Cirrhosis complete

The morphological spectrum may therefore range from steatosis, acute hepatitis, fulminant course, chronic hepatitis, aggressive episodes in chronic hepatitis and liver fibrosis through to micronodular cirrhosis. Complete cirrhosis can already exist in children aged 4-5 years. The development of hepatocellular carcinoma is extremely rare (360) it is assumed that copper has a protective effect against malignant transformation. (391,393)... 

Infection with one or more strains of viral hepatitis often causes acute inflammation of the liver, while chronic infection with hepatitis B or C can lead to cirrhosis. Hepatitis B and C are common in intravenous drug users and can also be transmitted through sexual contact, but many cases of hepatitis C are idiopathic.5,6 Hepatitis C is a more common cause of cirrhosis than hepatitis B in the United States while hepatitis B is more common in the rest of the world.7 See Chapter 21 on viral hepatitis for a complete discussion of infectious hepatitis. 

Obviously the best treatment for cirrhosis is removal of the injurious event. In the case of viral hepatitis, viral load can at least be temporarily reduced with anti-viral agents such as lamivudine, ribavirin and/or IFNa [76]. Unfortunately, complete removal of the injurious event is frequently not possible. Moreover, by the time cirrhosis is diagnosed the fibrotic process has usually progressed beyond the point of no return and removal of the injurious event will have little effect. Successful pharmacological treatment to reverse the fibrotic... 

Reversibility of Noncarcinogenic Systemic Effects. Most case reports of humans intoxicated with carbon tetrachloride indicate that, if death can be averted, clinical signs of renal and hepatic dysfunction diminish within 1-2 weeks, and recovery often appears to be complete. This is primarily because both liver and kidney have excellent regenerative capacity and can repair injured cells or replace dead cells (Dragiani et al. 1986 Norwood et al. 1950). However, high doses or repeated exposure can lead to fibrosis or cirrhosis that may not be reversible. The depressant effects of carbon tetrachloride on the central nervous system do appear to be reversible, although any neural cell death that occurs (Cohen 1957) is presumably permanent. 

Rapidly and almost completely absorbed after PO administration. Protein binding 20%. Extensively metabolized in the liver to active metabolite (reduced in patients with advanced cirrhosis). Primarily excreted in urine. Minimally removed by hemodialysis. Half-life 6-7 hr. 

This disorder usually disappears after several weeks, with a complete return to normal liver function expected. Rarely, a longer-lasting exanthematous biliary cirrhosis occurs, characterized by a more chronic course of 6 months to 1 year, but also eventually clears. This may be an allergic phenomenon, as evidenced by ... 

In contrast to the treatment of patients with chronic HBV infection, the primary goal of treatment in patients with HCV infection is viral eradication. In clinical trials, the primary efficacy end point is typically achievement of sustained viral response (SVR), defined as the absence of detectable viremia for 6 months after completion of therapy. SVR is associated with improvement in fiver histology and reduction in risk of hepatocellular carcinoma and occasionally with regression of cirrhosis as well. Late relapse occurs in less than 5% of patients who achieve SVR. 

Hepatic Effects. Chromium(VI) has been reported to cause severe liver effects in four of five workers exposed to chromium trioxide in the chrome plating industry. Derangement of the cells in the liver, necrosis, lymphocytic and histiocytic infiltration, and increases in Kupffer cells were reported. Abnormalities in tests for hepatic dysfunction included increases in sulfobromophthalein retention, gamma globulin, icterus, cephalin cholesterol flocculation, and thymol turbidity (Pascale et al. 1952). In a cohort of 4,227 workers involved in production of stainless steel from 1968 to 1984, excess deaths were observed from cirrhosis of the liver compared to expected deaths (0/E=55/31.6) based on national rates and matched for age, sex, and calender time having an SMR of 174 with confidence limits of 131-226 (Moulin et al. 1993). No measurements of exposure were provided. Based on limited information, however, the production of chromium compounds does not appear to be associated with liver effects. As part of a mortality and morbidity study of workers engaged in the manufacture of chromium(VI) compounds (84%) and chromium(III) compounds (16%) derived from chromium(VI) in Japan, 94 workers who had been exposed for 1-28 years were given a complete series of liver function... 

A 31-year-old white man with depression, hepatitis C, and cirrhosis of the liver was hospitalized for alcohol detoxification. He had taken methadone 50 mg bd for opium dependence for 6 months. He developed bilateral pedal edema and 27 kg weight gain. There was no ascites, portal hypertension, or congestive heart failure. Most of his laboratory tests were within the reference ranges, except for reduced prothrombin time and platelet count. After stopping alcohol, his methadone dose was reduced to 60 mg/day his edema resolved 15 days later. When the dose of methadone was increased to 70 mg/day there was a progressive increase in the edema. When methadone was withdrawn his edema completely resolved and he lost 8 kg in 2 weeks. 

