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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 98 patients dying with primary biliary cirrhosis only four developed hepatocellular carcinoma. It is suggested that the development of hepatocellular carcinoma is uncommon in this type of chronic liver disease because of its known female preponderance, and the fact that cirrhosis develops late in the course of the illness.
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PMID:Hepatocellular carcinoma in primary biliary cirrhosis: report of four cases. 22 Jan 48

The association of chronic liver disease with long-standing arsenic ingestion is well documented, although the spectrum and incidence of liver disease due to arsenic remain uncertain. We report two patients with chronic liver disease and arsenical skin changes that followed previous chronic arsenic ingestion. One patient developed macronodular cirrhosis and the other non-cirrhotic portal hypertension with perisinusoidal fibrosis. The latter patient developed a primary liver cell cancer. There is only one previously reported case of malignant hepatoma in a non-cirrhotic liver complicating chronic arsenicism. Lack of awareness of this uncommon but well described cause of chronic liver disease may account for a small proportion of patients with "cryptogenic" liver disease. Previous arsenic administration should be considered as a cause of chronic liver disease, especially when typical skin changes or internal neoplasia develop.
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PMID:Liver disease associated with chronic arsenic ingestion. 22 36

The activities of urea-cycle enzymes were measured in liver biopsies of patients suffering from chronic-persistent hepatitis (CPH), chronic-active hepatitis (CAH) and liver cirrhosis. Most of the activities of urea-cycle enzymes did not differ in the case of CPH as compared to controls. Chronic-active hepatitis and liver cirrhosis are associated with a significant (p less than 0.05) decrease of enzyme activity as compared to normal persons. Most of the urea-cycle enzymes are significantly decreased in patients with CAH in comparison with CPH. No significant differences can be demonstrated in the case of CAH as compared to patients with complete cirrhosis. In conclusion, progression of chronic liver disease is associated with increasing alterations of enzyme activities catalyzing a liver specific metabolic pathway. The decrease of the activities of the key enzymes of the urea cycle (Carbamylphosphate-Synthetase and Arginino-succinate-Synthetase) is nearly identical both in CAH and liver cirhosis, although CAH may be a reversible disease. Therefore, marked alterations in the metabolic pathway of ammonia detoxification seem to preceed the histological manifestation of irreversible liver damage.
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PMID:Activities of urea-cycle enzymes in chronic liver disease. 22 5

Until now, the hepatitis B virus has been thought to play a minor role in the aetiology of chronic liver disease in Australia. This is a report of 21 patients with cirrhosis and/or primary hepatocellular carcinoma with hepatitis B antigenaemia. Primary hepatocellular carcinoma occurred in six patients, five of whom had underlying cirrhosis. The disease occurred mainly in non-Australian born males, and was not often associated with a previous history of hepatitis. The death of 16 patients within 12 months of presentation is in contrast to previous concepts of the benign nature of hepatitis B associated cirrhosis.
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PMID:Emerging patterns of hepatitis B chronic liver disease in Australia. 22 47

A Farr technique has been used to assay antibodies to double-stranded DNA in the serum of patients with acute and chronic liver disease and carriers of HBsAg from the United Kingdom and Iraq. These antibodies were found in all groups from both countries. The highest levels were found in chronic active hepatitis and cirrhosis. In the Iraqi patients there was a strongly positive correlation between DNA-binding antibody levels and the presence of hepatitis B markers but not with disease activity. In the patients from the United Kingdom there was little correlation with disease activity and none with autoantibodies. Ninety-five per cent of asymptomatic carriers of HBsAG had elevated DNA-binding antibodies. It is suggested that hepatitis B-specific DNA might be one trigger to DNA antibody formation, though in liver disease a variety of factors are clearly operative.
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PMID:DNA-binding antibodies and hepatitis B markers in acute and chronic liver disease. 30 8

From 388 patients with upper G.I. bleeding investigated by endoscopy, radiology or emergent surgery, one third bled from duodenal ulcer, one third oesophageal varices, and from the remain the most frequent were gastric ulcer (14%) and gastric cancer (9%). From a sample of 53 patients with liver cirrhosis, 66% bled from varices and 34% from other lesions. The proportion of patients who bled from oesophageal varices is higher under 60 yrs. The mortality was higher after 60 yrs, except when there was associated chronic liver disease or renal or cardio-respiratory failure. In this group of patients, near half in our series, the mortality is the same under and above 60 years.
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PMID:Endoscopy in the upper G.I. bleedings. 31 42

