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)

Morphological observations of paraffin-embedded histological sections stained with H&E led to the discovery of some cytoplasmic changes which occur in different conditions, although they look alike under the light microscope. These hepatocytic changes consisted basically of homogeneous areas which are weakly eosinophilic in H&E-stained sections. They are frequently referred to as "inclusion" bodies, even when they are not true inclusions. The hepatocytic changes observed in HBsAg carriers, in chronic alcoholic patients treated with cyanamide to discourage them from drinking alcohol, in Lafora's disease, and in glycogenosis type IV, look very similar in paraffin sections stained with H&E. Nevertheless, they can be differentiated using ancillary techniques. On electron microscopy they do not look alike. Of particular interest are the "inclusion" bodies induced by cyanamide, a predictable and reproductible lesion, which in man eventually leads to cirrhosis. Other types of hepatocytic changes also giving a rather vague "ground-glass" appearance to the cytoplasm are those resulting from intracytoplasmic accumulation of proteins, particularly fibrinogen, and those observed in patients treated with different drugs.
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PMID:Ground-glass hepatocytes: light and electron microscopy. Characterization of the different types. 196 81

Liver transplantation in malignancies must be confined to patients with potentially curable disease. The indication is widely accepted, however, in non-resectable tumors or in patients with cirrhosis that excludes major resection. Without treatment prognosis is extremely poor in these patients. In our own experience 12 out of 13 non-cirrhotic patients with hepatocellular carcinoma (HCC) died within 9 months, and 17 out of 19 cirrhotic patients died within the first year of non-curative or explorative surgery. None of our patients with HCC in non-cirrhotic livers has lived longer than 38 months, and those with cirrhotic livers more than 61 months even after curative resection. After liver transplantation 1-year survival rate was 54% in 14 patients with primary hepatic carcinomas (12 HCC, 2 CCC). In cirrhotic patients with large or infiltrating HCC the results of resection are worse than after grafting, at least in the Western World, so liver transplantation must be taken into consideration. The lack of grafts limits treatment by transplantation in these patients. Transplantation is only exceptionally indicated for patients with metastatic liver disease.
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PMID:Primary hepatic malignancies: resection or liver transplantation? 216 24

Prognostically relevant factors and treatment were analysed in 103 patients suffering from primary epithelial liver tumors (88 HCC, 15 CCC). Ninety of them underwent operations: 14 liver transplantations, 32 resections, 44 explorative laparotomies. The resection rate was 38%, the 30-day mortality in transplantation 14%, in resection 22%. The 5-year survival after resection was about 25%. Liver transplantation resulted in 50% 1-year and 40% 2-year survival. Long-term prognosis was positively influenced by cirrhosis and formation of a tumor capsule. Indications for operative management depend only on extension of tumor growth and concomiting liver cirrhosis as biology of epithelial liver tumors is poorly understood.
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PMID:[Prognosis and therapy of primary epithelial liver tumors. Evaluating a personal patient sample]. 217 93

In 94 patients liver transplantations for malignant tumors of the liver have been performed in this institution from 1972 to 1987. The long-term overall results in hepatic transplantation for irresectable tumors are disappointing in spite of good short-term palliation in most of the patients. Tumor recurrence is the rule. But individual long-living patients demonstrate the potentials of this treatment. Thus the crucial question will be a proper selection of patients. The relative suitability (in descending order of favorableness) of the kinds of tumors may range from HCC without cirrhosis, to central bile duct tumors, to HCC in cirrhosis, to CCC, and finally to secondaries. But this range can only give some probability for the success rate. More important is the tumor stage. Survival in lymph node-positive stages is by far worse than in lymph node-negative stages. The 6-month, 1-year, and 2-year actuarial survival data in our experience for lymph node-negative (lymph node-positive) HCC without cirrhosis are 83%, 75%, 75% (33%, 11%, 11%); in bile duct carcinomas in lymph node-negative stages (lymph node-positive) they are 6 months, 100% (40%); 1 year, 100% (13%); and 2 years, 83% (0%). Hepatic transplantation for selected tumor patients furthermore seems justified and is essential for a detailed analysis of the chance of different tumor types for success with this method of treatment.
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PMID:Is there a place for liver grafting for malignancy? 245 Apr 17

