Hepatocellular inflammation

Jean Ann Tonich. Jean Ann Tonich s signs and symptoms, as well as () her laboratory profile, were consistent with the presence of mild reversible alcohol-induced hepatocellular inflammation (alcohol-induced hepatitis) superimposed on a degree of irreversible scarring of liver tissues known as chronic alcoholic (Laennec s) cirrhosis of the liver. The chronic inflammatory process associated with long-term ethanol abuse in patients such as Jean Ann Tonich is accompanied by increases in the levels of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Her elevated bilirubin and alkaline phosphatase were consistent with hepatic damage. Her values for ALT and... 

Primary biliary cirrhosis is characterized by progressive inflammatory destruction of the bile ducts. Immune-mediated inflammation of intrahepatic bile ducts results in remodeling and scarring, causing retention of bile within the liver and subsequent hepatocellular damage and cirrhosis. The number of patients affected with primary biliary cirrhosis is difficult to estimate because many people are asymptomatic and incidental diagnosis during routine health care visits is common. 

Diagnosing viral hepatitis may be difficult because most infected individuals are asymptomatic. Because symptoms cannot identify the specific type of hepatitis, laboratory serologies must be obtained (Table 21-2). In addition, liver function tests may be obtained to assess the extent of cholestatic and hepatocellular injury. However, the definitive test to determine the amount of damage and inflammation of hepatic cells is a liver biopsy. 

A wide spectrum of hepatic lesions has been reported in AIDS (H4), but it is not known whether the changes are related to the presence of HIV-1. Therefore, sections from livers of autopsied patients with AIDS were examined for the presence of HIV-1 antigen p 24 (core) and gp 41 (envelope) by the avidin-biotin-peroxidase complex methods using monoclonal antibodies. The most common histologic abnormalities were steatosis, portal inflammation, Kupffer cell hyperplasia, and focal hepatocellular and bile duct damage. Immunoreactivity for HIV-1 antigens was demonstrated in 80% of cases. 

In a follow-up study in mice, exposure to DEA, via drinking water or by topical application, caused dose-dependent toxic effects in the liver (hepatocellular cytological alterations and necrosis), kidney (nephropathy and tubular epithelial necrosis in males), heart (cardiac myoqn e degeneration), and skin (site of application ulceration, inflammation, hyperkeratosis, and acanthosis). Doses ranged from 630 to 10,000 ppm in the drinking water and from 80 to 12 50 mg/kg in the topical application study. 

Toxicology. Pentachloroethane is an irritant of the eyes and respiratory tract and may cause mild narcosis chronic exposure causes hepatocellular carcinomas in mice and inflammation of the kidneys in rats. 

Hepatic cirrhosis is an end stage process of hepatic inflammation characterised by lobular scarring, distortion of the hepatocellular architecture and disordered function, frequently with associated portal hypertension. 

Allergic reactions to drugs produce foci of necrosis that are scattered throughout the liver. Other agents cause severe (chlorpromazine) or mild (estrogens) cholestatic liver damage, including cholestasis and inflammation of the portal triad and hepatocellular necrosis. 

Barr virus confirmed that he had infectious mononucleosis. He was kept in bed for 2 weeks, by which time the signs of inflammation and hepatocellular damage entirely disappeared. However, mild anemia (hemoglobin 110-120 g/L) with reticulocytosis (50%-6.0%), increased serum unconjugated bilirubin, and splenomegaly still remained, suggesting the presence of persistent hemolysis. The physician therefore performed further examinations to confirm the diagnosis of hemolytic anemia. 

Pathologic changes included inflammation of the respiratory tract, minor hepatocellular cytoplasmic changes. 

Injury to the hepatocytes, for example by hepatotoxins or viruses, will result in hepatocellular damage. This generally manifests itself as fatty infiltration (steatosis), inflammation (hepatitis) or cell death (necrosis). If the assault is mild and remits, the liver will recover and overall liver function will remain normal. Snstained injnry causing hepatocyte cell death will, however, nltimately lead to fibrosis and cirrhosis and potentially severe liver dysfimction. 

