic HBV.
HDV infection relates to a much more severe type of hepatitis in terms of both fractional cases and percentage of cases progressing to chronic hepatitis. In North America, duplicated infections of HDV occur mainly in high-risk groups such as injectable drug users and haemophilia patients, and in less than 9% of high-risk patients who are HBV-infected.
United states that the prevalence of HDV coinfection of populations infected with common HBV is not well recognized. HEV is an unclassified RNA virus Trojan that spreads through the bowel route as well as HAV. Clinical illness is similar to hepatitis A, but HEV virus can cause fulminant hepatitis in pregnant women.
Toxic hepatitis: Most cases of drug-induced liver disease exist as acute hepatitis, but exist as cholestasis or other patterns. The incidence of drug-induced hepatitis may be rising. Acetaminophen is currently the most common cause of United Seeds and fulminant hepatitis in the UK.
Hepatotoxicity is defined as the hepatotoxicity is predictable and further subdividing into individuals that are dose-dependent in individuals that cause unpredictable (peculiar) responses regardless of most individuals (eg, acetaminophen) and dosages You can do.
A specific response to a drug may be due to a genetic predisposition of an individual susceptible to a particular pathway of drug metabolism that produces toxic intermediates. Acute hepatic failure has occurred in thromogazone sulfuric acid, a thiazolidinedione used as a drug for improving insulin resistance in diabetes, and bromfenac, a nonsteroidal antiinflammatory drug.
Other thiazolidinediones such as rosiglitazone and pioglitazone do not appear to have the same complications although routine examinations of transaminases may be recommended for people who take medicines. HMG-CoA reductase inhibitors such as atorvastatin and lovastatin have few cases of acute liver failure in less than 3% of patients and are associated with high levels of transaminase.
Time course of acute hepatitis is very variable. In hepatitis A, jaundice is usually observed 4 to 8 weeks after exposure, but in hepatitis B it occurs generally after 8 to 20 weeks from exposure. Hepatitis induced by drugs and toxins usually occurs either during coverage or immediately after coverage and is resolved by discontinuation of the drug in question.
This actually applies to both specific reactions and dose-dependent reactions. Acute hepatitis typically resolves in 3 to 6 months. A hepatic disorder that lasts more than 6 months is arbitrarily defined as chronic hepatitis and suggests that immunity or other mechanisms are working in the absence of continuous coverage of harmful substances.
