Patients with either viral, autoimmune and alcoholic hepatitis may present with a wide variety of symptomatology during their acute and chronic phase of inflammations. The following signs and symptoms are seen in hepatitis:

• Low grade fever
• Anorexia and vomiting
• Dehydration with drying of mucous membranes
• Telangiectasis (spider angiomata) and esophageal varices
• Jaundice
• Ascites
• Utricarial rashes
• Portal Hypertension
• Hepatomegaly and Splenomegaly
• Signs of encephalopathy (i.e. seizure and delirium)
• Malnutrition

The following diagnostic modalities and tests are used in patients with hepatitis:

• Qualitative and quantitative analysis of immunoglobulins for infectious hepatitis
• Liver biopsy will reveal the histologic state of the liver
• Autoimmune assay like Anti-nuclear antibodies (ANA) and anti-smooth muscle antibodies (ASMA).
• Blood tests (Liver enzymes, C-reactive proteins, etc.)
• Imaging studies of the liver

The following treatment approaches are done in all cases of hepatitis among patients:

• Antiviral therapy for viral Hepatitis (nucleoside analogs)
• Interferon therapy for infectious hepatitis
• Autoimmune hepatitis is treated with intravenous corticosteroids
• Cyclosporine and azathioprine
• Naltrexone and acomprosate
• Liver transplantation may be indicated for end stage liver disease cases

In viral hepatitis, the prognosis is primarily dependent on the causative agents. Hepatitis A is usually self-limiting and benign while hepatitis B is insidious and chronic in nature which may lead to hepatocellular carcinoma in 10-15% of cases. Autoimmune hepatitis outlook is gravely dependent on the extent of inflammation. In severe cases, patients usually die within 10 years, those without treatment will usually die within 5 years from diagnosis [9].

The long term outlook of patients with alcoholic hepatitis is dependent whether they are continually on alcohol and whether cirrhosis has already developed. In general, the mortality rate of patients with severe alcoholic hepatitis reaches 66% in most cases [10].

Hepatitis may be clinically caused by infectious agents which commonly involves hepatitis A, hepatitis B, and hepatitis C virus. Less common infectious causes includes cytomegalovirus infections, leptospirosis, malaria, infectious mononucleosis, yellow fever and tuberculosis. Autoimmune hepatitis disease usually follows a hepatitis virus or Epstein Barr virus infection. Some cases of autoimmune hepatitis are caused by drugs like minocycline, methyldopa, nitrofurantoin, and infliximab [1]. Drug induced hepatitis may resolve with the immediate cessation of drugs, but some cases may persist even after drug withdrawal [2]. The most common toxin involved in hepatitis is alcohol. Alcoholic hepatitis usually progresses to cirrhosis and liver failure if heavy alcohol intake is continued.

In the United States, it was estimated that there are 25,000 new hepatitis A infection as of 2007 [3]. The new cases recorded for hepatitis B reached 43,000 as of 2007 in the US. On a worldwide scale, hepatitis A numbers up to 1.5 million infected individuals while those with hepatitis B infections reaches 4 million in numbers [4].

Autoimmune hepatitis occurs in 1-1.2 cases per 100,000 individuals as its global incidence rate. This type of hepatitis accounts for 6% of all liver transplantation done in the United States. In Japan, autoimmune hepatitis has been identified as one of the major causative agent in the development of liver cirrhosis [5].

The relationship of alcohol to the development of severe liver inflammation has been established since antiquity. Genetic polymorphism has been postulated to play a great role in the development of alcoholic damage to the liver cells [6]. Majority of patients who develop alcoholic hepatitis have some degree of malnutrition.

At the incubation period of the hepatitis virus, the host remains asymptomatic but viral shedding are passed out to the stools which potentially infective. After several weeks of unexplained malaise and weakness, patient will develop a cholestasis that leads to generalized hepatic inflammation marked by alalnine aminotransferase (ALT) and alkaline phosphatase elevation. In hepatitis B infection, liver damage is immune mediated and directly cytotoxic at the same time. In some patients, hepatitis undergoes an immune tolerant phase where viral DNA is abundant in the serum while ALT remains normal [7].

The pathogenesis of autoimmune hepatitis is an active interplay of genetic factors and environmental factors in a patient. Genetic predisposition makes the host more susceptible to hepatic insults from foreign antigens and antibodies. Environmental antigens trigger an autoimmune response and a necroinflammatory response in the hepatocytes which causes direct damage, fibrosis and eventually cirrhosis.

