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)

The authors have performed 631 urgent suprapubic transvesical adenomectomies in patients with prostate adenoma complicated by acute urine retention or hemorrhage. Prearranged and urgent interventions had, by the authors' experience, virtually the same rate of postoperative complications and lethal outcomes. The risk in urgent adenomectomy performed in 294 patients was attributed to their concurrent affections: postinfarction cardiosclerosis, myocardial ischemia or hypertensive crisis, hemiparesis after brain apoplexy, bronchial asthma, diabetes mellitus, hepatic cirrhosis, chronic lymphoid leukemia, drug polyallergy, multiple tumors of the urinary bladder, stomach, etc., in stage T1-3NOMO. 80 patients had intermittent chronic renal failure. In compensation of severe concurrent diseases and satisfactory condition of the patients urgent adenomectomy was conducted within 24 hours since hospitalization. Longer interval (within 24-72 hours) was necessary in subcompensation of the concurrent diseases, intermittent chronic renal failure which were intensively treated. The authors achieved uneventful postoperative course for 272 (92.5%) high-risk patients. Postoperative lethality made up 3.06%. According to 1-11-year follow-up 7 patients died, for the most part of blood and respiratory diseases. Functional long-term outcomes were good in 83.5% of the patients. Basing on their experience, the authors specify indications to urgent adenomectomy and optimal time of its conduction. Contraindications to urgent adenomectomy were revised and narrowed.
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PMID:[The indications and contraindications for emergency adenomectomy in patients with severe concomitant diseases]. 753 45

The clinicopathological findings of eight children with hepatic adenoma in the absence of cirrhosis are presented. The lesions ranged in diameter from 0.1 to 14.5 cm. Associated disorders were Fanconi's anemia, type I glycogen storage disease. Hurler's disease, and severe combined immunodeficiency with ADA deficiency. The remaining three children had adenoma without known associated disorders. In the children with glycogenosis and Hurler's disease the adenomas were multiple. Significant dysplasia occurred in the two children with Fanconi's anemia; however, the lesions behaved in a benign fashion--one with regression of the tumor after cessation of androgen therapy and the other with nonrecurrence after complete resection. Proliferating cell nuclear antigen (PCNA) labeling index (LI) of the adenoma arising in patients with Fanconi's anemia was significantly greater than the PCNA-LI of adenoma in the other children (mean 4.1% versus 0.9% of nuclei), approaching the lower end of the spectrum for reported hepatocellular carcinoma cases. We emphasize that the worrisome pathology that may occur in hepatic adenoma in children, particularly with Fanconi's anemia, does not necessarily predict malignant behavior. The association of hepatic adenoma with Hurler's disease or severe combined immunodeficiency has not been reported previously.
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PMID:Hepatic adenoma in the pediatric age group. Clinicopathological observations and assessment of cell proliferative activity. 757 76

The prolonged half-life of mutant p53 makes feasible its immunocytochemical detection. In order to assess the pathogenetic role of mutant p53 in regenerative and neoplastic liver disease we studied its immunohistochemical expression in cases of hepatic cirrhosis, hepatocellular carcinoma (HCC), cirrhosis with areas of HCC, hepatocellular adenoma and focal nodular hyperplasia. The study included needle and wedge biopsies of 50 cirrhotic livers, 59 HCCs (36 of them with associated cirrhosis), six adenomas and two focal nodular hyperplasias. Sixty-five HCC fine-needle cytology specimens were also included in the study. There was no immunohistochemical evidence of mutant p53 expression in any of the cases of cirrhotic liver (except for one instance associated with HCC) adenoma or focal nodular hyperplasia. In contrast p53 was detected in 8.5% of HCC cases in the biopsy series and 24% of HCC cases in the fine needle aspiration series. In addition, mutant p53 expression in HCC was positively correlated with tumour grade. According to grade, the distribution of p53 positive immunoreactivity among HCCs was as follows: Grade I-II, 0% of cases in the biopsy series and 9% in the fine needle aspirates; Grade III, 18% in the biopsy series and 55% in the fine needle aspirates; and Grade IV, 40% in the biopsy series. Therefore, mutant p53 expression does not seem to be associated with benign liver lesions but seems to correlate with the progression of HCC through various grades of increasing malignancy.
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PMID:p53 immunoreactivity in hepatocellular adenoma, focal nodular hyperplasia, cirrhosis and hepatocellular carcinoma. 771 85

