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

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

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