Absorption of theophylline from the gastrointestinal tract is usually rapid and complete. Some 90% is metabolised by the liver and there is evidence that the process is saturable at therapeutic doses. The tis 8 h, with substantial variation, and it is prolonged in patients with severe cardiopulmonary disease and cirrhosis. Obesity and prematurity are associated with reduced rates of elimination, whereas tobacco smoking enhances theophylline clearance by inducing hepatic P450 enzymes. Because of these pharmacokinetic factors and low therapeutic index, monitoring of the plasma theophylline concentration is necessary to optimise its therapeutic effect and minimise the risk of adverse reactions the optimum concentration range is 10-20 mg/1 (55-110 mmol/1). 

Caffeine is completely absorbed within the intestine, and about 97% is metabolized selectively by the liver - relatively independently of perfusion - by way of microsomal demethylation (E. Renner et af, 1984). After intravenous administration of 125 mg caffeine (with 125 mg sodium benzoicum) - equivalent to 1 cups of coffee -a plasma caffeine increase was detected in liver patients, corresponding to the limited demethylation capacity via paraxanthin. The prolongation of half-life and the limitation of plasma clearance (PC) were clearly altered in patients suffering from cirrhosis. The result can be influenced by age, smoking, contraceptives and numerous medicaments, etc. The test shows no side effects, it is cost-favourable and easy to carry out. (56, 70, 73,81,87)... 

The criteria for the development and completion of liver cirrhosis can be assessed according to their importance ... 

Total abstinence from alcohol renders the prognosis considerably more favourable some 30% of patients enjoy a return to full health a further 50-60% develop a chronic course lasting several years, whereby approx, half of this latter group ultimately experience complete recovery. Cirrhosis is found in some 20% of all patients. 

The prognosis for alcoholic fatty liver is good when abstention is uncompromisingly maintained, and complete reversibility can be expected within a few weeks or months. In contrast, alcoholic hepatitis has a fatal outcome in 10-20% of cases. When alcohol consumption is continued, about 40% of patients develop cirrhosis, while some 60% persist for several years. However, when alcohol abstention is maintained, only 15-20% of cases develop cirrhosis, some 50-60% persist for up to 3 years, and 20-30% recover completely. Half of the persistent cases normalize again. There is a five-year survival rate in 50-70% of patients (depending on severity), with the mortality rate remaining almost constant after the third year. In alcoholic cirrhosis, the two-year mortality rate can reach 85% with continued alcohol consumption, but falls to 10% with strict abstention. (2)... 

While the formation of nodes is a typical finding on the liver surface (s. figs. 28.13 35.2-35.4), in sectional preparations (s. fig. 35.5) and under the microscope (s. fig. 35.4), it is not an obligate criterion. It is hardly recognizable in many cases, such as in haemochromatotic, biliary and alcoholic cirrhosis. Smooth cirrhosis, showing a smooth liver surface despite complete transformation, is likewise found it is micronodular and poor in fibres, (s. fig. 14.3)... 

Fig. 35.2 Complete, coarse-nodular liver cirrhosis due to chronic viral hepatitis B...

Fig. 35.3 Complete, coarse-bulbous cirrhosis after years of alcohol abuse and superimposed acute viral hepatitis B, showing a chronic course. Mild tendency towards cholestasis pronounced subcapsu-lar vascularization and vascular stasis. Occasional funnel-shaped parenchymal depressions...

Fig. 35.4 Complete, micronodular, progressive liver cirrhosis with formation of pseudoacini (Sirius red)...

Fig. 35.5 Complete, micronodular to medium-nodular liver cirrhosis after chronic viral hepatitis B (section, native preparation)...

Fig. 35.6 Complete, mixed-nodular (toxin-induced) liver cirrhosis due to years of alcohol abuse and long-term oxyphenisatin abuse...

Another important criterion is to determine whether the nodular transformation in the liver is complete or incomplete. This morphological characteristic can be found both in progressive and stationary cirrhoses. In complete cirrhosis, the parenchyma is completely partitioned by connective tissue septa. The collapse of fibres (due to portocentral bridging necroses) results in the development of portocentral septa (= passive septa). Due to the spreading of the inflammation to the periportal parenchyma, septa develop and branch out from the portal fields (= active septa). Generally, they lead to capillarization of the sinusoidal walls as well. (s. fig. 35.7) Incomplete cirrhosis only displays the formation of short septa (= subsepta), so that there are areas of incomplete (partial) subdivision of the parenchyma. 

Fig. 35.10 Splenic infarction in splenomegaly due to complete liver cirrhosis. (Postpartum blood transfusion into the umbihcal vein, with subsequent severe viral hepatitis B and rapid transition into early infantile cirrhosis)...

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