Isolated cases of chronic paracetamol toxicity have been reported, such as hepatocellular necrosis, hepatic inflammation and fibrosis. These cases occurred in patients taking 2-6 g of paracetamol daily for months... 

Hepatic lesions in the case of yellow fever are more likely to correspond to those of hepatosis, (s. p. 404) There is also evidence of distinct acidophilic hepatocellular necrosis as well as microvesicular fatty degeneration of the hepatocytes. Hyaline, eosinophilic inclusions in the cytoplasm of degenerated hepatic cells (so-called Councilman bodies) are characteristic and were first identified by w.T. Councilman in 1890 in yellow fever (s. p. 396). Acidophilic inclusion bodies in the hepatocellular nuclei which are arranged concentrically around the nucleolus (so-called Torres corpuscles) correspond to the yellow fever virus (C.M. Torres, 1928). The liver does not present any significant signs of inflammation. The reticular fibre structure is maintained, so that the liver architecture is usually completely restored-provided the outcome of the disease is favourable, (s. fig. 23.4)... 

Lobular inflammation Whereas lobular, diffusely distributed inflammation is more evident, in acute hepatitis portal and periportal inflammation predominates in chronic hepatitis and lobular hepatitis is less pronounced. Generally, it consists of separate small clusters of mononuclear cells. Scattered necrotic hepatocytes (= acidophilic / Councilman bodies) are found the hepatocellular nuclei are in disarray (= anisonucleosis) there is swelling of the hepatocytes, and mitoses are present. Marked lobular hepatitis in conjunction with considerable portal and periportal inflammation is typical of flares of chronic viral hepatitis or autoimmune hepatitis. In addition to single-cell necroses, there are confluent necroses, which affect entire lobules. Bridging necroses link portal tracts with other portal tracts or with terminal venules, (l)... 

A 27-year-old Hispanic man presented with nausea and vomiting, diarrhea, and upper abdominal pain 12 months after starting to take chaparral capsules. A liver biopsy showed hepatocellular injury with necrosis and periportal inflammation. His liver function stabilized after withdrawal of chaparral. 

CosgroveBD, KingBM, Hasan MA, etal. Synergistic drug-cytokine induction of hepatocellular death as an in vitro approach for the study of inflammation-associated idiosyncratic drug hepatotoxicity. Toxicol Appl Pharmacol. 2009 237(3) 317-330. 

The skin lesions are often the first sign of underlying liver cell damage. Clinically, overt liver disease is uncommon, but minor alterations in biochemical tests of liver function are present in more than 50% of patients. Needle biopsy of the liver reveals hepatic siderosis in most patients, usually accompanied by minor histopathological abnormalities nfild fatty infiltration, focal necrosis of hepatocytes, and inflammation of portal tracts. Cirrhosis is unusual, being present in less than 15% of patients, but carries a high risk of hepatocellular carcinoma. 

Epidemiological evidence points to a connection between long-term inflammation and the development of cancer that is characterized by dysplasia, hyperplasia, and sometimes irreversible cancer transformations. Nearly 15% of worldwide cancer incidence in humans is associated with microbial infection (Kuper et al. 2002). Chronic infections, with human papilloma virus or with hepatitis B or C viruses in immunocompetent human hosts, can lead to cervical and hepatocellular carcinomas, respectively. Infection with the human herpes virus can produce Kaposi s sarcoma in the skin. Karposi s cancers are seen more often in the IDS-compromised AIDS patients. After protracted inflammation, Helicobacter pylori can cause stomach irrita-... 

Decreased liver weights, liver body weight ratio, SGPT activity in male rats decreased SGPT activity, presence of liver nodular hyperplasia in high-dose female rats decreased incidence of adenomas in male high-dose mice increased liver inflamm atory infiltrates, incidence of hepatocellular adenomas in high-dose female mice... 

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