Liver necrosis pathology

Aragno M, Tamagno E, Danni O, et al. 1992. In wVo studies on halogen compound interactions. III. Effect of carbon tetrachloride plus 1,2- dichloroethane on liver necrosis and fatty accumulation. Research Communication in Chemical Pathology and Pharmacology 76 341-354. 

Aminlari, M., T. Vaseghi, M. J. Sajdianfard, and M. Samsami. 1994. Changes in arginase, aminotransferases and rhodanes in sera of domestic animals with experimentally induced liver necrosis. Journal of Comparative Pathology 110 1-9. 

Elevations of serum iron occur in various other pathological conditions hemolytic anemia, lead toxicity, pyridoxine deficiency, pernicious anemia, acute liver necrosis, and iron poisoning. Serum transferrin levels usually decrease in these cases and the percent saturation increases in response to increased iron in the extracellular fluid. Desferrioxamine, a siderophote from actinomycetes, has been used to treat patients with acute iron toxicity (30,31]. The toxicity of iron was reviewed in a previous volume of this series [6]. 

The lesions produced in avitaminosis E vary greatly, depending upon the animal used for the experimentation. The pathological observation can be classified into four main groups interference with reproduction muscular degeneration pigment formation in adipose tissue and liver necrosis. 

In the course of studies on other pathological amino acidurias, the accompanying peptiduria has also been observed by many authors. Rapp de Eston et al. (R2) observed a marked increase in the excretion of both free amino acids and peptides in patients with diffuse hepatic necrosis. Using a simplified chromatographic method adapted to clinical purposes and suitable for analysis of amino acids excreted with urine, Skarzynski et al. (S5) demonstrated a raised level of a certain peptide which is always present in normal urine in smaller quantities, as well as the appearance of some new peptides in cases of jaundice and liver cirrhosis. Some abnormal peptide spots were also detected on the chromatograms in cases of progressive muscular dystrophy (K4) and in patients irradiated with X-rays (S2). 

However, as well as the changes going on in the hepatocyte, other events contribute to the hepatic necrosis such as the Kupffer cells. These release chemical mediators that contribute to the pathological response. Changes to the microcirculation of the liver also seem to play a part as indicated by the role of nitric oxide. 

---