In a retrospective review of 2400 consecutive liver biopsy specimens, 60 cases with ground-glass hepatocytes were identified, 41 specimens gave a positive reaction to orcein stain and 19 a negative staining. These 19 specimens were obtained from chronic alcoholics who had been admitted to a detoxication program that used aversive drugs and who were hepatitis B surface antigen negative. The use of cyanamide (Colme), an inhibitor of aldehyde dehydrogenase could be documented in 11 instances. In addition to ground-glass hepatocytes, which were periodic acid-Schiff positive and had a periportal or paraseptal distribution, these liver specimens showed a variety of hepatic lesions: cirrhosis in five cases, portal and periportal inflammation in six, triaditis in five, portal fibrosis in two, and minimal changes in one. Patients with shorter courses of cyanamide were those who had less severe histologic lesions. In three patients who had a liver biopsy carried out before the cyanamide treatment ground-glass hepatocytes were not found. These data indicate that ground-glass hepatocytes that stain with periodic acid-Schiff may develop after cyanamide treatment. They are associated with structural hepatic damage of varied severity in patients submitted to a long-term treatment.
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PMID:Hepatic disease associated with ground-glass inclusions in hepatocytes after cyanamide therapy. 302 Oct 86

Ground-glass hepatocytes resembling those seen in HBsAg carriers on hematoxylin and eosin and on trichrome stained sections, but giving a negative reaction to orcein and a positive one to PAS, were found in liver biopsy specimens from nine asymptomatic former alcoholics who were on treatment with cyanamide, in one of four who had been treated with cyanamide several months before the liver biopsy procedure, in none of 15 treated with disulfiram, and in one of eight who had apparently not received aversive drugs. Portal and periportal inflammatory changes and fibrosis were more frequently observed in biopsy specimens containing PAS-positive ground-glass hepatocytes than in those without, but cirrhosis was found with a similar frequency. It is concluded that periportal PAS-positive ground-glass hepatocytes are a histological marker of cyanamide treatment.
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PMID:Cyanamide hepatotoxicity. Incidence and clinico-pathological features. 368 93

We report here on the hepatic lesions produced in 17 alcoholic patients who had received Cyanamide or Disulfiram as aversion therapy. The characteristic lesion consists of cytoplasmic inclusions, similar to Lafora bodies. They are found predominantly in periportal hepatocytes, including those lining the cholangioles. They appear to be persistent but are lost after death of the inclusion-bearing liver-cell when both the inclusion body and the dead hepatocyte are removed by macrophages. As well as the inclusion bodies, portal or periportal inflammation and necrosis of isolated liver-cells are seen. The inflammatory infiltrate is usually denser in the periportal areas and is associated with liver-cell destruction. The inflammation is usually followed by portal fibrosis which can be severe if treatment is prolonged. In one case, in which two biopsies were performed, cirrhosis developed while that patient was on Cyanamide.
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PMID:Hepatitis induced by drugs used as alcohol aversion therapy. 630 16

The authors present the clinical and histological findings in a series of 42 liver biopsies from 39 chronic alcoholics treated with cyanamide as aversion therapy. All biopsies displayed characteristic cytoplasmic inclusions in the liver-cells. Fibrosis and disruption of the parenchymal-connective tissue interface were observed in all cases. According to the severity and extension of fibrosis, three stages could be depicted: Stage I. Periportal activity cholangiolar type (ACT), which is defined by cholangiolar proliferation, fibroblastic activation and inflammatory infiltrate, which together cause a blurred appearance of the parenchymal-connective tissue junction. It is the elementary lesion and was observed alone in 26 biopsies. Stage II. Portal-to-portal linkage. It was observed in 10 biopsies, all of which also showed periportal ACT. Three of these came from patients with two biopsies in which transition from stage I (first biopsy) to stage II (second biopsy) was observed. Stage III. Nodular parenchymal regeneration, associated with changes observed in stage I and II. It was found in six patients. The histological picture resembles the biliary type of cirrhosis. There is a clear-cut correlation between the length of treatment and the stage of the hepatic lesion.
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PMID:Structural hepatic changes associated with cyanamide treatment: cholangiolar proliferation, fibrosis and cirrhosis. 632 77