In order to explain the increase of total IRI frequently observed at basal status, and after glucose administration, in patients with chronic liver disease, plasma proinsulin-like component and insulin levels have been studied in fourteen patients with liver cirrhosis associated or not with clinical or subclinical diabetes mellitus. A significative increase of plasma insulin was observed at basal status and after a glucose load not only in subjects with clinical or subclinical diabetes but also in those patients without carbohydrate abnormalities. This increase is apparently not correlated to any clinical characteristic and is associated in fasting and after glucose load with increased proinsulin-like component levels especially in patients with clinical or subclinical diabetes.
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PMID:Plasma proinsulin-like components and insulin in chronic liver disease. 32 82

A review of literature is given concerning the incidence, pathogenesis and clinical relevance of peptic ulcer in chronic liver disease. 1. Today there is no doubt about a highly significant incidence of peptic ulcer in chronic liver diseases, especially in cirrhosis of the liver. Therefore it seems reasonable to use the term "hepatogenic ulcer". 2. Assuming a relation between chronic liver disease and peptic ulceration several theories are discussed with regard to the causality and etiology. Most investigators suppose the diseased liver as "primum movens" in peptic ulceration by means of conditioning different ulcerogenic factors. 3. The clinical finding of increased frequency of peptic ulcer in cirrhotics despite of reduced gastric acid output is no contradiction. It can be explained by relative disturbance of the balance between aggressive and protective mechanism, the latter being diminished. Although a dysfunction of gastric mucus is recently assumed, the specific pathogenetic factor is not clear up to now. 4 Nevertheless, there is no doubt about the clinical relevance of this type of ulcer, given by diagnostic and therapeutic problems and pitfalls.
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PMID:["Hepatogenic ulcer": theories and facts (author's transl)]. 34 9

Four cases of hepatic angiosarcoma are reported with a review of 99 other cases in the English literature. Angiosarcoma of the liver is associated with chronic exposure to thorotrast, vinyl chloride, arsenicals, radium and possibly copper and with chronic idiopathic hemochromatosis. Although 40% of patients have hepatic fibrosis or cirrhosis at autopsy, the nature of the association between chronic liver disease and hepatic angiosarcoma is unknown. The clinical presentation of hepatic angiosarcoma is nonspecific with abdominal pain, weakness and weight loss common complaints and with hepatomegaly, ascites and jaundice common findings. Liver function tests are usually abnormal but there is no one liver function test or set of tests specific for the tumor. The occurrence of thrombocytopenia and disseminated intravascular coagulation is characteristic of hepatic angiosarcoma and may be related to local consumption of clotting factors and formed blood elements in the tumor. Catastrophic intraabdominal bleeding is also characteristic and occurs in one-fourth of all cases. This complication is likely related to the high incidence of clotting abnormalities and the vascular nature of the neoplasm. Selective hepatic arteriogram and open liver biopsy are the foundations of diagnostic evaluation. Percutaneous liver biopsy should be avoided. Failure to appreciate the possibility of hepatic angiosarcoma in the proper clinical setting, leading to blind percutaneous biopsy, may result in failure to make the diagnosis at the cost of significant morbidity and mortality. Survival of patients with hepatic angiosarcoma is brief; only 3% live longer than 2 years. Treatment of the tumor to date is empirical. There are probably a few patients who might benefit from radical surgery with curative intent. For all others chemotherapy is indicated. Adriamycin is active against hepatic angiosarcoma, but optimal dose and mode of administration require further investigation. Further study is also required to delineate the cause of hepatic angiosarcoma in the 60% of cases without definite epidemiologic association.
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PMID:The clinical features of hepatic angiosarcoma: a report of four cases and a review of the English literature. 36 8

Routine performance of a dynamic study as part of the liver scan results in a significant rate of discovery (19%) of intraabdominal abnormalities such as aortic aneurysms, cystic masses, ischemic intestinal diseases and collateral circulation. The procedure aids in the demonstration of space-occupying hepatic lesions and is often decisive in the diagnosis of chronic liver disease. Alterations in the perfusion of the liver as reflected in the dynamic scan may have a predictive value in the course of alcoholic hepatic disease as to the ultimate development of cirrhosis. Therefore, the dynamic study assumes an important role in the management of the alcoholic patient.
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PMID:Value of routine abdominal nuclide angiography as part of liver scan. 42 6


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