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

114 patients with cryptogenic or "hepatitic" cirrhosis of the liver (toxic or biliary causes excluded) were followed for a period of 15 years. The time of first manifestation of the disease was known because all patients had been in hospital or under serial outpatient observation, with clinical and biopsy studies every six months for chronic hepatitis. In addition, diagnosis of the liver cirrhosis was confirmed by laparoscopy and histomorphology, which further confirmed the exact timing of first manifestation. In 37 patients (32.5%) the disease healed out completely by way of reactionless fibrosis after, in some of them, a long period of observation, while in 47 (41.2%) the active disease continued, and 30 (26.3%) died in liver coma or bleeding from varices or surgical shunt procedures or from carcinoma of the liver. Prognosis of cirrhosis of the liver is thus much better than previously thought.
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PMID:[Prognosis of cirrhosis of the liver (15-year follow-up from time of first manifestation (author's transl)]. 12

For the purpose to study the citrate metabolism in liver diseases, blood citrate, blood glucose and serum non-esterified fatty acids (NEFA) in fasting state were measured in the subjects with chronic hepatitis and with liver cirrhosis. Citrate and glucose were measured by the enzymatic methods. NEFA was measured colorimetrically. Fasting blood citrate level was investigated in relation to the type and extent of these liver diseases. Results revealed the following: 1. Fasting blood citrate level rose with the severity of liver diseases, especially in decompensated liver cirrhosis. 2. No significant difference in fasting blood citrate level was found between the subjects with and without glucose intolerance. 3. Fasting blood citrate level had a closer correlation with serum NEFA level than with blood glucose level. From these results, it has been concluded that the increase in blood citrate level in liver diseases is due to the impaired uptake of citrate by the liver and the increased release of citrate from peripheral tissues.
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PMID:Studies on citrate metabolism in liver injuries. 1. Fasting blood citrate level in chronic hepatitis and liver cirrhosis. 12 99

Cirrhotic livers of different types were subjected to three-dimensional graphic reconstruction of nodules, interstitial septa and blood vessels from serial histologic sections. It was found that in all cases adjacent cirrhotic nodules were connected to one another so as to form a nodular network, in spite of their apparent separation in histologic sections. The nodules were linked in the form of chains with abundant anastomoses, and the network was 'conjugate' with the intrahepatic vascular tree, as revealed by its close relationship to blood vessels. A parenchymal network of the same type was also found in livers with subacute or chronic hepatitis, suggesting that this type of structure was common to cirrhosis and its precursor lesions and represents the geometrical configuration of hepatic parenchyma surviving zonal hepatic necrosis. A Re-examination of chronic liver disease in terms of its structural framework provided a new viewpoint from which to analyse the morphogenetic problems of these disorders.
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PMID:Three-dimensional morphology of the liver in cirrhosis and related disorders. 14 61

Cirrhotic and precirrhotic livers consist of three-dimensional parenchymal networks. Topological analysis has been carried out using the total connectivity number p1 on the livers from 6 autopsy cases of chronic liver diseases of different types. The total p1 amounts to 6,100,000 in chronic hepatitis of periportal type and 6,350,000 in portal cirrhosis, but to only 100,000 in posthepatitic cirrhosis of coarse-nodular type. In view of the similarity of values for p1 in chronic hepatitis and portal cirrhosis, the former is considered to give rise to the latter by continuous change in structure or through "piecemeal" progression of the periportal lesion. Development of posthepatitic cirrhosis from chronic hepatitis is possible only through a substantial reduction in p1, which is brought about by parenchymal necrosis sufficient in extent to cause multiple disconnection of the network.
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PMID:Topological analysis of the morphogenesis of liver cirrhosis. 14 49