The present report concerns a patient who was first diagnosed as having adenoma in the duodenal bulb and subsequently was discovered to have adenomas in the stomach and colon. Surgical procedures including endoscopic resection could not be carried out because the patient had advanced liver cirrhosis. Follow-up colonoscopy no longer detected any polyp in the colon. Ultrasonography demonstrated a slowly growing hypoechoic mass in the liver, which was indicative of hepatocellular carcinoma. Then, single chemotherapy with oral administration of 5'-deoxy-5-fluorouridine was initiated. Surprisingly, repeated esophagogastroduodenoscopy revealed gradual regression of the gastric and duodenal tumors. Findings from the endoscopy and biopsy materials 10 months after the start of therapy showed disappearance of the gastric and duodenal adenomas. Despite enlargement of the hepatic mass, no recurrence of gastric and duodenal tumors has been noted during the past 1 1/2 yr.
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PMID:Simultaneous occurrence of adenomas in stomach, duodenal bulb, and colon: disappearance of gastric and duodenal adenomas during oral administration of 5'-deoxy-5-fluorouridine. 794 42

The development of hepatocellular adenoma has been recognized in association with glycogen storage disease type I and, less often, with glycogen storage disease type III, but, to our knowledge, it has not been reported in glycogen storage disease type IV. We had the opportunity to study an 11-month-old male infant who underwent orthotopic liver transplantation for cirrhosis that developed in the setting of glycogen storage disease type IV. A clinically unsuspected hepatocellular adenoma was present in the explanted liver. Glycogen storage disease type IV should be considered as a potential precursor to the development of hepatocellular adenoma. Recognition of this association is important, both in terms of the differential diagnosis of tumors that occur in this setting and also to anticipate potential complications of this benign neoplasm.
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PMID:Hepatocellular adenoma in glycogen storage disease type IV. 828 39

Hepatic silicosis, cirrhosis, liver cell adenoma, and carcinomas developed in nude mice (NCr-Nu) given quartz by the subcutaneous and intraperitoneal routes. Syrian golden hamsters (15:16 EHS:cr) given quartz by both routes developed extensive fibrosis and cirrhosis and had higher morbidity and mortality rates after 3 months. Crystalline silica (quartz) induces fibrosis, adenomas, and carcinomas in the lungs of Fisher 344 rats, but certain strains of mice and hamsters are resistant to quartz-induced pulmonary carcinogenesis. Pulmonary fibrosis, however, is minimal in mice and absent in hamsters who received quartz intratracheally. To determine whether species differences are due to organ-specific rather than species-specific factors, susceptibility of the liver to quartz toxicity was investigated in nude mice and hamsters. The present study shows that the differential manifestations of quartz toxicity by these rodent species are dependent on factors that are organ-specific rather than host-specific. At 3 months, hepatocytes in mice were immunostained with intracellular transforming growth factor (TGF) beta 1 (LC 1-30) but not with TGF-beta 1 latency-associated peptide (LAP) protein (266-278); at 12 months, hepatocytes were immunostained with TGF-beta 1 LAP (266-278) but not with TGF-beta 1 (LC1-30). The hepatocytes of hamsters at 3 months showed immunoreactivities to TGF-beta 1 LAP (266-278) and TGF-beta 1 (LC1-30); immunostaining to TGF-beta 1 (LC1-30) was detected in nonparenchymal cells. Extracellular TGF-beta 1 (CC1-30) was detected in the silicotic granulomas and fibrous tissue in livers of both species. Quartz-induced liver carcinoma did not express TGF-beta 1 LAP (266-278) and LC (1-30) proteins, but these were detected in the cells of the adenoma in the same liver. Control animals showed no hepatic lesions nor immunoreactivity to TGF-beta 1. The spatial and temporal patterns of expression of TGF-beta 1, TGF-beta 2, TGF-beta receptor type II messenger RNAs (mRNAs), and TGF-beta 1 proteins in the different hepatic lesions suggests that TGF-beta isoforms may play a role in the pathogenesis of quartz-induced fibrosis, cirrhosis, liver cell adenoma, and carcinoma.
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PMID:Hepatic silicosis, cirrhosis, and liver tumors in mice and hamsters: studies of transforming growth factor beta expression. 862 Nov 63

Hepatocellular carcinoma (HCC) is a common type of cancer, with approximately 260,000 new cases each year, and liver cirrhosis is generally considered a major predisposing factor for HCC. However, specific changes of gene expression in liver cirrhosis and HCC remain obscure. The expression of genes for hepatocyte growth factor (HGF), its receptor c-met proto-oncogene, c-myc proto-oncogene, and albumin was analyzed. Gene expression was studied by PCR in seven normal human livers, nine cases of hepatitis C cirrhosis, 12 cases of alcoholic cirrhosis, two cases of liver adenoma, and 12 cases of HCC. HGF and c-met protein were revealed by immunofluorescent staining. HGF mRNA was not expressed in normal livers but was detected in adenomas, in 80% of HCC, and in some cirrhoses. Paraffin-embedded and fresh-frozen tissue samples yielded similar results. Immunohistochemical data correlated with PCR results regarding the overexpression of the HGF/c-met system in HCC. Albumin gene expression was decreased in HCC vs normal livers, consistent with altered function of tumor hepatocytes. The elevated expression of the HGF/c-met system in HCC may play a role in tumor development and/or progression. Tissue localization studies of HGF and its receptor c-met protein support the existence of both autocrine and paracrine mechanisms of action of HGF in HCC vs only a paracrine mechanism in normal liver.
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PMID:Expression of HGF, its receptor c-met, c-myc, and albumin in cirrhotic and neoplastic human liver tissue. 901 Apr 72

