Fulminant hepatitis, or massive hepatic cell death, is a rare and life-threatening complication of acute hepatitis that can occur in cases of hepatitis B, D, and E, in addition to drug-induced and autoimmune hepatitis. The complication more frequently occurs in instances of hepatitis B and D co-infection at a rate of 2–20% and in pregnant women with hepatitis E at rate of 15–20% of cases. In addition to the signs of acute hepatitis, people can also demonstrate signs of coagulopathy (abnormal coagulation studies with easy bruising and bleeding) and encephalopathy (confusion, disorientation, and sleepiness). Mortality due to fulminant hepatitis is typically the result of various complications including cerebral edema, gastrointestinal bleeding, sepsis, respiratory failure, or kidney failure.

Acute cases of hepatitis are seen to be resolved well within a six-month period. When hepatitis is continued for more than six months it is termed chronic hepatitis. Chronic hepatitis is often asymptomatic early in its course and is detected only by liver laboratory studies for screening purposes or to evaluate non-specific symptoms. As the inflammation progresses, patients can develop constitutional symptoms similar to acute hepatitis, including fatigue, nausea, vomiting, poor appetite, and joint pain. Jaundice can occur as well, but much later in the disease process and is typically a sign of advanced disease. Chronic hepatitis interferes with hormonal functions of the liver which can result in acne, hirsutism (abnormal hair growth), and amenorrhea (lack of menstrual period) in women. Extensive damage and scarring of the liver over time defines cirrhosis, a condition in which the liver's ability to function is permanently impeded. This results in jaundice, weight loss, coagulopathy, ascites (abdominal fluid collection), and peripheral edema (leg swelling). Cirrhosis can lead to other life-threatening complications such as hepatic encephalopathy, esophageal varices, hepatorenal syndrome, and liver cancer.

People with neonatal hepatitis caused by rubella or cytomegalovirus are at risk of developing an infection of the brain that could lead to mental retardation or cerebral palsy. Many of these infants will also have permanent liver disease from the destruction of liver cells and the resulting scarring (cirrhosis).

Infants with giant cell hepatitis usually recover (80 percent of cases) with little or no scarring to their liver. Their growth pattern resumes as bile flows normally into the small intestine for digestion and to absorb vitamins.

About 20 percent of the infants with neonatal giant cell hepatitis develop chronic liver disease and cirrhosis. Their liver becomes very hard, due to the scarring, and the jaundice does not disappear by six months of age. Infants who reach this point in the disease eventually will require a liver transplant.

Because of the blockage of the bile ducts and the damage caused to liver cells, infants with chronic neonatal hepatitis will not be able to digest fats and will not be able to absorb vitamins A, D, E and K. The lack of vitamin D leads to poor bone and cartilage development (rickets). Vitamin A is also needed for normal growth and good vision. Vitamin K deficiency is associated with easy bruising and a tendency to bleed, whereas the lack of vitamin E results in poor coordination.

Chronic neonatal hepatitis will lead to the inability of the liver to eliminate toxins in the bile. This causes itching, skin eruptions and irritability.

The infant with neonatal hepatitis usually has jaundice (yellow eyes and skin), that appear at one to two months of age, is not gaining weight and growing normally, and has an enlarged liver and spleen. The infant cannot absorb vitamins for proper growth.

About 80% of those exposed to the virus develop a chronic infection. This is defined as the presence of detectable viral replication for at least six months. Most experience minimal or no symptoms during the initial few decades of the infection. Chronic can be associated with fatigue and mild cognitive problems. Chronic infection after several years may cause cirrhosis or liver cancer. The liver enzymes are normal in 7–53%. Late relapses after apparent cure have been reported, but these can be difficult to distinguish from reinfection.

Fatty changes to the liver occur in about half of those infected and are usually present before cirrhosis develops. Usually (80% of the time) this change affects less than a third of the liver. Worldwide hepatitis C is the cause of 27% of cirrhosis cases and 25% of hepatocellular carcinoma. About 10–30% of those infected develop cirrhosis over 30 years. Cirrhosis is more common in those also infected with hepatitis B, schistosoma, or HIV, in alcoholics and in those of male gender. In those with hepatitis C, excess alcohol increases the risk of developing cirrhosis 100-fold. Those who develop cirrhosis have a 20-fold greater risk of hepatocellular carcinoma. This transformation occurs at a rate of 1–3% per year. Being infected with hepatitis B in addition to hepatitis C increases this risk further.