Most of the knowledge of post-hepatitic cirrhosis comes from studies performed in the last five years on the hepatitis B antigen-related variety. The position of other types of hepatitis (particularly type A) as an aetiological factor in cirrhosis remains conjectural. In general, the post-hepatitic cirrhosis develops insidiously after a mild or unrecognised acute episode of hepatitis. General progress is slow. Early deaths are due to liver failure. Later, primary hepatocellular carcinoma assumes increasing importance. Needle biopsy of the liver is usually necessary to confirm the diagnosis of cirrhosis and to estimate the degree of activity. Sampling errors when such a small specimen of liver is obtained must be taken into account, when formulating a diagnosis and prognosis. Prednisolone therapy is usually given if the patient is symptomatic, biochemical tests are abnormal and the liver biopsy confirms active chronic hepatitis with or without cirrhosis. The evidence of benefit is not so strong as for other forms of active hepatitis and cirrhosis such as the lupoid type. The management of the cirrhosis is otherwise along orthodox lines.
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PMID:Viral hepatitis and cirrhosis. 16 21

The frequency of occurrence of hepatitis B antigen (HBAg) and certain tissue autoantibodies [antinuclear antibody (ANA), smooth muscle antibody (SMA) and mitochondrial antibody (MIA)] were studied with the microtiter complement fixation and immunofluorescence techniques respectively in a group of patients suffering from chronic liver diseases. These were chronic hepatitis (30), cirrhosis of the liver (66) and hepatocellular carcinoma, mostly with underlying cirrhosis (100). A group of closely matched hospital in-patients served as controls. HBAg was found in high frequency in the patients with liver disease (60% in chronic hepatitis, 36.4% in cirrhosis and 49% in hepatocellular carcinoma) whereas tissue auto-antibodies were found in lower frequencies (16.7%, 10.6% and 13% in the three groups respectively). However, in both the frequency was significantly higher than that in the controls (9.2% for HBAg and 0.8% for auto-antibodies). There was a negative correlation between HBAg and tissue auto-antibodies in the group of patients with liver disease when taken as a whole (x2=14.3, P less than 0.001). These results suggest a possible aetiological role played by hepatitis virus B in hepatocellular carcinoma through chronic hepatitis and cirrhosis in Hong Kong while the mutual exclusion between HBAg and auto-antibodies supports the hypothesis of heterogeneity in the aetiology of chronic liver diseases. The patients with auto-antibodies may belong to the auto-immune category but no definate conclusion can be reached until the role played by hepatitis virus A in chronic liver diseases is clarified when more reliable techniques for its identification are available.
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PMID:Hepatitis B antigen and auto-antibodies in chronic liver diseases in Hong Kong. 16 80

Maximum motor and sensory nerve conduction velocities, amplitudes of muscle action potentials (surface electrodes) and of sensory nerve action potentials, and needle electromyograms were studied in 80 patients with alcoholic neuropathy and in 5 chronic alcoholics without clinical signs of neuropathy. The electrophysiological results were compared to the clinical findings. Neurographic criteria compatible with the diagnosis "alcoholic neuropathy" were defined. Neurographic findings contrary to a diagnosis of alcoholic etiology were demonstrated in 3 patients. Only in a smaller group of patients could a reduction of conduction velocity be found, especially in regions of peripheral nerve entrapment. A decrease in conduction velocity outside of the entrapment sites can be explained in some cases by segmental demyelination in chronic hepatitis or cirrhosis of the liver.
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PMID:[Alcoholic polyneuropathy. Electrophysiological and clinical findings in 85 patients (author's transl)]. 17 Aug 84