The precise mechanism in the pathogenesis of alcoholic hepatitis is still unknown. Although some studies postulate that genetic predisposition and susceptibility of patients to alcohol play a major role in the development of alcoholic hepatitis. Toxicity studies reveal that aldehyde or the metabolite of ethanol metabolism has been shown to directly damage the hepatocyte membranes. The other byproducts of alcohol like free radicals, superoxides, and hydroperoxides are thought to facilitate cell damage through oxidative stress and induce hepatic inflammations. The accumulation of lipid laden hepatocytes from the nonoxidative metabolism of ethanol may rupture and cause hepatic granuloma reactions and fibrosis that my lead to cirrhosis if left unchecked [8].

Hepatitis A is effectively prevented with proper sanitation and good hygiene. Immunizations against hepatitis B is the best preventive option available for uninfected individuals. Because a great deal of hepatotoxic drugs can cause hepatitis, it is most prudent to abide strictly on prescription medications and avoid self-medication at all cost. The use of alcohol should be regulated to prevent the onset of alcoholic hepatitis.

Hepatitis is a clinical disorder characterized by the inflammation of the liver. It is marked by diffuse and patchy necrosis of the liver parenchyma. It is most commonly caused by viruses, alcohol and drugs.

Hepatitis is a serious liver disorder and could either be infectious, autoimmune, or toxic in nature. Hepatitis can be classified as acute if inflammation resolves within 6 months, or chronic if persists beyond 6 months. Patient with chronic hepatitis are more prone to serious complications like liver cirrhosis or liver failure. Severe toxic or alcoholic hepatitis can lead to neurologic complications which carry a high mortality and morbidity rate.

Definition

Hepatitis is the inflammation of the liver which can eventually cause liver parenchymal damage. It is a serious liver disorder that could either be infectious, autoimmune, or toxic in nature.

Cause

Hepatitis is a condition caused most commonly by viruses. Few medications also can cause secondary hepatitis. Chronic alcohol consumption is also implicated to cause hepatitis.

Symptoms

Symptoms of hepatitis are similar though the causative agent varies. The symptoms are due to liver damge. They include jaundice, flu-like symptoms, vomiting, hepatosplenomegaly and malnutrition.

Diagnosis

The common diagnostic methods are serum immunoglobulin assays, blood test of liver enzymes, autoimmune assay and imaging studies (ultrasound, CT-scan, and MRI).

Treatment

The common treatment modalities are antiviral drugs, interferon, corticosteroids, and the final treatment option is liver transplantation.

1. Fairhurst DA,Sheehan-Dre R. Autoimmune hepatitis associated with infliximab in a patient with palmoplanter pustular psoriasis. Clin Exp Dermatol. 2009/04; 34(3):421-2.
2. Liu ZX, Kaplowitz N. Immune-mediated drug-induced liver disease. Clin Liver Dis. Aug 2002; 6(3):755-74.
3. Wasley A, Grytdal S, Gallagher K. Surveillance for acute viral hepatitis--United States, 2006. MMWR Surveill Summ. Mar 21 2008; 57(2):1-24.
4. Previsani N, Lavanchy D. World Health Organization. Hepatitis A (WHO/CDS/CSR/EDC/2000.7). 2000.
5. Michitaka K, Nishiguchi S, Aoyagi Y, Hiasa Y, Tokumoto Y, Onji M. Etiology of liver cirrhosis in Japan: a nationwide survey. J Gastroenterol. Sep 30 2009.
6. Zintzaras E, Stefanidis I, Santos M, Vidal F. Do alcohol-metabolizing enzyme gene polymorphisms increase the risk of alcoholism and alcoholic liver disease? Hepatology. Feb 2006; 43(2):352-61.
7. Keeffe EB, Dieterich DT, Han SH, Jacobson IM, Martin P, Schiff ER, et al. A treatment algorithm for the management of chronic hepatitis B virus infection in the United States: 2008 update. Clin Gastroenterol Hepatol. Dec 2008; 6(12):1315-41; quiz 1286.
8. Testino G, Sumberaz A, Ancarani AO, Borro P, Ravetti G, Ansaldi F, et al. Influence of body mass index, cholesterol, triglycerides and steatosis on pegylated interferon alfa-2a and ribavirin treatment for recurrent hepatitis C in patients transplanted for HCV and alcoholic cirrhosis. Hepatogastroenterology. Mar-Apr 2009; 56(90):501-3.
9. Kirk AP, Jain S, Pocock S, et al. Late results of the Royal Free Hospital prospective controlled trial of prednisolone therapy in hepatitis B surface antigen negative chronic active hepatitis. Gut. Jan 1980; 21(1):78-83.
10. Horie Y, Ishii H, Hibi T. Severe alcoholic hepatitis in Japan: prognosis and therapy. Alcohol Clin Exp Res. Dec 2005; 29(12 Suppl):251S-8S.