Liver cirrhosis may lead to portal hypertension, ascites (accumulation of fluid in the abdomen), easy bruising or bleeding, varices (enlarged veins, especially in the stomach and esophagus), jaundice, and a syndrome of cognitive impairment known as hepatic encephalopathy. Ascites occurs at some stage in more than half of those who have a chronic infection.

infection causes acute symptoms in 15% of cases. Symptoms are generally mild and vague, including a decreased appetite, fatigue, nausea, muscle or joint pains, and weight loss and rarely does acute liver failure result. Most cases of acute infection are not associated with jaundice. The infection resolves spontaneously in 10–50% of cases, which occurs more frequently in individuals who are young and female.

Acute infection with virus is associated with acute viral hepatitis, an illness that begins with general ill-health, loss of appetite, nausea, vomiting, body aches, mild fever, and dark urine, and then progresses to development of jaundice. It has been noted that itchy skin has been an indication as a possible symptom of all hepatitis virus types. The illness lasts for a few weeks and then gradually improves in most affected people. A few people may have a more severe form of liver disease known as (fulminant hepatic failure) and may die as a result. The infection may be entirely asymptomatic and may go unrecognized.

Chronic infection with virus either may be asymptomatic or may be associated with a chronic inflammation of the liver (chronic hepatitis), leading to cirrhosis over a period of several years. This type of infection dramatically increases the incidence of hepatocellular carcinoma (HCC; liver cancer). Across Europe, hepatitis B and C cause approximately 50% of hepatocellular carcinomas. Chronic carriers are encouraged to avoid consuming alcohol as it increases their risk for cirrhosis and liver cancer. virus has been linked to the development of membranous glomerulonephritis (MGN).

Symptoms outside of the liver are present in 1–10% of HBV-infected people and include serum-sickness–like syndrome, acute necrotizing vasculitis (polyarteritis nodosa), membranous glomerulonephritis, and papular acrodermatitis of childhood (Gianotti–Crosti syndrome). The serum-sickness–like syndrome occurs in the setting of acute , often preceding the onset of jaundice. The clinical features are fever, skin rash, and polyarteritis. The symptoms often subside shortly after the onset of jaundice but can persist throughout the duration of acute . About 30–50% of people with acute necrotizing vasculitis (polyarteritis nodosa) are HBV carriers. HBV-associated nephropathy has been described in adults but is more common in children. Membranous glomerulonephritis is the most common form. Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia have been described as part of the extrahepatic manifestations of HBV infection, but their association is not as well-defined; therefore, they probably should not be considered etiologically linked to HBV.

Early symptoms of hepatitis A infection can be mistaken for influenza, but some sufferers, especially children, exhibit no symptoms at all. Symptoms typically appear 2 to 6 weeks (the incubation period) after the initial infection. About 90% of children do not have symptoms. The time between infection and symptoms, in those who develop them, is between 2 and 6 weeks with an average of 28 days.

The risk for symptomatic infection is directly related to age, with more than 80% of adults having symptoms compatible with acute viral hepatitis and the majority of children having either asymptomatic or unrecognized infections.

Symptoms usually last less than 2 months, although some people can be ill for as long as 6 months:

- Fatigue

- Fever

- Nausea

- Appetite loss

- Jaundice, a yellowing of the skin or the whites of the eyes owing to hyperbilirubinemia

- Bile is removed from the bloodstream and excreted in the urine, giving it a dark amber colour

- Diarrhea

- Light, or clay-coloured faeces (acholic faeces)

- Abdominal discomfort

While usually an acute disease, in immunocompromised subjects—particularly in solid organ transplant patients—hepatitis E may cause a chronic infection. Occasionally this may cause liver fibrosis and cirrhosis.

The incubation period of hepatitis E varies from 3 to 8 weeks. After a short prodromal phase symptoms lasting from days to weeks follow. They may include jaundice, fatigue, and nausea. The symptomatic phase coincides with elevated hepatic aminotransferase levels.

Viral RNA becomes detectable in stool and blood serum during incubation period. Serum IgM and IgG antibodies against HEV appear just before onset of clinical symptoms. Recovery leads to virus clearance from the blood, while the virus may persist in stool for much longer. Recovery is also marked by disappearance of IgM antibodies and increase of levels of IgG antibodies.

Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that affects the liver. It can cause both acute and chronic infections. Many people have no symptoms during the initial infection. Some develop a rapid onset of sickness with vomiting, yellowish skin, tiredness, dark urine and abdominal pain. Often these symptoms last a few weeks and rarely does the initial infection result in death. It may take 30 to 180 days for symptoms to begin. In those who get infected around the time of birth 90% develop chronic while less than 10% of those infected after the age of five do. Most of those with chronic disease have no symptoms; however, cirrhosis and liver cancer may eventually develop. These complications result in the death of 15 to 25% of those with chronic disease.

