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)

Peritoneovenous shunt placement has been reported as a treatment of refractory ascites by general surgeons, but without a clearly established role. The authors successfully inserted shunts under ultrasonographic and fluoroscopic guidance in 12 patients who had symptomatic refractory ascites (nine men, three women; mean maintenance duration, 88.5 d). Nine patients had advanced liver cirrhosis (five with superimposed hepatoma). Other patients had stomach cancer, colon cancer, and complicated polycystic kidney disease. The mortality rate was 83%. Causes of death included bleeding from preexisting varices, sepsis, hepatic failure, rupture of hepatoma, and disseminated intravascular coagulation. The authors describe the feasibility, technical details, and short-term results of percutaneous peritoneovenous shunt placement.
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PMID:Percutaneous peritoneovenous shunt creation for the treatment of benign and malignant refractory ascites. 1174 23

The effectiveness of repeated hepatic dearterialization (RHD) therapy was evaluated in 26 patients with unresectable primary and secondary liver tumors. RHD was performed in 12 patients with hepatocellular carcinoma (HCC), 7 with hepatic metastases from colorectal carcinoma, and 7 with hepatic metastases from gastric carcinoma. It was repeatedly carried out by occluding the hepatic artery for 1 h twice daily. All patients concurrently received an intra-arterial infusion of anticancer drugs. More than 50% remission of the hepatic tumors, defined as a partial response (PR), was demonstrated in 8 patients (31%). A higher PR was seen in hepatic tumors from metastatic gastric cancer (5 out of 7 patients; 71%). Most patients who suffered severe complications had HCC with liver cirrhosis. These preliminary results suggest that RHD with intra-arterial chemotherapy is an acceptable palliative treatment for patients with unresectable liver metastasis from gastric cancer; however, the majority of patients with HCC are not responsive to such treatment, primarily because most have underlying cirrhosis predisposing to the development of postoperative complications at an unacceptably high rate.
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PMID:Repeated hepatic dearterialization for unresectable carcinomas of the liver: report of a 10-year experience. 1176 86

Prognosis for patients with early gastric cancer who undergo gastric resection is far better than that for patients with advanced disease. However, patients with advanced liver cirrhosis may not be suitable for general anesthesia and major surgery. We used a less invasive endoscopic mucosal resection (EMR) with a cap-fitted endoscope to resect an early gastric cancer in a 58-year-old male with decompensated liver cirrhosis. Although postoperative pathology revealed that the tumor had focal invasion to the submucosa, the patient had an uneventful course and was well during 4 years' follow-up. This method may be effective for the treatment of early gastric cancer with focal submucosal invasion when patients are not suitable for major surgery.
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PMID:Endoscopic mucosal resection with a cap-fitted endoscope for early gastric carcinoma with focal submucosal invasion in a patient with decompensated liver cirrhosis. 1180 27

European experience in endoscopic mucosal resection (EMR) for early gastric cancer is still relatively low, since early stomach cancer is diagnosed at a much lower rate in Europe than in Japan and generally operable patients are referred to surgery for radical resection. Endoscopic mucosal resection or mucosectomy was developed as a promising technology to diagnose and treat mucosal lesions in the esophagus, stomach and colon. In contrast to surgical resection, EMR allows "early cancers" to be removed with a minimal cost, morbidity and mortality. We present the case of a patient with hepatic cirrhosis incidentally diagnosed with an elevated-type IIa early gastric cancer. Echoendoscopy was performed in order to assess the depth of invasion into the gastric wall confirming the only mucosal involvement. We performed an EMR using "cup and suction" method. After the procedure, the patient experienced an acute upper gastrointestinal bleeding from the ulcer bed requiring argon plasma coagulation. The histopathological examination confirmed an early cancer, without involvement of muscularis mucosae. The patient has had an uneventful evolution being well at six months after the procedure
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PMID:Endoscopic mucosal resection for early gastric cancer. A case report. 1209 12

