Cirrhosis systemic complications

Liver transplantation may be indicated in patients with considerable cirrhosis-related complications. However, NASH can also reoccur in the transplanted liver. (45, 63) This observation points to a systemic disorder of the lipid metabolism. 

Acetyls alley lie acid was shown to prevent cirrhosis under certain experimental conditions [125]. Naproxen and indomethacin partially protected against LPS and D-galactosamine-in-duced hepatotoxicity [126] Acetylsalicylic acid and ibuprofen were also protective in endo-toxic shock [127]. Endotoxaemia is one of the complications in cirrhotic patients [128] and is probably caused by an impaired ability of the liver to take up and detoxify gut-derived LPS [116]. The presence of portosystemic shunts in cirrhotic patients may also contribute to this spill-over of LPS into the systemic circulation [129]. NSAIDs, however, are also reported to provoke deleterious effects on renal function in cirrhosis [130], and can therefore not be used in cirrhotic patients. Cell-specific delivery of NSAIDs to SECs and/or KCs may make application of these drugs in cirrhosis feasible by circumventing the renal side-effects. 

The use of lUDs in patients with CLD has complicating factors. Owing to reduced hepatic complement synthesis and reticuloendothelial system dysfunction, patients with cirrhosis and ascites are prone to develop repeated episodes of spontaneous bacterial peritonitis (SBP). Historically, the risk of pelvic inflammatory disease (PID) was considered to be increased in lUD users during the first year after insertion, therefore it was thought that the presence of an lUD in approximation with the peritoneal surface in a patient with cirrhotic ascites might lead to SBP... 

Wong, F., Blendis, L.M. Ascites and portal-systemic encephalopathy as complications of cirrhosis. Curr. Opin. Gastroenterol. 1993 9 391-396... 

There is also a significantly increased incidence of IgA deficiency in patients with autoimmune or potentially autoimmune disorders, and usually it is not clear which came first. It can be argued that autoimmunity is a complication of immune imbalance subsequent to inborn IgA deficiency (H24). With inborn absence of IgA, exposure to normal human colostrum, plasma, and saliva can result in the production of antibodies to IgA. By the time such patients are discovered the etiological mechanisms are often obscured and IgA treatment is out of the question. The incidence of IgA deficiency is known to be 1-4% in the following conditions Still s disease, systemic lupus erythematosus, rheumatoid arthritis, Sjogren s disease, warm hemolytic anemia, megaloblastic anemia, idiopathic pulmonary hemosiderosis, thyrotoxicosis, and cirrhosis. 

Alcoholism affects about 10% of the drinking population and alcohol (ethanol) abuse has been implicated in at least 20% of admissions to general hospitals. This chronic disease exhibits high mortality due to a wide variety of factors. Ethanol produces effects in virtually every organ system. The biochemical effects of ethanol are due to increased production of NADH that decreases the [NAD ]/[NADH] ratio in the cytoplasm of liver cells at least tenfold from the normal value of about 1000. Increased production of lactate and inhibition of gluconeo-genesis (Chapter 15) result. The hyperuricemia associated with ethanol consumption has been attributed to accelerated turnover of adenine nucleotides and their catabolism to uric acid (Chapter 27). Alcohol increases hepatic fatty acid and triacylglycerol synthesis and mobilization of fat from adipose tissue, which can lead to fatty liver, hepatitis, and cirrhosis. These effects are complicated by a deficiency of B vitamins and protein. 

Hepatic encephalopathy is a common complication of cirrhosis and requires clinical vigilance and treatment with dietary restriction, elimination of central nervous system depressants, and therapy to lower ammonia levels. 

Rare complications of liver cirrhosis are chronic persistent hepatic encephalopathy and hepatic myelopathy. Both occur in less than 1% of the patients, and both are accompanied by extensive porto-systemic shunts. Chronic persistent hepatic encephalopathy is also known as acquired hepato-lenticular degeneration (Victor, Adams and Cole, 1965). In contrast to the nsnal cirrhotic patient with HE, these patients show obvions neuronal alterations a patchy, spongy degeneration most consistently observed in the deep layers of the cerebral cortex and subcortical white matter, particularly in the parieto-occipital cortex, basal ganglia and cerebellum. 

In a large retrospective multicenter study by Pic-ciNiNO et al. (1986) including 68,276 fiver biopsies with a Tru-Cut system, a complication rate of only 0.4% was found. Deaths after fiver biopsy were rarely observed, usually due to hemoperitoneum in patients with malignant disease or cirrhosis. The rate of tumor cell seeding after percutaneous tumor puncture of hepatocellular carcinoma (HCC) has been reported to be in the range between 1% (Llovet et al. 2001) and 5% (Takamori et al. 2000). In biopsy of subcapsular lesions, the rate can even increase up to 12% (Llovet et al. 2001). 

Chemoembolization can be used in patients with ether primary or metastatic malignant hepatic tumors who are not surgical candidates (Table 2.5.1). Surgery is not feasible in advanced malignant disease involving both lobes of the liver, or complicating factors such as cirrhosis or failure of systemic chemotherapy. Likewise, TACE should be reserved for those patients who have liver-dominant disease, because the predominant effect is local. 

Persons aged 2 to 64 years who are at increased risk for pneumococcal disease or its complications if they become infected should be vaccinated. Persons at increased risk for severe disease include those with chronic illness such as chronic cardiovascular disease (e.g., congestive heart failure [CHF] or cardiomyopathies), chronic pulmonary disease (e.g., chronic obstructive pulmonary disease [COPD] or emphysema, and asthma that occurs with chronic bronchitis, emphysema, or long-term use of systemic corticosteroids), diabetes melli-tus, alcoholism, chronic liver disease (cirrhosis) (36-39), or cerebrospinal fluid leaks. 

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