Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver specimens from 103 patients with various hepatic diseases and from 297 consecutive liver biopsies examined routinely were stained with orcein after oxidation of the tissue sections with potassium permanganate. Orcein-positive dark brown cytoplasmic material could be demonstrated in 27 cases with long-standing cholestasis. These patients had either primary biliary cirrhosis, the cholestatic liver disease of ulcerative colitis or chronic active hepatitis, advanced alcoholic cirrhosis or secondary biliary cirrhosis due to extrahepatic biliary obstruction. Orcein-positive material could not be demonstrated in congenital disorders of bilirubin metabolism or in hemochromatosis. Similarly, it could not be found in acute, toxic, alcoholic or chronic persistent hepatitis.
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PMID:The occurrence of orcein-positive hepatocellular material in various liver diseases. 6 38

The serum alpha-fetoprotein level was measured by radioimmunoassay in 200 patients when admitted to hospital, 63 with idiopathic hemochromatosis and 137 with liver cirrhosis. In addition, repeated controls were performed in 19 subjects of each group for a mean period of 11 months (range 3--18 months). Elevated alpha-fetoprotein levels were observed initially or during the study period in 15 patients, a malignant liver tumor being demonstrated in 12 of them. In 4 of these patients, the abnormal alpha-fetoprotein concentration was the clue to the diagnosis of an unsuspected malignant hepatoma, but in none of these cases could the tumor be resected. The present results indicate that screening the serum alpha-fetoprotein level may contribute to the detection of malignant hepatoma in high-risk clinical groups, but the practical interest of such screenings may keep limited until more efficient therapeutic methods are developed.
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PMID:alpha-Fetoprotein screening in patients with idiopathic hemochromatosis and liver cirrhosis. 7 12

Diurnal variations of plasma testosterone and urinary excretion rates of testosterone-, androsterone-, aetiocholanolone-, and DHA-glucuronide, as well as DHA-sulphate were measured before and after selective Leydig-cell stimulation (with 3 X 5000 IU human gonadotrophin) in eight patients with alcoholic liver cirrhosis, ten with acute hepatitis and four with haemochromatosis. The circadian variation of plasma testosterone and the maximal testosterone concentration after human gonadotrophin stimulation were decreased in patients with cirrhosis and haemochromatosis, while in those with acute hepatitis the diurnal variations were evened out, whereas individual values were within the normal range. Urinary excretion of free testosterone and testosterone glucuronide was significantly reduced in those with cirrhosis and haemochromatosis before and after stimulation. The urinary pattern of C19 steroid metabolites was markedly changed in favour of the 5 alpha-steroids in acute heaptitis, cirrhosis, and haemochromatosis.
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PMID:[Androgen metabolism and Leydig-cell function in acute and chronic liver disease (author's transl)]. 12 98

In 74 patients admitted to hospital for primary hemochromatosis, the authors observed in 5 cases, the development of primary carcinoma of the liver. The frequency of this complication was definitely greater than in alcoholic or post-hepatitic cirrhosis, whether one considers patients in hospital or on autopsy. The best signs of malignant change are alterations in the surface of the liver and the development of hemorrhagic ascites. Using modern methods of clinical investigation, it is possible to make the diagnosis during the patient's life. Laparoscopy, permitting biopsy under direct vision, is the best investigation but it is not always possible. A search for alpha 1 foeto-protein was positive in one third of cases and the demonstration by hepatic arteriography of characteristic vascular abnormalities and, perhaps in future, information supplied by ultra-sonic echography, usually permit one to make the diagnosis. The course was fatal within a few months, and it seems that metastases and vascular spread are less frequent than in carcinoma developing on cirrhosis due to other causes.
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PMID:[Idiopathic hemochromatosis and primary cancer of the liver]. 17 70

Hemochromatosis is a disorder characterized by the association of portal cirrhosis with deposition of excess amounts of iron in the parenchymal cells of many organs. Arthralgia and arthritis occur in about 50% of patients. The role of the radiologist is often significant in the recognition of this condition because hemochromatosis may be unsuspected clinically since the hepatic cirrhosis is frequently inactive at the time the arthritis develops. The possibility of hemochromatosis should be considered when the characteristic involvement of the metacarpophalangeal, radiocarpal, and proximal interphalangeal joints of the hand and wrist is present. In addition, articular and fibrocartilage calcification is often noted, particularly in the knee, triangular cartilage of the wrist, hip, elbow, symphysis pubis, and shoulder. Although localized chondrocalcinosis may be seen in association with many disorders, as well as in asymptomatic elderly persons, generalized chondrocalcinosis is a significant finding and is commonly associated with hemochromatosis. Recognition of the typical distribution of the arthropathy plus its characteristic roentgenographic features should aid in the identification of patients with the disorder who do not demonstrate the typical clinical features of hemochromatosis.
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PMID:Hemochromatosis: a disease often silent but not invisible. 17 3