The virus is transmitted by exposure to infectious blood or body fluids. Infection around the time of birth or from contact with other people's blood during childhood is the most frequent method by which hepatitis B is acquired in areas where the disease is common. In areas where the disease is rare, intravenous drug use and sexual intercourse are the most frequent routes of infection. Other risk factors include working in healthcare, blood transfusions, dialysis, living with an infected person, travel in countries where the infection rate is high, and living in an institution. Tattooing and acupuncture led to a significant number of cases in the 1980s; however, this has become less common with improved sterility. The viruses cannot be spread by holding hands, sharing eating utensils, kissing, hugging, coughing, sneezing, or breastfeeding. The infection can be diagnosed 30 to 60 days after exposure. The diagnosis is usually confirmed by testing the blood for parts of the virus and for antibodies against the virus. It is one of five known hepatitis viruses: A, B, C, D, and E.

The infection has been preventable by vaccination since 1982. Vaccination is recommended by the World Health Organization in the first day of life if possible. Two or three more doses are required at a later time for full effect. This vaccine works about 95% of the time. About 180 countries gave the vaccine as part of national programs as of 2006. It is also recommended that all blood be tested for hepatitis B before transfusion and condoms be used to prevent infection. During an initial infection, care is based on the symptoms that a person has. In those who develop chronic disease, antiviral medication such as tenofovir or interferon may be useful; however, these drugs are expensive. Liver transplantation is sometimes used for cirrhosis.

About a third of the world population has been infected at one point in their lives, including 343 million who have chronic infections. Another 129 million new infections occurred in 2013. Over 750,000 people die of hepatitis B each year. About 300,000 of these are due to liver cancer. The disease is now only common in East Asia and sub-Saharan Africa where between 5 and 10% of adults are chronically infected. Rates in Europe and North America are less than 1%. It was originally known as "serum hepatitis". Research is looking to create foods that contain HBV vaccine. The disease may affect other great apes as well.

Hepatitis A is an infectious disease of the liver caused by the hepatitis A virus (HAV). Many cases have few or no symptoms, especially in the young. The time between infection and symptoms, in those who develop them, is between two and six weeks. When symptoms occur, they typically last eight weeks and may include nausea, vomiting, diarrhea, jaundice, fever, and abdominal pain. Around 10–15% of people experience a recurrence of symptoms during the six months after the initial infection. Acute liver failure may rarely occur, with this being more common in the elderly.

It is usually spread by eating food or drinking water contaminated with infected feces. Shellfish which have not been sufficiently cooked are a relatively common source. It may also be spread through close contact with an infectious person. While children often do not have symptoms when infected, they are still able to infect others. After a single infection, a person is immune for the rest of his or her life. Diagnosis requires blood testing, as the symptoms are similar to those of a number of other diseases. It is one of five known hepatitis viruses: A, B, C, D, and E.

The hepatitis A vaccine is effective for prevention. Some countries recommend it routinely for children and those at higher risk who have not previously been vaccinated. It appears to be effective for life. Other preventive measures include hand washing and properly cooking food. No specific treatment is available, with rest and medications for nausea or diarrhea recommended on an as-needed basis. Infections usually resolve completely and without ongoing liver disease. Treatment of acute liver failure, if it occurs, is with liver transplantation.

Globally, around 1.4 million symptomatic cases occur each year and about 114 million infections (symptomatic and asymptomatic). It is more common in regions of the world with poor sanitation and not enough safe water. In the developing world, about 90% of children have been infected by age 10, thus are immune by adulthood. It often occurs in outbreaks in moderately developed countries where children are not exposed when young and vaccination is not widespread. Acute hepatitis A resulted in 11,200 deaths in 2015. World Hepatitis Day occurs each year on July 28 to bring awareness to viral hepatitis.

Hepatitis D (hepatitis delta) is a disease caused by the "hepatitis D virus" ("HDV"), a small spherical enveloped virusoid. This is one of five known hepatitis viruses: A, B, C, D, and E. HDV is considered to be a subviral satellite because it can propagate only in the presence of the hepatitis B virus (HBV). Transmission of HDV can occur either via simultaneous infection with HBV (coinfection) or superimposed on chronic hepatitis B or hepatitis B carrier state (superinfection).

