Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0239946 (liver fibrosis)
 8,268 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

C-reactive protein titre was estimated in serum and ascitic fluid in 23 patients, 12 with cancer stomach accompanied by liver metastatases and 11 with bilharzial liver fibrosis. The results showed no statistically significant differences between the titre in serum and ascitic fluid in the group of cancer with mean of serum/ascitic level ratio 1.3, while in bilharzial group there was significant difference with ratio mean 6.3.
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PMID:Study of C-reactive protein in bilharziasis and malignancy as causes of ascites. 176 87

Androgen receptors (AR) and estrogen receptors (ER) were consecutively assayed for hepatocellular carcinoma (HCC) and the surrounding liver was removed surgically from 19 female patients. Patient age ranged from 43 to 79 years, with an average of 61 +/- 9 years. All patients had underlying liver disease (liver cirrhosis in 16, liver fibrosis in two, and chronic hepatitis in one). Seven (37%) of 19 HCC had AR ranging from 2.3 to 82.6 fmol/mg of cytosol protein. The AR titer was higher in the HCC than in the liver in these cases. Three cases also had ER. ER existed in seven (37%) tumors (range, 2.4 to 25.6 fmol/mg of protein). AR and ER were detected in 11 (65%) and ten (58%) of 17 nonneoplastic liver tissues, respectively. Serum alpha-fetoprotein (AFP) level, hepatitis B virus markers, or histopathologic types of HCC had no correlation with the presence or absence of AR or ER and their titers. Also, there was no correlation between the AR and ER positivities. Further studies are mandatory to determine the genuine role of sex hormone receptors in the development and growth of HCC in humans.
Cancer 1989 Jan 01
PMID:Androgen and estrogen receptors in hepatocellular carcinoma and the surrounding liver in women. 253 50

During the past 6 years, 150 consecutive hepatic resections were performed for hepatocellular carcinoma on 129 male and 21 female patients. Their ages ranged from 17 years to 78 years, with an average of 57.0 years. All but two patients had an underlying parenchymal disease of the liver; 131 had liver cirrhosis, 16 chronic hepatitis, and one liver fibrosis. The operations performed were extended right lobectomy in 10 cases, right lobectomy in 13, left lobectomy in 5, left lateral segmentectomy in 11, other segmentectomies in 31, and partial wedge resection in 80 instances. The operative and in-hospital mortality rates were 6.0% and 12.0% respectively. In the 122 patients with curative resection, the 1-, 3- and 5-year survival rates were 75.2%, 49.0% and 30.0% respectively. The 1- and 3-year survival rates were 14.3% and 7.1% in the 28 patients with palliative resection. The tumor size and Child's classification generally reflected the survival rate.
Cancer Chemother Pharmacol 1989
PMID:Liver resection for hepatocellular carcinoma: results from 150 consecutive patients. 253 69

Only a few cases of Duodenal Varices (DV) have been reported in the world literature mostly by radiological studies, at operations, or autopsies. Alberti described DV for the first time in 1931. The visualisation of DV by fiberoptic endoscope was first made in 1973 by Kunisaki et al. (one case) and later by Kunert and Ottenjann in 1976 (one case). In this study we present 13 cases of DV diagnosed in the period from June 1979 to May 1983 out of 5664 endoscopic examinations performed in the Endoscopy Unit of Riyadh Central Hospital and giving a prevalence of 1:435. 598 cases of Oesophageal Varices (OV) were found in these series, so that the relation DV:OV is 1:46 in this study. The etiology of DV is mostly liver fibrosis due to schistosomiasis (9 cases). In the rest of the cases we found av-malformation (one case), cancer of the head of pancreas (one case) and Hodgkin's disease with enlarged lymph-nodes and ascites in association with chronic duodenal ulcer (one case). In one case the etiology remained unknown. 4 patients had no oesophageal involvement (isolated DV). The cases will be discussed in detail.
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PMID:Duodenal varices. Report of 13 cases. 310 Dec 97

Eighty-six children were diagnosed with cancer in infancy, followed for at lest 5 years, and assessed for late effects of disease and therapy. One child subsequently died from respiratory failure and 3 died from second primary cancers. Another patient survived second primary cancers of the skin. The high frequency of new cancers (4 observed, 0.09 expected) was attributable to host susceptibility factors and treatment effects. Kyphoscoliosis was diagnosed in 44 patients, 40 of whom had received radiotherapy to the spine. Other patients had neurologic deficits, pulmonary fibrosis, hypoplastic breasts, bowel adhesions, thyroid nodules, musculoskeletal defects, and liver fibrosis associated with tumor therapy. Sequelae of cancer were more common after treatment in infancy than in later childhood. Improved treatments and knowledge of natural history can reduce adverse effects of therapy.
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PMID:Late effects of treatment of cancer in infancy. 628 89