Observations on the clinical effects of venesection therapy in 85 treated, as compared with 26 untreated, patients with idiopathic haemochromatosis showed decreased pigmentation and hepatomegaly together with a return to normal tests of liver function in half the patients who had abnormal tests at presentation. Control improved in 28 per cent of those patients with diabetes mellitus, although some patients developed it during the period of observation, despite venesection. Portal hypertension, testicular atrophy and arthropathy were not improved. In only 12 patients was there sufficient reaccumulation of iron after the initial course of venesection to merit further treatment. Rates of iron accumulation in these patients varied between 1-4 mg and 4-8 mg per day and chelatable iron levels were noted to be inappropriately high in relation to body iron stores during the early stages of the reaccumulation period. Life table data shows that the percentage survival five and ten years after diagnosis was 66 and 32 per cent respectively for the treated patients, and 18 and 6 per cent respectively for the untreated patients, both statistically highly significant differences (p less than 0-01). Possible clinical differences such as age of presentation, the presence of diabetes mellitus, cirrhosis, clinical hepatic failure and hepatoma between the treated and untreated groups that might otherwise have weighted survival in favour of the treated group were corrected by the use of covariant analysis. This gave mean log survival values of 4-15 and 2-88 for the treated and untreated patients respectively, equivalent to 63-4 months and 17-8 months, a highly significant difference (p less than 0-01). Ten patients, all of whom had cirrhosis at the time of diagnosis, died of malignant hepatoma between three and 15 years after completing venesection therapy. There was also a high rate of death from neoplasms in a variety of other sites--22 per cent in the venesected group, strikingly higher than that rate predicted for a similarly aged population using national cancer mortality rates.
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PMID:Long term results of venesection therapy in idiopathic haemochromatosis. 18 63

An analysis of 294 patients who died with cirrhosis showed that 24% had developed hepatocellular carcinoma. Haemochromatosis and HBsAg positive chronic active hepatitis were high risk groups (36% and 42% respectively) and the frequency was lowest in primary biliary cirrhosis and HBsAg negative chronic active hepatitis (3% and 11% respectively). Those with hepatocellular carcinoma showed a striking male preponderance (11:1) and further analysis has shown that the proportion developing this tumour in each group was closely related to the proportion of males in that group (r=0.97). Age was the only other significant factor, malignant change occurring more commonly in those over the age of 50 years than those below (30% and 7% respectively, P less than 0.005). The indluence of HBsAg was largely accounted for by the known predisposition of males to carry HBsAg. The group of patients who had developed this tumour without cirrhosis were younger (mean age 39 years) and had a lower male to female ratio of 1.1:1 and the place of contraceptive-related tumour within this group is dicussed.
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PMID:Hepatocellular carcinoma in Great Britain: influence of age, sex, HBsAg status, and aetiology of underlying cirrhosis. 21 96

A 65 years old, female patient with acquired aplastic anemia secondary to frequent exposure to hair dye. While on treatment with anabolic steroids hormone became jaundiced and developed hepatomegaly eight months later. During laparotomy the liver was enlarged, hard, with multiple whitish nodules on its surgace but was otherwise normal. Liver biopsy showed hepatocellular carcinoma, there were not cirrhosis niether hemochromatosis. A review of the related literature was done and discussed on the experimental and clinical evidences that suggested that androgens may play same role on the etiology of liver cancer.
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PMID:[Androgenic therapy and hepatocellular carcinoma. Report of a case]. 22 17

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

To clarify further the etiology of the carbohydrate intolerance in idiopathic hemochromatosis, we investigated the glucose, insulin, C-peptide, and glucagon responses to arginine (0.5 g/kg) infused during 30 min in lean normal subjects; in insulin-requiring subjects with hemochromatosis, genetic diabetes, and total pancreatectomy; and in nondiabetic cirrhotic subjects without portosystemic shunting. Serum insulin, C-peptide, and glucagon responses (30K antibody) were determined by RIA, and glucose level was determined by a glucose oxidase technique. Hemochromatotic and genetic diabetic subjects had similar basal glucose (157 +/- 25 vs. 168 +/- 40 mg/dl) and C-peptide (0.73 +/- 0.42 vs. 0.65 +/- 0.22 ng/ml) values, with subnormal C-peptide peak responses to stimulation (1.05 +/- 0.38 and 1.40 +/- 0.83 vs. 3.95 +/- 0.4 ng/ml in normals; P less than 0.05). No glucagon or C-peptide response to arginine was seen in any pancreatectomized subject. Similar but excessive glucagon levels were present in hemochromatosis, diabetes, and cirrhosis under basal conditions (166 +/- 24, 232 +/- 111, and 263 +/- 116 vs. 76 +/- 15 pg/ml; P less than 0.05) and after arginine stimulation (782 +/- 80, 834 +/- 123, and 902 +/- 275 vs. 489 +/- 81 pg/ml; P less than 0.05) when compared with normals. The excessive glucagon levels found in hemochromatosis, diabetes mellitus, and cirrhosis contrast to the absent response in pancreatectomized subjects and indicate that generalized islet cell destruction is not the major factor in diabetic hemochromatotic subjects.
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PMID:Pancreatic alpha-cell function in diabetic hemochromatotic subjects. 38 22


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