We describe the case of a patient with gastric cancer complicated by portal hypertension due to liver cirrhosis. Endoscopy showed esophageal varices in the lower third of the esophagus and a superficially depressed lesion in the middle third of the stomach, while a biopsy suggested signet-ring cell carcinoma. Laboratory data showed pancytopenia, the indocyanine green fraction after 15 min was 29%, and the symptoms corresponded to the Child B criteria. A preoperative arteriogram revealed a remarkably dilated left gastric vein and the development of collateral pathways. We performed a distal subtotal gastrectomy with a reconstruction by the Billroth I method combined with a distal splenorenal shunt (DSRS) and a splenopancreatic disconnection (SPD). The endoscopic findings of the esophageal varices 15 months after surgery showed only a few white veins and the red color sign had disappeared. Now 7 years have passed since surgery, the risk of variceal hemorrhage has disappeared, and the patient is ambulatory and well. These results seems to be attributable to the long-term maintenance of the shunt selectivity and good portal hemodynamics. In patients with gastric cancer complicated with esophageal and/or gastric varices, it is recommended that DSRS with SPD be performed after a reconstruction using the Billroth I method.
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PMID:Gastrectomy in combination with a distal splenorenal shunt in a patient with gastric cancer and portal hypertension: report of a case. 1218 26

We describe the case of an 87-year-old woman who presented to Tokyo Kousei Nenkin Hospital because of appetite loss and general fatigue. Multiple liver masses and Borrmann type 2 gastric tumor were detected. A clinical diagnosis of hepatocellular carcinoma and gastric cancer was made based on the patient's high levels of serum alpha-fetoprotein (AFP; 490 200 ng/mL) and protein induced by vitamin K absence or antagonist-II (PIVKA-II, 2284 mAU/mL). The patient's general condition worsened gradually and she died 42 days after admission. Autopsy revealed that the predominant histological structure of the gastric tumor was trabecular or sheet-like, although a tubular structure was also found. Venous invasion was prominent. Immunohistochemically, the tumor tissue was positive for AFP and a few tumor cells were positive for PIVKA-II. The histological appearance and immunohistochemical features of the hepatic tumors resembled that of the gastric tumor. This case was pathologically diagnosed as AFP- and PIVKA-II-producing gastric carcinoma with multiple liver metastases. When tumors are found in the stomach and liver and serum PIVKA-II level is abnormally high, the possibility of PIVKA-II-producing gastric cancer with liver metastasis should be considered, especially when hepatitis virus markers are negative and liver cirrhosis is not present.
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PMID:Des-gamma carboxy prothrombin (PIVKA-II) and alpha-fetoprotein producing gastric cancer with multiple liver metastases. 1267 68

An increased risk for gastric cancer in patients with liver cirrhosis has recently been reported in epidemiological studies. The present endoscopic study was performed to further evaluate whether people with cirrhosis are at increased risk for gastric cancer development. We reviewed the medical records of all cirrhotic patients referred to our Endoscopic Service for portal hypertension screening and, therefore, cases of latent gastric cancer were observed. For a comparison, the prevalence (age and sex standardized) of latent gastric cancer in the general population was estimated hypothesizing a latency period of 5 years. Overall, 1379 patients with cirrhosis were selected from a total of 15 791 endoscopically examined different patients observed during the period 1982-1997. Histological assessment revealed the presence of gastric cancer in 10 patients (9 males and 1 female). There was a significant 2.6-fold (P<0.01) increase in prevalence of gastric cancer compared with that expected in our cirrhotic patients. In conclusion, our findings confirm that liver cirrhosis would seem to be a risk factor for the development of gastric cancer. Other studies are needed to evaluate the pathogenic mechanisms involved.
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PMID:Gastric cancer prevalence in patients with liver cirrhosis. 1277 54

