As a student, my sister likes reading a book. She has many books collection. But, she has bad style if she is reading a book. She often taking lie down style and standing on her room with slightly dark lamp. And now, she has complaint of decrease her vision.
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The hepatitis D virus (HDV) is an infectious RNA agent. Biological expression of this agent in man requires the concomitant obligatory association of hepatitis B surface antigenemia.
HDV can cause both acute and chronic hepatitis. Clinically, HDV hepatitis may be indistinguishable from other forms of acute and chronic viral hepatitis, although on average, it is more severe. The mortality of icteric acute HDV hepatitis ranges from 2-20% (the mortality for HBV is approximately 1%). Likewise, chronic delta hepatitis tends to be more severe than chronic HBV and HCV infection.
In delta virus there are about 300 million B carriers and about 20 million delta carriers now. You should think of delta when you see fulminant hepatitis B infection. Up to 70% can have delta. Patients lining up for a liver transplant in Pittsburgh were found to be delta positive. The one time we don’t find delta with increased frequency is in patients with chronic hepatitis B and hepatoma. That at first glance appears as a paradox. How come? The answer or the hypothesis is that delta is so bad for the patients that it kills the patient from complications of end stage liver disease, hypertension, or they get referred for a liver transplant before the required incubation of 20 or 30 or 50 years for hepatoma development. In 3 different parts of the world where people have looked at the prevalence of delta in patients with chronic hepatitis B and hepatoma it is actually very low. Delta occurs in 2 cases adds core infection or super infection. Core infection is simultaneous delta and B. You might say a double peak in ALT. That could be a clue, my patients have delta as well. Super infection is the patient with chronic hepatitis B who is doing well, and then out of the blue decompensates. They start with encephalopathy, ascites, and one of the possibilities is delta. What are the other possibilities? Hepatoma, portal vein thrombosis, spontaneous reactivation, seroconversion from e antigen to e antibody as a flare, and delta, which is about 4 or 5 reasons why a patient with chronic hepatitis B who is doing well suddenly decompensates. Super infection is often fatal. It can be very severe.
Number developing primary hepatocellular carcinoma unknown The characteristic clinical features of hepatitis C, can be summarized as follows:
1) It has an incubation period of 2-22 weeks; and ultra-short incubation period of 4 days to 4 weeks has been reported in hemophiliacs
2) The acute disease is clinically indistinguishable from acute hepatitis A or hepatitis B virus infection 3). In the United States, it accounts for a significant percentage (20%) of sporadic acute viral hepatitis 4). One of the characteristic features of chronic hepatitis C hepatitis is the cyclical pattern of transaminase elevations.
The hepatitis C virus is in the togavirus family. It is enveloped, sensitive to lipid solvents, and 50-60 nm in diameter. It contains a linear, single-stranded RNA and bears no genomic homology to hepatitis B virus, hepatitis D virus, or retroviruses. Hepatitis C virus is a major cause of acute and chronic hepatitis. It can also lead to cirrhosis and may be an important factor in the development of primary hepatocellular carcinoma. The putative role of chronic hepatitis C infection in primary hepatocellular carcinoma is predicated on a number of observations, including the following: 1) HBV-negative primary hepatocellular carcinoma appears to be on the rise in Japan. 2) A third of hepatitis B surface antigen-negative hepatocellular carcinoma patients have a previous history of receipt of blood transfusions. 3) HBV-negative primary hepatocellular carcinoma patients have been
shown in some studies to lack HBV DNA. 4) There are anecdotal case reports of
acute hepatitis C progressing to chronic hepatitis C, eventuating in cirrhosis and,
over a 10-20 year period, culminating in primary hepatocellular carcinoma. 5)
Some investigators have noted liver cell dysplasia in a significant proportion of
patients with chronic hepatitis C.
The hepatitis C virus antibody test is used to detect both acute and chronic HCV
infection. It takes on average three months for the antibody test to become positive
and, on occasion, may take up to a year for the antibody test to become positive in
patients with acute HCV infection. In contrast, in approximately 80-90% of patients
with chronic hepatitis C, the hepatitis C virus antibody test will be positive.
The prevalence of hepatitis C virus antibody in male homosexuals is relatively 1ow
(5%). A recent study has suggested that household and sexual contacts of chronic
HCV-infected patients do not appear to have HCV infection. Based on these
observations, it has been suggested that sexual transmission of HCV is most
inefficient.
The major factors in community-acquired HCV infection include blood
transfusions, intravenous drug abuse, and inapparent percutaneous exposure.
Vertical transmission (mother-to-infant transmission) appears to be uncommon. It is
possible that HCV infection is more likely to be transmitted if the mother also has
HIV infection.
With the current availability of the HCV antibody, and the use of autologous blood,
it is estimated that in 1996, post-transfusion hepatitis will occur in 1% or less of
recipients.
Recent studies have established a key role for HCV in the pathogenesis of at least
some cases of essential mixed cryoglobulinemia (EMC). EMC is a multisystem
syndrome more common in women. Characteristic features include purpura,
arthritis, neuropathy, vasculitis, and glomerulonephritis. HCV RNA has been noted
to be present not only in the serum, but also in cryoprecipitates from patients with
EMC. In addition, the disappearance of cryoglobulinemia, with successful alfa
interferon therapy, strengthens the case of the role of this virus in the pathogenesis
of this syndrome.
Hepatitis C also has been reported to be an important pathogenetic factor of the
liver disease present in patients with porphyria cutanea tarda.
There are three antigen-antibody systems related to hepatitis B Hepatitis B surface Hepatitis B surface antigen is a spherical particle about 22 nm in size. This is extra core material was not incorporated during the assembly of the virus during its replication within the liver. The actual virus is 42-nm donut shape particle called the Dane particle. It contains a core surface antigen, core antigen, e antigen, DNA polymerase, and DNA. Then 3 antigen antibodies systems related to hepatitis B are surface antigens, core antigen, and e antigen. The Corresponding antibodies are surface antibody, core antibody, and e-antibody.