Hepatitis B virus (HBV) with T-1856 of the precore region is always associated with C-1858 (i.e., TCC at nucleotides 1856 to 1858), and it is reported only in genotype C HBV isolates. We aimed to investigate the phylogenetic, virological, and clinical characteristics of HBV isolates bearing TCC at nucleotides 1856 to 1858. We have previously reported on the presence of two major subgroups in genotype C HBV, namely, HBV genotype Cs (Southeast Asia) and HBV genotype Ce (Far East). We have designed a novel 5' nuclease technology based on the nucleotide polymorphism (C or A) at nucleotide 2733 to differentiate the two genotype C HBV subgroups. The mutations at the basal core promoter and precore regions were analyzed by direct sequencing. Among 214 genotype C HBV-infected patients, 31% had TCC, 37% had CCC, 3% had CTC, and 29% had CCT at nucleotides 1856 to 1858. All except one HBV strain with TCC at nucleotides 1856 to 1858 belonged to subgroup Cs, which has been reported only in Hong Kong; Guangzhou, China; and Vietnam. HBV with TCC at nucleotides 1856 to 1858 was associated with the G1898A mutation (64%). Patients infected with HBV harboring TCC had more liver cirrhosis than those infected with HBV harboring CCC (18% versus 5%; P = 0.008), and more of the patients infected with HBV harboring TCC were positive for HBeAg (58% versus 36%; P = 0.01) and had higher median alanine aminotransferase levels (65 IU/liter versus 49 IU/liter; P = 0.006); but similar proportions of patients infected with HBV harboring TCC and those infected with HBV harboring CCT had liver cirrhosis (18% versus 13%; P = 0.43). In summary, we report that HBV with TCC at nucleotides 1856 to 1858 of the precore region might represent a specific HBV strain associated with more aggressive liver disease than other genotype C HBV strains.
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PMID:Phylogenetic, virological, and clinical characteristics of genotype C hepatitis B virus with TCC at codon 15 of the precore region. 1651 39

Alcoholic myopathy is characterized by biochemical and morphological lesions within muscle, ranging from impairment of muscle strength and loss of lean tissue to cellular disturbances and altered gene expression. The chronic form of the disease is five times more common than cirrhosis and is characterized by selective atrophy of type 11 (anaerobic) fibres: type I (aerobic) fibres are relatively protected. Although the causative agent is known (i.e. ethanol), the intervening steps between alcohol ingestion and the development of symptoms and lesions are poorly understood. However, acetaldehyde appears to have an important role in the aetiology of the disease. For example, alcohol is a potent perturbant of muscle protein synthesis in vivo, and this effect is exacerbated by cyanamide pre-dosage, which raises acetaldehyde concentrations. Acetaldehyde alone also reduces muscle protein synthesis in vivo and proteolytic activity in vitro. The formation of acetaldehyde protein adducts is another mechanism of putative importance in alcoholic myopathy. These adducts are formed within muscle in response to either acute or chronic alcohol exposure and the adducts are located preferentially within the sarcolemmal and sub-sarcolemmal regions. However, the significance of protein adduct formation is unclear since we do not currently know the identity of the adducted muscle proteins nor whether adduction alters the biochemical or functional properties of skeletal muscle proteins.
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PMID:Alcoholic myopathy and acetaldehyde. 1759 Sep 94


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