Viral hepatitis diagnosis

Since cases of hepatitis E are not clinically distinguishable from other types of acute viral hepatitis, diagnosis is made by blood tests which detect elevated antibody levels of specific antibodies to hepatitis E in the body or by reverse transcriptase polymerase chain reaction (RT-PCR). Unfortunately, such tests are not widely available. 

At the second consultation, the patient said that he felt better but the GP noticed he was now clinically jaundiced (yellow discolouration of the skin and the whites of the eyes) which supported the suspicion of viral hepatitis. To confirm the diagnosis, the GP took another blood sample for analysis. The results were ... 

Hoofnagle,J.H.,andA.M.DiBisceglie,5 erc>-logic diagnosis of acute and chronic viral hepatitis. Semin Liver Dis, 1991.11 73-83. 

A 61-year-old woman developed symptoms of acute hepatitis 6 weeks after she began to take fluvastatin sodium 20 mg/day for hypercholesterolemia (3). Ultrasonography and liver biopsy confirmed the diagnosis of non-obstructive intrahepatic jaundice. Studies of viral markers and autoimmune factors excluded viral hepatitis and autoimmune hepatitis. There was a high serum concentration of a metabolite of fluvastatin, suggesting a possible anomaly of drug metabolism. All liver function tests normalized 8 weeks after the withdrawal of fluvastatin. 

Elevation of y-GT is found in cholestasis, liver cirrhosis, viral hepatitis, fatty liver, porphyria, toxic liver damage, pancreatitis and pancreatic cancer, myocardial infarction, nephrotic syndrome, diabetes mellitus, right heart failure, obesity, nicotine abuse, and brain tumours. There is a good correlation of y-GT with CEA in colon cancer, involving a metastatic spread to the liver - an increase in y-GT in neoplastic disease is likewise supportive of the diagnosis of hepatic metastases. 

Similarly, in various liver diseases, thought should be given to the presence of HE if neuropsychiatric disturbances occur. This is true for acute liver diseases (severe acute viral hepatitis, acute liver failure) and for severe (particularly alcohol-related) fatty liver, Wilson s disease, severe chronic hepatitis, severe infectious or parasitic liver diseases such as schistosomiasis, metastatic liver, nodular regenerative hyperplasia, and liver cirrhosis. (1,16,17, 22, 24,28,29, 67,76,78,95,104) The diagnosis of HE can prove difficult if the liver disease is (still) unknown. 

Direct detection of HAV and HAAg in the blood or stools is only necessary for scientific purposes. Serological diagnostics is based on the specific detection of anti-HAV IgM, the presence of which confirms acute viral hepatitis A. In differential diagnosis, it is necessary to rule out acute viral hepatitis E, with which anti-HAV IgM may likewise occur Anti-HAV IgM rises in the serum during the first 2 weeks of the disease, i. e. 3 to 4 weeks after infection. It persists for about 2 or 3... 

As with HAV infection (s. p. 421), the clinical features of viral hepatitis B can be influenced by certain courses of disease. As a result, it can prove difficult to draw up a differential diagnosis, and thus further examination becomes necessary. Some of these initially unpredictable courses of disease may be a considerable impediment to the self-limiting capacity of viral hepatitis B. (s. fig. 22.10)... 

On the whole, the histological picture resembles that of toxic hepatitis. As a result, it can be most difficult to make a differential diagnosis. In contrast to HAV and HBV infections, viral hepatitis C displays some specific histological features (310, 325, 326, 334, 358, 362, 376, 384) ... 

The diagnosis of acute viral hepatitis C is based on the following parameters, whereby especially alcoholic liver damage must first be ruled out (353, 377) ... 

Just as with acute viral hepatitis A and B, an HCV infection can induce extrahepatic manifestations and syndromes. (300,313,357, 358) Such associations with various diseases not only make differential diagnosis very difficult, but they also have an unfavourable influence on the course of disease in certain cases. The capability of the C virus to induce autoimmunity is of special significance, (s. tab. 22.8) (see chapter 34.6.2)... 

Lemon, S.M. Type A viral hepatitis epidemiology, diagnosis and prevention. Clin. Chemist. 1997 43 1494-1499... 

Differential diagnosis of typhoid fever includes other Salmonella infections, leptospirosis, schistosomiasis, disseminated tuberculosis, malaria, brucellosis, viral hepatitis. Yersinia enterocolitis, influenza, lymphoma, toxoplasmosis, infectious mononucleosis, tuphus, encephalopathy and connective-tissue disorders. 

Pawlotsky JM.Molecular diagnosis of viral hepatitis. Gastroenterology 2002 122 1554-1568 Perz JF, Elm JL Jr, Fiore AE, Huggler JI, Kuhnert WL, Effler PV (2006a) Near elimination of hepatitis B virus infections among Hawaii elementary school children after universal hepatitis B vaccination. Pediatrics 118 1403... 

Another emergent viral hepatitis is that causes by E virus, a single stranded RNA virus, which is endemic in many areas like North America and Asia. It can be transmitted via the faecal-oral ronte, water and also food. This virus causes acute hepatitis and it is important to distinguish it from other kind of viral hepatitis. The pathogenesis of hepatitis E is not well known and the diagnosis is actually mainly serological even if a molecular method represents that preferable to be developed. 

In normal, healthy subjects, the fasting level of serum bile acids is low imd is less than 5 p,mol/liter. This level is greatly increased in various hepatobiliary diseases (A9, B6, F2, F3, P9, S34, Til). For example, some liver diseases and their reported range of fasting serum bile acid concentrations (in brackets) are liver cirrhosis (5-100 pmol/liter), viral hepatitis (78—405 p,mol/liter), and extrahepatic biliary obstruction (5-230 p,mol/liter) (P9). An elevated serum bile acid concentration is highly specific for liver disease, but there is no specificity as to the type of liver disease. Determination of the profile of individual bile acids and calculations such as the cholic to che-nodeoxycholic acid ratio have been proposed as useful in the differential diagnosis of liver disease (P9). In practice, however, there is too much overlap between diseases, so that the pattern of serum bile acids does not normally provide useful diagnostic information. 

Immunohistochemical staining has been used in the histopathologic diagnosis of viral hepatitis C however, IFIC for this virus is not as effective as serologic assays and detection of FICV RNA in serum. 

By far the most likely diagnosis in this case is that the woman has acute viral hepatitis. 

A diagnosis of acute viral hepatitis type A was made, probably contracted from virus-contaminated food Percy had eaten while on his cruise. His physician explained that there was no specific treatment for type A viral hepatitis but recommended symptomatic and supportive care and prevention of transmission to others by the fecal-oral route. Percy took acetaminophen 3 to 4 times a day for fever and arthralgias throughout his illness. 

Percy Veere s symptoms and laboratory abnormalities did not slowly subside over the next 6 weeks as they usually do in uncomplicated viral hepatitis A infections. Instead, his serum total bilirubin, ALT, AST, and alkaline phosphatase levels increased further. His vomiting became intractable, and his friend noted jerking motions of his arms (asterixis), facial grimacing, restlessness, slowed mentation, and slight disorientation. He was admitted to the hospital with a diagnosis of hepatic failure with incipient hepatic encephalopathy (brain dysfunction caused by accumulation of various toxins in the blood), a rare complication of acute type A viral hepatitis alone. The possibility of a superimposed acute hepatic toxicity caused by the use of acetaminophen was considered. 

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