Both superinfection and coinfection with HDV results in more severe complications compared to infection with HBV alone. These complications include a greater likelihood of experiencing liver failure in acute infections and a rapid progression to liver cirrhosis, with an increased risk of developing liver cancer in chronic infections. In combination with hepatitis B virus, hepatitis D has the highest fatality rate of all the hepatitis infections, at 20%.

Cirrhosis has many possible manifestations. These signs and symptoms may be either a direct result of the failure of liver cells, or secondary to the resultant portal hypertension. There are also some manifestations whose causes are nonspecific but which may occur in cirrhosis. Likewise, the absence of any signs does not rule out the possibility of cirrhosis. Cirrhosis of the liver is slow and gradual in its development. It is usually well advanced before its symptoms are noticeable enough to cause alarm. Weakness and loss of weight may be early symptoms.

Liver disease (also called hepatic disease) is a type of damage to or disease of the liver.

The following features are as a direct consequence of liver cells not functioning.

- Spider angiomata or spider nevi are vascular lesions consisting of a central arteriole surrounded by many smaller vessels (hence the name "spider") and occur due to an increase in estradiol. One study found that spider angiomata occur in about 1/3 of cases.

- Palmar erythema is a reddening of palms at the thenar and hypothenar eminences also as a result of increased estrogen.

- Gynecomastia, or increase in breast gland size in men that is not cancerous, is caused by increased estradiol and can occur in up to 2/3 of patients. This is different from increase in breast fat in overweight people.

- Hypogonadism, a decrease in male sex hormones may manifest as impotence, infertility, loss of sexual drive, and testicular atrophy, and can result from primary gonadal injury or suppression of hypothalamic/pituitary function. Hypogonadism is associated with cirrhosis due to alcoholism or hemochromatosis.

- Liver size can be enlarged, normal, or shrunken in people with cirrhosis.

- Ascites, accumulation of fluid in the peritoneal cavity (space in the abdomen), gives rise to "flank dullness". This may be visible as an increase in abdominal girth.

- Fetor hepaticus is a musty breath odor resulting from increased dimethyl sulfide.

- Jaundice, or "icterus" is yellow discoloration of the skin and mucous membranes, (with the white of the eye being especially noticeable) due to increased bilirubin (at least 2–3 mg/dL or 30 µmol/L). The urine may also appear dark.

There are more than a hundred different kinds of liver disease. Symptoms may include jaundice and weight loss. These are some of the most common:

- Fascioliasis, a parasitic infection of liver caused by a Liver fluke of the "Fasciola" genus, mostly the "Fasciola hepatica".

- Hepatitis, inflammation of the liver, is caused by various viruses (viral hepatitis) also by some liver toxins (e.g. alcoholic hepatitis), autoimmunity (autoimmune hepatitis) or hereditary conditions.

- Alcoholic liver disease is a hepatic manifestation of alcohol overconsumption, including fatty liver disease, alcoholic hepatitis, and cirrhosis. Analogous terms such as "drug-induced" or "toxic" liver disease are also used to refer to disorders caused by various drugs.

- Fatty liver disease (hepatic steatosis) is a reversible condition where large vacuoles of triglyceride fat accumulate in liver cells. Non-alcoholic fatty liver disease is a spectrum of disease associated with obesity and metabolic syndrome.

- Hereditary diseases that cause damage to the liver include hemochromatosis, involving accumulation of iron in the body, and Wilson's disease. Liver damage is also a clinical feature of alpha 1-antitrypsin deficiency and glycogen storage disease type II.

- In transthyretin-related hereditary amyloidosis, the liver produces a mutated transthyretin protein which has severe neurodegenerative and/or cardiopathic effects. Liver transplantation can give a curative treatment option.

- Gilbert's syndrome, a genetic disorder of bilirubin metabolism found in a small percent of the population, can cause mild jaundice.

- Cirrhosis is the formation of fibrous tissue (fibrosis) in the place of liver cells that have died due to a variety of causes, including viral hepatitis, alcohol overconsumption, and other forms of liver toxicity. Cirrhosis causes chronic liver failure.

- Primary liver cancer most commonly manifests as hepatocellular carcinoma and/or cholangiocarcinoma; rarer forms include angiosarcoma and hemangiosarcoma of the liver. (Many liver malignancies are secondary lesions that have metastasized from primary cancers in the gastrointestinal tract and other organs, such as the kidneys, lungs.)

- Primary biliary cirrhosis is a serious autoimmune disease of the bile capillaries.

- Primary sclerosing cholangitis is a serious chronic inflammatory disease of the bile duct, which is believed to be autoimmune in origin.

