Hepatic damage/disease detection

Biomarkers of Disease. Since acute NDMA poisoning in humans caused severe liver disease, sensitive clinical biochemistry liver function tests might detect early hepatic damage from toxic exposure to NDMA. Recently,... 

In a variety of liver diseases, it often happens that only certain partial functions or cellular structures are impaired this impairment can differ widely in intensity and extent in the individual patient. Therefore, when applying only a few biochemical tests, pathological changes may well be overlooked. For the detection of hepatocellular damage or disorders of hepatic functions, a variety of examination methods will have to be employed in order to provide a comprehensive assessment derived from the various single findings. 

Central venules only contain a small amount of collagen, with the result that in this form of fibrosis, perivenous sinusoids are always involved as well. A typical example is perivenular fibrosis in chronic alcohol abuse, (s. fig. 21.16) Centrolobular fibrosis may also be detectable in healed viral hepatitis or following slight liver damage (e.g. Meulengracht s disease). Central hyaline sclerosis, which is due to chronic alcohol abuse with intermittently recurring alcohol hepatitis, is known to be a particularly severe form of fibrosis, (s. p. 526)... 

HBsAg-negative/anti-HBs-positive course This rare course of disease can occasionally be detected in fulminant hepatitis with rapid elimination of the virus, in cases of infection with HBV mutants, in HDV superinfection with suppression of the HBV infection and in non-apparent HBV infection in patients suffering from alcohol-related liver damage. 

Non-specific toxic liver damage may be evident in this connection, possible tuberculostatic toxic effects must also be considered. With severe courses of tuberculosis, peliosis hepatis is often observed. Frequently, retothelial nodules are detectable, as demonstrated for the first time in tuberculosis patients by H. Hamperl in 1953. (50) In the course of chronic pulmonary tuberculosis,infiltration of liver cells was noted, as reported in several publications. (50) It was attributed to toxic effects and/or undernourishment or malnutrition. Secondary hepatic amyloidosis, developing in the course of chronic lung tuberculosis, has also been postulated. (50) A restriction of hepatic function in chronic tuberculosis, which was first observed by E. Leuret et al. in 1922, has been described in a number of publications. (51, 60, 63) Depending on the severity and duration of the disease as well as the tuberculostatic pretreatment, we found pathological laboratory parameters in 15-20% and 25-40% of cases respectively. (50)... 

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