Liver cell necrosis

Systemic treatment of 13-cis retinoic acid frequently leads to cheilitis and eye irritations (e.g., unspecific cornea inflammation). Also other symptoms such as headache, pruritus, alopecia, pains of joints and bone, and exostosis formation have been reported. Notably, an increase of very low density lipoproteins and triglycerides accompanied by a decrease of the high density lipoproteins has been reported in 10-20% of treated patients. Transiently, liver function markers can increase during oral retinoid therapy. Etretinate causes the side effects of 13-cis retinoid acid at lower doses. In addition to this, generalized edema and centrilobulary toxic liver cell necrosis have been observed. 

Another fatal poisoning occurred in a woman who intentionally ingested a capsule containing 6480 mg ethylene dibroinide [140 mg/kg]. On admission to hospital, the patient was drowsy, disoriented and jaundiced with mild hepatomegaly. She died eight days later and a post-mortem liver biopsy revealed congestion and focal liver cell necrosis (Singh et al., 1993). 

Inorganic cobalt is transported in the blood by albumin and transferrin it is taken up by the liver. The serum concentration amounts to 1.9-7.6 mmol/1. An increased value is a sign of liver cell necrosis (e. g. acute hepatitis). Its biological significance is attributed to its position as a central atom in vitamin B12 and its involvement in the release of renin and erythropoietin. 

Elevated iron, which usually corresponds to increased ferritin, is found primarily in idiopathic haemochromatosis and secondarily in acute viral hepatitis, liver cell necrosis and necrotic episodes, alcoholic liver diseases, porphyria cutanea tarda, oestrogen administration, etc. 

Acute hepatitis In the early stages of the disease, the T2-scan shows an increase in signal intensity, whereas a prolongation of Ti tends to be observed before the occurrence of liver cell necrosis. 

Acquired liver diseases (e.g. cirrhosis, liver cell necrosis in severe shock (11), pronounced toxic liver damage, cardiac congestion (ll, 17), alcohol-related and medication-induced diseases of the liver) very frequently... 

A categorization of the clinical picture of HE is not liver-specific , but encompasses encephalopathy and its multiple aetiological aspects. Similarly, the phenomena of the individual stages do not allow conclusions to be drawn as to the type of liver coma (liver cell necrosis or functional liver cell failure). However, the course of HE with acute liver cell necrosis is more progressive and more severe. 

Acute liver failure (ALF) is defined as an acute clinical picture with jaundice due to a most severe disorder in the liver function and/or massive liver cell necrosis which, without any pre-existing liver disease, culminates in hepatic coma (= endogenous coma) within 8 weeks. Potentially, the condition is fully reversible (C. Trey et al., 1970). In addition, coagulopathy must also be present (D.F. Schafer et al., 1989). 

Fig. 20.3 Centrilobular, two-week-old liver cell necrosis resulting from paracetamol intoxication (HE)...

Liver collapse fibrosis must be differentiated from proper liver fibrosis, which displays increased deposition of a qualitatively altered extracellular matrix. It results from a collapse of the reticular fibres following liver cell necrosis. A primary collapse arises subsequent to confluent cell-group necrosis in a previously normal parenchyma. A secondary collapse develops as a result of extensive necrosis in previously damaged parenchyma (e.g. cirrhosis). 

Confluent liver cell necrosis, possibly developing into bridging necroses (32) or multilobular (< 3% of cases) or even massive necroses in B, B/D and C hepatitis, as well as in E hepatitis during pregnancy collapse of the lattice fibre network. Formation of passive septa, cholestasis, accumulation of ceroid and siderin in macrophages and stellate cells. 

Escherichia coii In the case of sepsis, the occasionally massive endotoxinaemia may lead to major liver cell damage, accompanied by jaundice. Histologically, focal liver cell necrosis, giant-cell transformation, inflammatory infiltrations and signs of cholestasis are detectable. Escherichia coli is the most frequent causative agent of liver abscesses, followed by Friedlander s bacillus and Yersinia enterocolitica. In the case of bacteraemia, a toxic shock syndrome can develop with a so-called chol-angiolitis lenta (M. Vyberg et af, 1984). 

Jaundice is often observed. Histologically, signs of nonspecific reactive hepatitis with spotty liver cell necrosis are generally detectable. (87-90)... 