- Budd–Chiari syndrome is the clinical picture caused by occlusion of the hepatic vein.

Alcoholic hepatitis is hepatitis (inflammation of the liver) due to excessive intake of alcohol. It is usually found in association with fatty liver, an early stage of alcoholic liver disease, and may contribute to the progression of fibrosis, leading to cirrhosis. Signs and symptoms of alcoholic hepatitis include jaundice, ascites (fluid accumulation in the abdominal cavity), fatigue and hepatic encephalopathy (brain dysfunction due to liver failure). Mild cases are self-limiting, but severe cases have a high risk of death. Severe cases may be treated with glucocorticoids.

Alcoholic hepatitis is characterized by myriad symptoms, which may include feeling unwell, enlargement of the liver, development of fluid in the abdomen (ascites), and modest elevation of liver enzyme levels (as determined by liver function tests). Alcoholic hepatitis can vary from mild with only liver enzyme elevation to severe liver inflammation with development of jaundice, prolonged prothrombin time, and even liver failure. Severe cases are characterized by either obtundation (dulled consciousness) or the combination of elevated bilirubin levels and prolonged prothrombin time; the mortality rate in both severe categories is 50% within 30 days of onset.

Alcoholic hepatitis is distinct from cirrhosis caused by long-term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Some alcoholics develop acute hepatitis as an inflammatory reaction to the cells affected by fatty change. This is not directly related to the dose of alcohol. Some people seem more prone to this reaction than others. This is called alcoholic steatonecrosis and the inflammation probably predisposes to liver fibrosis.

There is a rapid onset of clinical signs over the period of 2–7 days, beginning with anorexia, lethargy, and hyperbilirubinemia (icterus and discolored urine). Signs of hepatic encephalopathy (ataxia, blindness, aggression, and coma) and fever can also occur. Other signs include photodermatitis, hemorrhagic diathesis, dependent edema, and colic. The reason for colic is unknown, but is thought to be due to rapid decrease in the size of the liver, and the increased risk of gastric impaction. Rarely, weight loss can occur.

Signs of chronic liver disease detectable on clinical examination can be divided into those that are associated with the diagnosis of chronic liver disease, associated with decompensation and associated with the cause.

Viral hepatitis is liver inflammation due to a viral infection. It may present in acute (recent infection, relatively rapid onset) or chronic forms.

The most common causes of viral hepatitis are the five unrelated hepatotropic viruses hepatitis A, hepatitis B, hepatitis C, hepatitis D, and hepatitis E. In addition to the nominal hepatitis viruses, other viruses that can also cause liver inflammation include cytomegalovirus, Epstein–Barr virus, and yellow fever. Up to 1997 there has been also 52 cases of viral hepatitis caused by herpes simplex virus.

There is the opportunity to prevent or treat the most common types. Hepatitis A and hepatitis B can be prevented by vaccination. Effective treatments for hepatitis C are available but expensive.

In 2013 about 1.5 million people died from viral hepatitis. Most deaths are due to hepatitis B and hepatitis C. East Asia is the region of the world most affected.

Note that "other diseases can involve the liver" and cause hepatomegaly but would not be considered part of the spectrum of chronic liver disease. Some examples of this would include chronic cancers with liver metastases, infiltrative haematological disorders such as chronic lymphoproliferative conditions, chronic myeloid leukaemias, myelofibrosis and metabolic abnormalities such as Gaucher's disease and glycogen storage diseases.

Autoimmune hepatitis may present completely asymptomatic (12–35% of the cases), with signs of chronic liver disease, or acute or even fulminant hepatic failure.

People usually present with one or more nonspecific symptoms, sometimes of long lasting duration, as fatigue, general ill health, lethargy, weight loss, mild right upper quadrant pain, malaise, anorexia, nausea, jaundice or arthralgia affecting the small joints. Rarely, rash or unexplained fever may appear. In women, amenorrhoea is a frequent feature. Physical examination may be normal, but it may also reveal signs and symptoms of chronic liver disease. Many people have only laboratory abnormalities as their initial presentation, as unexplained increase in transaminases and are diagnosed during an evaluation for other reasons. Others have already developed cirrhosis at diagnosis.

Autoimmune hepatitis frequently appears associated with other autoimmune conditions, mainly celiac disease, vasculitis, and autoimmune thyroiditis.

This is quite extensive and includes

- acute infectious hepatitis

- acute mycotoxicosis

- acute pyrrolizidine toxicosis

- acute infectious hepatitis

- acute mycotoxicosis

- haemolytic disease

- hepatotoxins