Hepatomas arising as a result of prolonged injection of CCl4 consist of cells in which the processes of dystrophy and intracellular regeneration are pronounced to a different degree. In the late stages of development, hepatomas tend to malignancy, exhibiting cells that bear ultrastructural resemblance to the cells of malignant hepatomas. Histological examination revealed high aerobic glycolysis and decreased activity of oxidizing enzymes. Discontinuance of CCl4 injection did not entail normalization of the liver structure. The sinusoidal cells are likely to play an essential role in the development of intralobular liver fibrosis.
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PMID:[Electron microscopic and histochemical characteristics of hepatomas arising during long-term administration of carbon tetrachloride]. 739 69

Although effective treatments are available for many children with LCH, there are many others for whom no definitive therapy yet exists. These patients include those with 1) multisystem disease and associated organ dysfunction, 2) chronic, relapsing disease, 3) new onset pituitary involvement associated with diabetes insipidus and 4) long-term complications such as pulmonary fibrosis, liver fibrosis or CNS involvement. This introductory paper discusses these clinical problem areas and then reviews several new therapeutic approaches including novel chemotherapeutic agents, immunosuppressive strategies, bone marrow transplantation and gene therapy.
Br J Cancer Suppl 1994 Sep
PMID:Treatment options--commentary. 807 10

From 1971 to 1990, 18 children were surgically managed for choledochal cysts at two Berlin pediatric surgical units. Eight patients underwent an internal drainage procedure, eight a Roux-en-Y hepaticojejunostomy and one a choledochoplasty. The children were followed-up 2 to 20 years later (median: 8.4 years). Three children died in the early postoperative period, but the immediate postoperative course was uneventful in all other cases. Later, five patients suffered from recurrent gastrointestinal disease, cholangitis and pancreatitis and, in two cases, from progressive liver fibrosis. Four of the five patients with symptoms had undergone internal drainage procedures; one developed cholangitis after a hepaticojejunostomy. In one case of internal drainage, the anastomosis was transformed into a hepaticojejunostomy. No patient had cancer.
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PMID:Late results in the management of choledochal cysts. 808 89

Hepatic necrosis is a common reaction to liver injury of various etiologies. The response is regeneration. As reviewed earlier, reconstitution of liver mass may proceed via two mechanisms: (1) re-entry of surviving, functionally intact differentiated liver cells into the cell cycle, where they may remain for several rounds of replication, and (2) recruitment of hepatic progenitor cells, whereby the liver mass is replaced by extensive proliferation and differentiation of more primitive cell types. Although both mechanisms appear to share a number of regulatory factors, distinct differences exist that are reflected in the complex and intricate networks of interacting cells, cytokines, and ECM molecules constituting the regenerative process. The development of liver fibrosis or cirrhosis is probably an unwanted but frequent byproduct of the regenerative process, similar to scar formation in any other tissue following extensive damage. Although intensive research in recent years has yielded a wealth of information about regenerative processes, a better understanding of the elements regulating the regenerative process is crucial for effective intervention to prevent or minimize fibrosis while providing optimal conditions for regeneration. Because our only experimental tool is observation in human studies, we must continue the use of experimental animal models including those of transgenic mice to further elucidate the complex interactions of cytokines, ECM, and target cells in the development of liver fibrogenesis, cirrhosis, and cancer.
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PMID:Hepatic regeneration. The role of regeneration in pathogenesis of chronic liver diseases. 879 75

Basic fibroblast growth factor (FGF) is thought to be involved in carcinogenesis and, to clarify its clinical significance, the study of its blood level in cancer patients is important. Plasma levels of basic FGF are reported to be elevated in some cancers. However, little is known of basic FGF levels in plasma in hepatocellular carcinoma (HCC). In this study, we measured basic FGF plasma levels in patients with chronic liver disease and compared the levels in chronic hepatitis (CH), liver cirrhosis (LC), and HCC. We also examined whether these levels were related to serum levels of asparate aminotransferase, alanine aminotransferase, gamma-glutamyl transpeptidase, alkaline phosphatase, leucine aminopeptidase, total bilirubin, total protein, and albumin, and to the indocyanine green test (i.e., liver function tests) and to type III procollagen. 7S domain of IV type collagen, and hyaluronic acid (i.e., markers of liver fibrosis). Levels of basic FGF, determined by a quantitative "sandwich" enzyme immunoassay, were significantly elevated with the progression of liver disease; being 3.67 +/- 2.37 (mean +/- SD). 7.78 +/- 6.61, and 12.37 +/- 7.67 pg/ml in the CH, LC, and HCC groups, respectively. FGF levels were elevated to a greater extent in the HCC patients than in the CH (P < 0.0001) and LC patients (P = 0.0117). Levels were higher in LC than in CH (P = 0.0204). None of the liver function test findings or levels of markers of liver fibrosis were correlated with levels of basic FGF. These results suggest that circulating basic FGF could serve as a new indicator of the progression of chronic liver disease. The extremely elevated plasma of level basic FGF in the HCC group suggests that basic FGF may be related to the development of HCC.
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PMID:Plasma level of basic fibroblast growth factor increases with progression of chronic liver disease. 905 7


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