Liver amoebiasis The propagation of amoebae in the liver leads to focal liver cell necrosis, which regresses spontaneously. Eurther episodes of focal necrosis may follow. Occasionally, granulomas are formed as well. The liver is generally enlarged and sensitive to pressure. The transaminases are slightly elevated. This involvement is called nonsuppurative amoebiasis of the liver. Liver amoebiasis does not lead to cirrhosis. (There is no evidence of hepatitis , chronic non-suppurative hepatitis or chronic amoebic hepatitis .)... 

In children and adults, signs of non-specific reactive hepatitis have also been observed. (42, 47) Acidophilic liver cell necrosis occasionally develops, depending on the type of red corpuscles. The endothelial cells are distended, the portal zones show inflammatory infiltration and granulomas or retothelial nodules are frequently found, (s. fig. 25.4) The pathogens can be demonstrated in the liver. Cirrhosis may develop, especially after the destruction of the lobular architecture as a sequela of extensive parenchymal necrosis. There are various serological tests available, including the Sabin-Feldmann... 

Kava extracts can, if overdosed (>60-120 mg kavapyr-ones/day) and/or taken over a longer period (>3 months), cause hepatotoxicity in the form of hepatic reactions and liver cell necrosis in rare cases, they may even cause cholestasis and acute liver failure (possibly leading to liver transplantation). Risk factors include the concomitant intake of medicaments and alcohol as well as a genetically based deficiency of cytochrome P450 2D6. (99, 116)... 

Chlorinated halogenated hydrocarbons can be taken up via the respiratory tract and via the skin (even perorally in suicide attempts). In addition, they are also dangerous in their solid form. The so-called perna disease is named after an insulating material mainly consisting of perchloronaphthalene . This substance, which is commonly used in the electrical industry, produces toxic vapour during soldering that may cause severe liver cell necrosis and acute liver dystrophy. 

Isomers of hexachlorocyclohexane (HCH) are found in air, soil, water, food and even breast milk. Lindane is used in large quantities in agriculture and forestry as a wood preservative as well as in veterinary medicine. Provided that the required safety measures are adhered to, no liver damage occurs during the production of lindane. On the other hand, liver cell necrosis was observed in animal experiments after HCH isomers were added to the feed a carcinogenic effect was seen after long-term administration. An increased toxic potential is to be expected when there is simultaneous exposure to DDT, PCB, contraceptives, etc. 

Lead Lead poisoning (= saturnism) results in mild, rapidly regressive toxic hepatitis in about 30% of cases. Occasionally, eosinophilic, acid-resistant inclusions are found in the nuclei of the liver cells (so-called lead protein complexes). Steatosis and liver-cell necrosis have also been witnessed. Although there is a correlation between exposure to lead and severity of damage, individual sensitivity to lead can nevertheless vary. In addition, lead intoxication causes an inhibition of erythrocyte 5-aminolaevulinic acid dehydratase and an induction of 5-aminolaevulinic acid synthase. This brings about the manifestation of acute intermittent porphyria. (8)... 

There have been repeated reports of intoxication by still largely unknown phytotoxins liver cell necrosis and cholestasis following the consumption of herbal medicine made from mulberry tree bark (S. Tozuka et al., 1983), liver cell necrosis (even fatal) following the intake of a root extract from the distaff thistle (G. Lemaigre et al., 1975), poisoning by a decoction from Callilepsis laureola (J. Wainwright et al., 1977) and due to mint oil (J.B. Sullivan et al., 1979). 

Babany, G., Bernuau, J., Cailleux, A., Cadranel, J.-F., Degott, C., Erlinger, S., Benhamou, J.-P. Severe monochlorobenzene-induced liver cell necrosis. Gastroenterology 1991 101 1734-1736... 

After complete saturation of the copper-binding capacity of the liver, the copper absorbed from food can no longer be taken up by the liver. This means that copper is stored in the brain, skeletal system, heart, cornea and kidneys - as is also the case when copper stored in the hepatocytes is released into the circulation on a large scale due to extensive liver cell necrosis. (339)... 

The histological components of chronic hepatitis can be evaluated semiquantitatively and summarized in a histological activity index (HAI). This index combines the values for the inflammatory infiltrate, liver cell necrosis... 

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