Liver biopsy results from the patient with indometacin-induced acute hepatitis (A and B) that progressed to chronic autoimmune hepatitis (C and D).
(A) Low-power photomicrograph of the first liver biopsy sample, which was obtained 6 weeks after indometacin was discontinued (stained by hematoxylin and eosin, magnification 
100). Visible features of acute hepatitis include lobular disarray, and periportal and centrilobular hepatocyte dropout. (B) Higher-power view of the liver biopsy sample shown in Figure A, which reveals lobular inflammation and hydropic change in the hepatocytes (stained by hematoxylin and eosin, magnification 200). Portal inflammation is minimal. (C) Low-power photomicrograph of the second biopsy sample, which was obtained 20 months after therapeutic indometacin was discontinued (stained by hematoxylin and eosin, magnification 100). A dense mononuclear cell infiltrate is evident in the portal tract with little lobular inflammation typical of chronic hepatitis. (D) Higher-power view of the liver biopsy sample shown in Figure C, which reveals dense portal inflammation and focal piecemeal necrosis (stained by hematoxylin and eosin, magnification 200)
100). Visible features of acute hepatitis include lobular disarray, and periportal and centrilobular hepatocyte dropout. (B) Higher-power view of the liver biopsy sample shown in Figure A, which reveals lobular inflammation and hydropic change in the hepatocytes (stained by hematoxylin and eosin, magnification 200). Portal inflammation is minimal. (C) Low-power photomicrograph of the second biopsy sample, which was obtained 20 months after therapeutic indometacin was discontinued (stained by hematoxylin and eosin, magnification 100). A dense mononuclear cell infiltrate is evident in the portal tract with little lobular inflammation typical of chronic hepatitis. (D) Higher-power view of the liver biopsy sample shown in Figure C, which reveals dense portal inflammation and focal piecemeal necrosis (stained by hematoxylin and eosin, magnification 200)Treatment of acute viral hepatitis and chronic viral hepatitis are different. Treatment of acute viral hepatitis involves relieving symptoms and maintaining adequate intake of fluids. Treatment of chronic viral hepatitis involves medications to eradicate the virus and taking measures to prevent further liver damage.
Acute hepatitis
In patients with acute viral hepatitis, the initial treatment consists of relieving the symptoms of nausea, vomiting, and abdominal pain. Careful attention should be given to medications which can have adverse effects in patients with abnormal liver function. Only those medications that are considered necessary should be administered since the impaired liver is not able to eliminate drugs normally, and drugs may accumulate in the blood and reach toxic levels. In addition, sedatives and "tranquilizers" are avoided because they may accentuate the effects of liver failure on the brain and cause lethargy and coma. The patient must abstain from drinking alcohol since alcohol is toxic to the liver. It occasionally is necessary to provide intravenous fluids to prevent dehydration caused by vomiting. Patients with severe nausea and/or vomiting may need to be hospitalized for treatment and intravenous fluids.
Chronic hepatitis
Treatment of chronic infection with hepatitis B and hepatitis C usually involves medication or combinations of medications to eradicate the virus. Doctors believe that in properly selected patients, successful eradication of the viruses can stop progressive damage to the liver and prevent the development of cirrhosis, liver failure, and liver cancer. Alcohol aggravates liver damage in chronic hepatitis, and can cause more rapid progression to cirrhosis. Therefore, patients with chronic hepatitis should stop drinking alcohol. Smoking cigarettes also can aggravate liver disease and should be stopped.
Medications for chronic hepatitis C infection include:
- injectable interferon
- oral ribavirin
Medications for chronic hepatitis B infection include:
- injectable interferon
- oral lamivudine (Epivir)
- oral adefovir (Hepsera)
- oral entecavir (Baraclude)
Decisions regarding treatment of chronic hepatitis can be complex, and should be directed by gastroenterologists or hepatologists (doctors specially trained in treating diseases of the liver) for several reasons including:
The diagnosis of chronic viral hepatitis may not be straightforward. Sometimes a liver biopsy may have to be performed for confirmation of liver damage. Doctors experienced in managing chronic liver diseases must weigh the risk of liver biopsy against the potential benefits of the biopsy.
Not all patients with chronic viral hepatitis are candidates for treatment. Some patients need no treatment (since some patients with chronic hepatitis B and C do not develop progressive liver damage or liver cancer).
Medications for chronic infection with hepatitis B and hepatitis C are not always effective. Prolonged treatment (6 months to years) often is necessary. Even with prolonged treatment, rates of successful treatment (defined as complete and lasting eradication of the virus) often are low (usually less than 80% and often around 50%).
Some of the medications such as interferon and ribavirin can have serious side effects, and doses may have to be reduced.
There are several different strains of hepatitis C viruses with differing susceptibilities to medications. For example, hepatitis C type 3 is more likely to respond to interferon injections and ribavirin than type 1. Certain hepatitis B strains are resistant to lamivudine but respond to adefovir or entecavir.
Please read the hepatitis B and hepatitis C articles for more details in diagnosis and treatment.
Fulminant hepatitis. Treatment of acute fulminant hepatitis should be done in centers that can perform liver transplantation since acute fulminant hepatitis has a high mortality without liver transplantation.
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