Hepatitis(redirected from mycotic hepatitis)
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Previously endemic throughout much of the developing world, viral hepatitis now ranks as a major public health problem in industrialized nations. The three most common types of viral hepatitis (A, B, and C) afflict millions worldwide. Acute viral hepatitis is characterized by varying degrees of fever, malaise, weakness, anorexia, nausea, and abdominal distress. Hepatocellular damage causes bilirubin retention, often with jaundice, and a rise in serum levels of certain enzymes (particularly transaminases). Hepatitis A, caused by an RNA enterovirus, is spread by the fecal-oral route, most often through ingestion of contaminated food or water. The case fatality rate is less than 1% and recovery is complete. The presence of antibody to hepatitis A virus indicates prior infection or successful immunization, noninfectivity, and immunity to future attacks. Hepatitis B, due to a small DNA virus of the Hepadnaviridae family, is transmitted through sexual contact, sharing of needles by IV drug abusers, needlestick injuries among health care workers, and from mother to fetus. This disease is a leading cause of chronic hepatitis, cirrhosis, and hepatocellular carcinoma. The annual incidence of hepatitis B in the U.S. is 300,000 cases. The incubation period is 6-24 weeks. Some patients become carriers, and in some, an immune response to the virus induces a chronic phase leading to cirrhosis, hepatic failure, and risk of hepatocellular carcinoma. Hepatitis B surface antigen (HbsSAg) appears in the serum early in the disease; its persistence correlates with chronic infection and infectivity. Core antigen (HbcCAg) appears later and also indicates infectivity. The presence of antibodies to these antigens implies recovery and noninfectivity. Hepatitis C, caused by an RNA virus of the Flaviviridae family, was the principal form of transfusion-induced hepatitis before the early 1990s, when screening of donor blood for this virus was initiated. About two thirds of those currently infected have a history of IV drug abuse. The disease can also be transmitted by needles used for body piercing or tattooing and (less often) sexually or from mother to fetus. Early infection is usually asymptomatic. Antibodies to various components of the virus appear early but do not neutralize the virus. The disease is nonetheless self-limited in 15-20% of patients. The rest develop chronic infection, with persistence of detectable viral RNA, and about half experience slowly progressive deterioration of hepatic function. Cirrhosis occurs in 15-20% of patients with hepatitis C. Extrahepatic manifestations of hepatitis C virus infection include cryoglobulinemia, glomerulonephritis, and non-Hodgkin lymphoma. Acute infection with hepatitis B or C has a higher mortality rate than hepatitis A. Effective vaccines are available for active immunization against hepatitis A and hepatitis B. Interferon-alfa 2b and lamivudine are sometimes effective in hepatitis B. Combination therapy with interferon-alfa 2a, interferon-alfa 2b, and ribavirin brings about clinical remission in some cases of hepatitis C. Responsiveness depends in part on the genotype of the virus. Hepatitis D is due to a defective RNA virus capable of causing disease only in those previously infected by hepatitis B virus. People infected by both hepatitis B and hepatitis D viruses are at high risk of developing fulminant hepatitis and cirrhosis. Prolonged treatment with interferon is somewhat effective. Hepatitis E, which occurs chiefly in the tropics, resembles hepatitis A in that it is transmitted by the fecal-oral route and does not become chronic or lead to a carrier state, but it has a much higher mortality rate.
hepatitisA generic term for any type of liver inflammation.
• Viruses—HAV, HBV, hepatitis non-A, non-B (HCV, HDV, HEV, CMV), coxsackievirus, herpesvirus, EBV, measles, mumps, rubella, rubeola;
• Chemicals and toxins;
Anorexia, nausea, vomiting, malaise, jaundice, myalgia, arthralgia, photophobia, bleeding, diathesis.
Increased transaminases (ALA, AST, GGT, BR), immunoglobulins; decreased vitamin K-dependent coagulation factors, ergo increased prothrombin time. Viral hepatitis is diagnosed by serology, measuring viral antigen(s) or antibodies formed against the antigens; non-viral hepatitides are diagnosed by history and exclusion of virus.
Acute hepatitis—no treatment (steroids, IFN-a are not recommended); chronic hepatitis—corticosteroids, IFN-a may prolong survival and improve outcomes.
hepatitisHepatology Liver inflammation Etiology-infectious HAV, HBV, hepatitis non-A, non-B–HCV, HDV, HEV, CMV, coxsackievirus, herpesvirus, EBV, measles, mumps, rubella, rubeola, bacteria, parasites, fungi Etiology-noninfectious Alcohol, drugs, chemicals and toxins, hyperthermia, radiation Clinical Anorexia, N&V, malaise, jaundice, myalgia, arthralgia, photophobia, bleeding diathesis Lab ↑ Transaminases–ALA, AST, GGT, BR, Igs, ↓ vitamin K-dependent coagulation factors, ergo ↑ prothrombin time; viral hepatitis is diagnosed by serology, measuring viral antigen(s) or antibodies formed against the antigens; non-viral hepatitides are diagnosed by history and exclusion of virus Management Acute hepatitis, no treatment–steroids, IFN-α are not recommended; chronic hepatitis–corticosteroids, IFN-α may prolong survival and improve outcomes. See Acute hepatitis, Biochemical hepatitis, Chronic hepatitis, Giant cell hepatitis, Halothane hepatitis, Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis D, Hepatitis E, Hepatitis F, Hepatitis GB, Hepatitis non-A–G, Lupoid hepatitis, Neonatal hepatitis, Non-A, non-B hepatitis.
hepatitisa serious disorder of the liver that leads to severe jaundice, liver degeneration and even death. The condition is caused by two viruses: hepatitis A virus, which produces infective hepatitis transmitted by the intestinal-oral route, and hepatitis B virus, which produces serum hepatitis transmitted via infected blood or its products. Although these two viral types can be distinguished in tests, the acute diseases caused by each may be clinically indistinguishable, the chief difference being that type A usually has a shorter incubation period than type B. No specific therapy is available for hepatitis, although vaccines are being developed.
hep·a·ti·tis, vi·ral, non-A, non-B(NANB) (hepă-tītis, vīrăl)
Patient discussion about Hepatitis
Q. Do I have hepatitis? I'm volunteering in a shelter for homeless people, and there are many drug addicts there. Yesterday, as I was serving them food one of the residents of the shelter (who I know to be a long term drug addict that uses heroine) coughed and expelled blood on my bare hands (apparently he had some lung disease). Do I now have hepatitis? I know that it's very common among drug addicts, and that it's transmitted through blood contact. I checked my hands and I didn't have any wounds or scratches, but I heard the virus can infect you even if you don't have any wound, is that right?
Q. Is Hepatitis C contagious? My Girlfriend is a carrier for Hepatitis C. She got infected from a blood transfusion as a kid. Can I catch it from her?
Q. How Do You Become Infected With Hepatitis C? Can I get hepatitis C from touching someone with hepatitis?