Previously, we reported the identification and characterization of a novel cancer/testis antigen gene, CAGE(4), that was expressed in various histological types of tumors, but not in normal tissues, with the exception of the testis. To date, molecular mechanisms for the expression of CAGE have never been studied. In our expression analysis, we found that some cancer cell lines did not express CAGE. The expression of CAGE could be restored in these cell lines by treatment with 5(')-aza-2(')-deoxycytidine, suggesting that the expression of CAGE is mainly suppressed by hypermethylation. Bisulfite sequencing analysis of the 16 CpG sites of the CAGE promoter in various cancer cell lines and tissues revealed a close relationship between the methylation status of the CAGE promoter and the expression of CAGE. The transient transfection experiments displayed that the methylation of CpG sites inhibited the CAGE promoter activity in luciferase reporter assays. The methylation of the CpG sites inhibited the binding of transcription factors, shown by a mobility shift assay. A methylation-specific PCR analysis revealed that hypomethylation of the CAGE promoter was present at frequencies of more than 60% in breast, gastric, and lung cancers, and hepatocellular carcinomas, and at frequencies of less than 40% in prostate, uterine cervical, and laryngeal cancers. Promoter hypomethylation was found in chronic gastritis (19/55, 34.5%) and liver cirrhosis (13/22, 59%), but not in normal prostate, normal colon, or chronic hepatitis. These results suggest that the methylation status of the CpG sites of CAGE determines its expression, that the hypomethylation of CAGE precedes the development of gastric cancer and hepatocellular carcinoma, and that the high frequencies of hypomethylation of CAGE, in various cancers would be valuable as a cancer diagnostic marker.
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PMID:Promoter hypomethylation of a novel cancer/testis antigen gene CAGE is correlated with its aberrant expression and is seen in premalignant stage of gastric carcinoma. 1284 80

SAP-1 (stomach cancer-associated protein tyrosine phosphatase-1) is a transmembrane-type protein tyrosine phosphatase that has been implicated as a negative regulator of integrin-mediated signaling. The potential role of this enzyme in hepatocarcinogenesis has now been investigated by examining its expression in 32 surgically excised human hepatocellular carcinoma (HCC) specimens. Both immunohistochemical and immunoblot analyses revealed that normal liver tissue, as well as tissue affected by chronic hepatitis or cirrhosis, contained substantial amounts of SAP-1. The expression level of SAP-1 in 75% of well-differentiated HCCs was similar to or higher than that observed in the surrounding noncancerous tissue. In contrast, the abundance of SAP-1 in 85.7% of moderately differentiated HCCs and in all poorly differentiated HCCs was greatly reduced compared with that in the adjacent tissue. Indeed, SAP-1 was almost undetectable in 83.3% of poorly differentiated HCCs. Furthermore, expression of recombinant SAP-1 in two highly motile human HCC cell lines resulted in a change in morphology and a marked reduction in both migratory activity and growth rate. In conclusion, these results indicate that SAP-1 expression is downregulated during the dedifferentiation of human HCC, and that this downregulation may play a causal role in disease progression.
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PMID:Downregulation of stomach cancer-associated protein tyrosine phosphatase-1 (SAP-1) in advanced human hepatocellular carcinoma. 1287 10

This study examines the association between education and mortality from specific causes of death based on mortality records for 1996 and 1997, and 1996 population census data from the Region of Madrid (Spain). Poisson regression models were used to estimate the percentage increase in mortality associated with 1 year less education. The percentage increases in mortality from stomach cancer, lung, bladder and liver cancers, for aids, chronic obstructive pulmonary disease, pneumonia and influenza, and chronic liver disease and cirrhosis were higher in men than in women, whereas the percentage increases in mortality from colon cancer, diabetes mellitus, ischemic heart disease and nephritis, nephrosis and nephrotic syndrome were higher in women. The results found for some causes of death--lung cancer, ischemic heart disease, diabetes mellitus and chronic obstructive pulmonary disease--reflect the variations by educational level in the prevalence of lifestyle-related risk factors in men and women. Various hypotheses have been suggested for other causes of death, but it is not known why the magnitude of the association between education and mortality from some causes of death differs between men and women. Future studies of this subject may provide some clues as to the underlying mechanisms of this association.
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PMID:The size of educational differences in mortality from specific causes of death in men and women. 1288 84


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