Advances in operative, diagnostic and post-operative care technique have rendered liver resections safe. Consecutively, indications for operative interventions in primary and secondary liver tumors have changed. A current state of the art is presented. Focal nodular hyperplasia, if found incidentally during laparotomy, should be removed en-passant. Large or central lesions should be biopsied and can be observed if they remain asymptomatic and stable in size. Symptomatic or growing FNH should be removed. If the diagnosis is evasive resection should be favored. Most patients with hepatocellular adenoma are symptomatic and the lesion should therefore be removed. Hemangiomas are rarely causing symptoms. In case they truly are, or if they cause complications they should be excised. Anatomical resections for hepatocellular carcinoma are only feasible in non-cirrhotic livers or in patients with cirrhosis and compensated liver function. Other patients are candidates for liver transplantation if the cancer is stage I or II. Stage III and IVa lesions are subject of current studies. Surgical resection remains the only potentially curative treatment for intrahepatic cholangiocellular carcinoma. Because of their dismal prognosis these patients are not candidates for transplantation. Resection continues to be the most effective therapy for colorectal metastases to the liver. Patients with non-colorectal, non-neuroendocrine metastases are usually only candidates for surgical palliation. Cure can be achieved in patients with renal cell carcinoma or Wilms' tumor. Additionally, neuroendocrine metastases to the liver can be resected in curative intent if extrahepatic disease was excluded. In the few symptomatic patients in whom extrahepatic disease was excluded, symptomatic treatment has failed, and the lesions are not resectable, liver transplantation can provide a reasonable therapeutic choice.
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PMID:[Surgical therapy of primary and secondary liver tumors]. 906 25

Identification of gene products exclusively or abundantly expressed in cancer may yield novel tumour markers. We recently isolated a number of cDNA clones, including alpha-prothymosin, from rat hepatocellular carcinoma (HCC) using a subtraction-enhanced display technique. Alpha-Prothymosin is involved in cell proliferation and is regulated by the oncogene c-myc in vitro. In the present study, we analysed alpha-prothymosin gene expression and its correlation with c-myc in patients with HCC, cirrhosis and adenoma and in normal controls. Hepatic alpha-prothymosin messenger RNA (mRNA) levels were two- to 9.2-fold higher in tumoral tissues than in adjacent non-tumoral tissues in 14 of 17 patients with HCC, regardless of coexisting cirrhosis and viral hepatitis. No marked difference in alpha-prothymosin mRNA levels was present in patients with adenoma and hepatic cirrhosis and in healthy controls. The c-myc mRNA amounts were two- to fivefold increased in 11 of 17 patients with HCC and correlated significantly with those of alpha-prothymosin (P < 0.001). In situ hybridization revealed that increased alpha-prothymosin mRNA was localized in the tumour nodules of the patients with HCC. These data suggest that overexpression of alpha-prothymosin in HCC patients, correlated with c-myc, is possibly involved in the tumorigenic process and may be a novel molecular marker for human HCC.
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PMID:Overexpression of hepatic prothymosin alpha, a novel marker for human hepatocellular carcinoma. 936 69

The incidence and characteristics of hepatic tumors -primitive or secondary- were analyzed in a series of 596 patients with cirrhosis and on whom an autopsy was carried out. A hepatic tumor was discovered in 43.6%: 96.5% with histological findings of malignant disease and only 3.4% with benign disease. The tumors discovered showed the following in order of frequency: hepatocellular carcinoma (90.3%), hepatic metastases (4.2%), cholangiocarcinoma (2.3%), adenoma (1.5%), hemangioma (1.2%) and hamartoma (0.8%). Therefore, 10% of the neoplasms located in the cirrhotic liver were different from the hepatocellular carcinoma. In 2% of the subjects with hepatic tumors, two histologically different lesions were found to co-exist in the liver, and in every case it was found to be a hepatocellular carcinoma related to another tumor, which further complicated the diagnosis. The most frequent type of hepatocellular carcinoma was multinodular, although diffuse tumors most frequently developed metastases. When the hepatocellular carcinoma was uninodular and small, distal spread was exceptional. Metastatic infiltration of the liver by neoplasms of different origin, characteristically infrequent in cirrhosis, was always accompanied by spread to other organs and did not appear as a single nodule in any case. We conclude that the correct diagnosis of tumor-related lesions located, in a cirrhotic liver is occasionally difficult during life, especially when the neoplasms are different from the hepatocellular carcinoma.
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PMID:Hepatic tumors in patients with cirrhosis: an autopsy study. 940 34


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