Stages Of Liver Damage Research Articles

A simplified method for the quantitative analysis of 99Tc(m)-GSA liver scintigraphy using spectral analysis.

The aim of this study was to develop a simplified method for quantitative analysis of liver scintigraphy with 99Tc(m)-diethylenetriamine pentaacetic acid-galactosyl-human serum albumin (GSA) using spectral analysis. Dynamic liver scintigraphy using GSA was performed in three normal volunteers and 19 patients with chronic liver disease. Dynamic data were obtained with a gamma camera for 30 min after the injection of approximately 185 MBq GSA. The rate constant for the liver uptake of GSA from the blood (Ku, min(-1)), total excretion rate (Ke, min(-1)) and non-specific volume of distribution (Vh) were obtained by spectral analysis. Vh was defined as the volume in the liver region of interest (ROI) occupied by GSA which was in equilibrium with that in the blood. It should be noted that Vh had no units, since the counts in both the liver and heart ROIs were normalized by scan length to obtain counts pixel(-1) min(-). For comparison, compartmental analysis was also performed. A receptor index (LHL15) was calculated by dividing the radioactivity of the liver ROI by that of the liver plus heart ROIs 15 min post-injection. The Ku values obtained by spectral analysis (y) agreed well with those obtained by compartmental analysis (x) (y = 0.953x - 0.013, r = 0.992, S.E.E. = 0.016 min(-1)). The Ke and Vh values obtained by spectral analysis (y) correlated significantly with those obtained by compartmental analysis (x) (y = 1.149x - 0.016, r = 0.826, S.E.E. = 0.017 min(-1) for Ke; y = 1.191x + 0.044, r = 0.975, S.E.E. = 0.021 for Vh). The Ku values obtained by spectral analysis decreased as the severity of liver disease progressed, and were non-linearly related to the LHL15 values, suggesting that Ku is more sensitive to liver damage than LHL15, especially in the early stages of liver damage. These results suggest that spectral analysis applied to dynamic liver scintigraphy with GSA provides a simple, non-invasive and useful tool for the quantitative evaluation of liver function.

Trace Elements and Chronic Liver Diseases

The relationships between chronic liver diseases and trace element (TE) contents are debated. Particularly, no defined data are available about the TE levels in viral liver disease patients with or without malnutrition. In this study we evaluated blood and plasma levels of various trace elements in patients with HCV-related chronic liver disease, at different stages of liver damage (8 patients with chronic hepatitis and 32 with liver cirrhosis) with or without malnutrition. We also studied 10 healthy volunteers as control group. We found that cirrhotic subjects had a significant decrease of blood levels of Zn and Se, independently on the nutritional status, whereas plasma levels of Fe were significantly reduced only in malnourished cirrhotic patients. Our data indicate that liver impairment is the main cause of the blood decrease of Se and Zn levels in patients with non alcoholic liver disease, whereas the malnutrition affects Fe levels only.

Effect of partial liver resection and phenobarbital on the restoration of impaired drug metabolism in carbon tetrachloride induced liver damage.

The effect of partial liver resection and phenobarbital treatment on the restoration of hexobarbital, p‐nitrobenzoic acid and p‐nitrophenol metabolism and cytochrome P‐450 content in the rat liver was studied at different stages of liver damage after administration of carbon tetrachloride for 2, 4, 8, and 16 weeks. Restoration of p‐nitrophenol conjugation was very rapid in the resected animals and 10 days after the liver resection there were no significant differences between the operated groups and unoperated saline controls. Phenobarbital increased the conjugative activity in the same way both in the controls and the carbon tetrachloride treated rats. The rate of metabolism of p‐nitrobenzoic acid prior to and following liver resection was nearly the same as that of the unoperated controls up to 8 weeks. However, after 16 weeks of treatment the metabolism of p‐nitrobenzoic acid was significantly lower than that in controls even 28 days after the liver resection. Phenobarbital treatment caused an increase in the reductase activity as early as after 8 weeks of treatment. Before resection the rate of hydroxylation of hexobarbital decreased progressively during carbon tetrachloride treatment. However, after resection the hydroxylation activity did not differ from that found in the resected controls up to 8 weeks, but 10 days after the resection the activity was only half or less as compared with the unoperated controls. Only after 16 weeks of treatment was the rate of metabolism of hexobarbital lower than that in the controls after partial hepatectomy. Phenobarbital treatment increased the rate of hydroxylation of hexobarbital. The change in cytochrome P‐450 content was nearly parallel to that of the rate of hexobarbital metabolism. Phenobarbital accelerated the restoration of cytochrome P‐450.