Besides viral hepatitis there are also other forms of hepatitis, including alcoholic hepatitis, drug induced hepatitis, toxic hepatitis, hepatitis in metabolic syndrome, autoimmune hepatitis, etc.
Alcoholic hepatitis is suspected in case of a history of drinking. Symptoms onset is usually more gradual and there are signs of chronic alcohol use or alcoholic liver disease.
Drug induced hepatitis can be caused by a great number of drugs, including tuberculosis-specific antibiotics, amiodarone (anti-arrhythmic medication), certain antibiotics, certain antiviral drugs, paracetamol (when overdosed), etc.
Common toxins causing toxic hepatitis include: amatoxin (present in certain mushrooms), white phosphorus, chloroform, carbon tetrachloride (dry cleaning agent), and more.

Hepatitis treatment depends on the type, severity and evolution of the disease.
There is no specific treatment for hepatitis A and E. It is recommended an easy diet and restricted activity, as well as avoiding alcohol intake and drugs use during the recovery period.
Chronic hepatitis B can be cured (only in ? cases) with pegylated interferon-alpha. Treatment lasts six months. Alternative treatment includes other viral suppressors, such as lamivudine and adefovir. Individuals exposed to hepatitis B infection risk (healthcare workers, sexual partners of infected persons, newborns with infected mother, etc) should be vaccinated.
The most effective treatment for hepatitis C is a combination of pegylated interferon and ribavirin. Unfortunately, this treatment is not effective in all the cases and patients variably tolerate this therapy. It is important to notice that even moderate alcohol intake seriously aggravated existing hepatitis C and accelerated its evolution to cirrhosis and liver cancer.
Another option of treatment for patients with severe hepatitis evolution, leading to liver failure is liver transplantation.

Prevention of viral hepatitis is an important issue, since viral hepatitis may have severe evolution and complications and the treatment has limited efficacy.
Prevention of hepatitis A and E includes good personal hygiene and immunization of travelers to endemic areas.
Body fluids (blood, semen, saliva, etc.) of patients with hepatitis B and C are considered contagious. Thus, infection prevention includes protection during sexual intercourse, avoiding repeated use of needles and syringes, tattooing and piercing only at professional salons, etc.
An important step in hepatitis B prevention is vaccination in endemic areas. Hepatitis B vaccine includes three intramuscular injections: at baseline, at 1 month and at 6 months.

All the patients suspected of viral hepatitis are tested for hepatitis viruses A, B and C: IgM anti-HAV, HBsAg, IgM anti-HBc, anti-HCV. If any of these markers are positive, there are conducted further serological tests to differentiate acute infection from chronic infection or past infection. If there is confirmed the presence of hepatitis B virus, anti-HDV (antibody to hepatitis D virus) is measured.
Tests for IgM anti-HEV (IgM antibody to hepatitis E virus) are measured if the patient is (or have recently traveled to) an endemic area and if the test is available.
In uncertain cases HCV-RNA and HBV-DNA can be measured, although these are sophisticated tests and are not routinely available.

At its onset, acute hepatitis mimics various non-specific diseases. Usually, hepatitis is suspected only when jaundice develops. At this stage hepatitis should be differentiated from other disorders associated with jaundice.
Hepatitis diagnosis includes non-specific liver function tests: aminotransferases (ALT and AST), bilirubin, alkaline phosfatase, etc. AST and ALT are usually highly elevated in hepatitis (> 400 IU/L) and ALT is usually higher than AST. The level of aminotransferases not always correlates with clinical severity of hepatitis, which means that ALT and AST can be markedly increased, but the evolution of hepatitis can be relatively mild, and vice versa.
Hyperbilirubinemia can be variable in hepatitis and usually is preceded by urinary bilirubin (darkening of urine). Alkaline phosphatase is moderately elevated in hepatitis.
If viral hepatitis is suspected, it is necessary to effectuate serological studies, to determine the type of virus.

Hepatitis E virus is an RNA virus and is transmitted enterically (by mouth). Hepatitis E is more characteristic to certain geographical areas and usually evolutes in epidemics. Massive hepatitis E infections usually occur due to fecal contamination of water supply. Hepatitis E occurred in such countries as China, India, Mexico and central Africa, and no outbreaks have been registered in US or Western Europe.
Hepatitis E virus, similar to hepatitis A virus, does not produce chronic hepatitis.

Hepatitis D virus, also called delta virus, is a RNA virus which can replicate only in the presence of the hepatitis B virus. This is why it is impossible to have hepatitis D without having hepatitis B infection.
There are two types of hepatitis B+D infection: co-infection and super-infection. Co-infection is when both viruses B and D are inoculated at the same time – acute B+D hepatitis. Super-infection occurs when the individual already suffers from chronic hepatitis B and is infected with hepatitis D virus.
Most often hepatitis D virus is transmitted by blood contact (blood transfusions, parenteral drugs use, etc.), but can also be transmitted by sexual intercourse and from mother to child.

Cirrhosis is a severe consequence of chronic hepatitis and is characterized by replacement of normal liver tissue with fibrous tissue. This condition leads to progressive loss of liver function and is considered irreversible.
Cirrhosis can show no sign for a long period of time (years) and the sign can be unspecific: weight loss, fatigability, loss of appetite, etc.
Cirrhosis leads to serious complications, affecting all the systems and organs: portal hypertension, gastrointestinal bleeding, ascites, peritonitis, splenomegaly, hepatic insufficiency, coagulopathy, renal failure, cholestasis, osteoporosis, malnutrition, pancreatic insufficiency, various blood disorders and more.

Portal-systemic encephalopathy, also called hepatic encephalopathy or hepatic coma, is a neuropsychiatric syndrome, characterized by impaired brain function.
The causes of portal-systemic encephalopathy include acute metabolic stress and disorders leading to increased gut protein: toxins, which normally are detoxified by liver, are accumulating in blood stream and affecting brain functioning.
Portal-systemic encephalopathy can be present in acute hepatitis with fulminant evolution. However, most common conditions associated with portal-systemic encephalopathy are chronic liver diseases and cirrhosis.
Neuropsychiatric signs of portal-systemic encephalopathy include sleep disturbance, impaired concentration, anxiety, depression, memory disorders, somnolence, confusion, disorientation and coma.

Portal hypertension is a medical condition characterized by increased pressure in the portal vein. Portal vein is the blood vessel which drains blood from the gastrointestinal tract, spleen and pancreas into liver. Normal pressure in the portal vein is considered between 5 and 10 mm Hg.
Portal hypertension causes are classified into three categories: pre-hepatic, hepatic and post-hepatic causes.
Portal hypertension is frequently present in cirrhosis, which is a severe consequence of chronic hepatitis.
Portal hypertension shows no symptoms, but leads to severe complications, including: acute gastrointestinal variceal bleeding, ascites, splenomegaly and portal-systemic encephalopathy.