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Causes of liver disease and dysfunction

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. [Pg.50]

The liver is the principal organ of fat metabolism and, as a result, damage to the hepatocytes can disrupt normal fat metabolism and lead to steatosis the accmnnlation of fat within the hepatocytes. Steatosis or fatty liver can be classified into two categories based on the size of the fat droplets deposited within the hepatocyte microvesicular or [Pg.50]

This occurs typically in alcoholic steatosis. Macrovesicular steatosis has less effect on the function of the hepatocyte and liver function tests are usually only minimally abnormal. The accumulation of fat within the hepatocyte may trigger an inflammatory response this inflammation within the hepatocyte, or hepatitis related to steatosis, is termed steatohepatitis. Continued inflammatory responses further damage hepatocytes, and the liver disease may then progress to fibrosis and cirrhosis. [Pg.51]

Liver disease is defined as being acute when the history of the onset of symptoms does not exceed six months. The most common causes of [Pg.52]

Alcohol intake is the most important cause of liver cirrhosis in the Western world [2]. Data from the World Health Organization show that the incidence of chronic liver disease and cirrhosis associated with alcohol in the UK is 10.42 per 100 000 people [3]. Interestingly, only around [Pg.54]


Infection with SENV-D and -H adversely affected the outcome of antiviral therapy for HCV (572), whereas in another study SENV did not influence the clinical or histological features of HCV at all. (577) SENV infection is not associated with increased evidence of liver disease or the risk of HCC. (576, 579) Likewise, this virus does not play any role in graft dysfunction after liver transplantation, although SENV was found in 35% of unselected liver transplant recipients. It is possible that SENV is a causative agent of posttransfusion-associated hepatitis, especially since specific DNA could be detected in liver tissue. [Pg.451]

The acquired causes of hyperammonemia are advanced liver disease and renal failure. Severe or chronic liver failure (as occurs in fiilminant hepatitis and cirrhosis, respectively) leads to a significant impairment of normal ammonia metabolism. Reye s syndrome, which is primarily a central nervous system disorder with minor hepatic dysfunction, is also associated with hyperammonemia. Hepatic en-... [Pg.1790]

Use of anabolic steroids in attempting to improve athletic strength can cause numerous side effects in males—a reduction in testicle size, low sperm count and infertility, male pattern baldness, and breast development in females—facial hair, deepening of the voice, male pattern baldness, breast atrophy, and menstrual dysfunction. Possible long-term consequences of anabolic steroid use in both men and women include liver disease and tumors, depression, and heart complications, with an increased risk of prostate cancer for men. [Pg.537]

Defects of complex IV. These disorders, also termed COX deficiency, have clinical phenotypes that fall into two main groups one in which myopathy is the predominant or exclusive manifestation and another in which brain dysfunction predominates (Fig. 42-3). In the first group, the most common disorder is fatal infantile myopathy, causing generalized weakness, respiratory insufficiency and death before age 1 year. There is lactic acidosis and renal dysfunction, with glycosuria, phosphaturia and aminoaciduria, also termed DeToni-Fanconi-Debre syndrome. The association of myopathy and cardiopathy in the same patient and myopathy and liver disease in the same family has also been described [14]. [Pg.710]

On rare occasions, pemoline can cause a chemical hepatitis (liver dysfunction). For this reason, patients with known liver disease should not be prescribed pemoline. A baseline laboratory assessment of liver enzymes before starting therapy with pemoline is advised, and liver function monitoring must be repeated periodically. If liver abnormalities are detected, then pemoline must be discontinued. The recognition of this side effect resulting from therapy with pemoline has markedly restricted its use. [Pg.279]


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