In Asia, Africa, and other tropical areas, primary hepatic carcinoma (PHC) is associated with liver cirrhosis of the postnecrotic (macronodular) type. Chronic viral hepatitis is likely to be the cause of this cirrhosis in many patients from regions where chronic infection with the hepatitis B virus (HBV) is common. More than 95% of patients with hepatoma (in Mali and Senegal) have evidence of infection with HBV, a much higher frequency than in controls. Thirty-nine of 62 patients with PHC had hepatitis B surface antigen (HBsAg) (controls, 8 of 98) and 56 of 63 (controls, 26 of 100) had antibody against hepatitis B core antigen (anti-HBc). In earlier studies, we demonstrated a maternal effect of HBsAg. If the mother has the antigen and the father does not, the children are much more likely to also have HBsAg than if the father has the antigen and the mother does not (93/161 = 57.8% when mother is positive vs. 28/135 = 20.7% when father is positive; P = 0.6 X 10(-10)). Studies in Greece and in the Solomon Islands show that presence of HBsAg in parents affects the sex ratio of the offspring of the mating. This implies that the presence of the agent in a parent can affect the fetus early in life. Parental studies in the west African hepatoma patients showed that there is a very high frequency of HBsAg in mothers (71.6%), while the frequency in fathers (18.5%) is significantly less. This suggests that the development of hepatoma in offspring is related to infection in parents. Several years ago, we described a vaccine which may be useful in preventing infection with hepatitis B. Strategies are discussed which might be effective in preventing the development of carriers with, it is hoped, a consequent decrease in the frequency of HBV carriers, chronic hepatitis, and primary hepatic carcinoma. The strategy would employ methods for decreasing the frequency of the agent in the environment by the application of public health methods including the vaccination of appropriate newborns and other members of the population.
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PMID:The relation of infection with the hepatitis B agent to primary hepatic carcinoma. 17 34

In Asia, Africa and other tropical areas primary hepatic carcinoma (PHC) is associated with liver cirrhosis of the post-necrotic (macronodular) type. Chronic viral hepatitis is likely to be the cause of this cirrhosis in many patients from regions where chronic infection with the hepatitis B virus (HBV) is common. More than 95% of patients with hepatoma (in Mali and Senegal) have evidence of infection with HBV, a much higher frequency than in controls. Thirty-nine of 62 PHC patients had hepatitis B surface antigen (HBSAg) (controls: 8 of 98) and 56 of 63 (controls: 26 of 100) had antibody against hepatitis B core antigen (anti-HBC). In earlier studies we demonstrated a maternal effect of HBSAg. If the mother has the antigen and the father does not, the children are much more likely to also have HBSAg than if the father has the antigen and the mother does not (93/161 = 57.8% when mother is positive vs. 28/135 = 20.7% when father is positive; p = 0.6 X 10(-10)). Studies in Greece and in the Solomon Islands show that presence of HBSAg in parents affects the sex ratio of the offspring of the mating. This implies that the presence of the agent in a parent can affect the fetus early in life. Parental studies in the African hepatoma patients showed that there is a very high frequency of HBSAg in mothers (71.6%) while the frequency in fathers (18.5%) is significantly less. This suggests that the development of hepatoma in offspring is related to infection in parents. We described a vaccine several years ago which may be useful in preventing infection with hepatitis B. Strategies are discussed which might be effective in preventing the development of carriers with, it is hoped, a consequent decrease in the frequency of HBV carriers, chronic hepatitis and primary hepatic carcinoma. The strategy would employ methods for decreasing the frequency of the agent in the environment by the application of public health methods including the vaccination of appropriate newborns and other members of the population.
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PMID:[The relation of infection with the hepatitis B-agent to primary hepatic carcinoma (author's transl)]. 19 Apr 99

Hepatitis B surface antigen (HBsAg), anti-HBs, and anti-HB core (HBc) were measured in 124 patients with hepatocellular carcinoma (HCC) in comparison with 299 control subjects of comparable ages, and in 48 cases of chronic hepatitis and 52 cases of hepatic cirrhosis. It was found that 72.6% of the HCC patients were positive for anti-HBc, and 80.6% were positive for at least one test, whereas in the control, anti-HBc was positive in 30.1% and 34.1% were positive for at least one test, the differences between the two groups being significant (P less than 0.01). The frequencies of positive tests for HBsAg and anti-HBc were the highest in HCC followed in decreasing order by cirrhosis, chronic hepatitis and the control group. A possible role of HB virus infection in hepatocellular carcinoma is discussed in relation to other factors.
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PMID:Antibody to hepatitis B core antigen in patients with hepatocellular carcinoma. 19 26


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