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)

This investigation was undertaken to measure regional portal blood flow of the liver. The measurement was performed by injecting 133Xe into the proper hepatic artery through a balloon catheter and then occluding the proper hepatic artery with an inflated balloon. Data were collected using a gamma camera, and washout curves were generated. They were analyzed by the initial slope method and Kety Schmidt equation. The average regional portal blood flows were: 59.31 +/- 13.04 ml/100 g per min, 58.71 +/- 14.14 ml/100 g per min and 37.12 +/- 10.11 ml/100 g per min in hospital controls (11), patients with chronic hepatitis (10) and those with liver cirrhosis (56), respectively. In the patients with cirrhosis, the regional portal blood flow was significantly reduced (P less than 0.01). The reproducibility of this method was satisfactory. The measurement of regional portal blood flow will be useful to evaluate underlying liver injuries and determine indications of a transcatheter arterial embolization of the liver.
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PMID:A measurement of regional portal blood flow with Xe-133 and balloon catheter in man. 277 93

Plasma amino acid levels were determined in 23 patients in comparison with 16 normal subjects and 17 patients with liver cirrhosis. Patients with hepatocellular carcinoma had elevated levels of the aromatic amino acids and lowered levels of the branched-chain amino acids, as seen in liver cirrhosis; however, they had lowered levels of alanine and glutamine as compared with normal subjects and with liver cirrhosis patients. Following treatment with intraarterial chemotherapy and/or transcatheter arterial embolization, plasma levels of alanine and glutamine recovered. These results suggest that the consumption of alanine and glutamine increase in hepatocellular carcinoma.
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PMID:Plasma amino acid patterns in hepatocellular carcinoma. 282 52

Protein C, one of the vitamin K-dependent plasma proteins synthesized in the liver, was measured immunologically in normal subjects (n = 20), patients with hepatocellular carcinoma (n = 60), liver cirrhosis (n = 60), acute hepatitis (n = 16), chronic hepatitis (n = 19), malignant neoplasms other than hepatocellular carcinoma (n = 35) and patients on warfarin treatment (n = 20). We also assayed gamma-carboxyglutamic acid-complete (carboxylated) protein C in these population by using a monoclonal antibody directed against human protein C, JTC-1, which recognizes the gamma-carboxyglutamic acid domain-related conformational change induced by metal ions. We demonstrated that the plasma of patients with hepatocellular carcinoma contains considerable amounts of gamma-carboxyglutamic acid-incomplete protein C, evidenced by the significantly reduced protein C:gamma-carboxyglutamic acid/protein C:antigen ratios in hepatocellular carcinoma as compared to those seen in normal controls, other liver diseases and other malignant neoplasms (p less than 0.01). In two patients with hepatocellular carcinoma with the reduced protein C:gamma-carboxyglutamic acid/protein C:antigen ratios, successful treatment (transcatheter hepatic arterial embolization or lipiodolization of antitumor agent) led to the very rapid normalization of the ratios. Intravenous administration of vitamin K, however, induced no such effects in three other patients with hepatocellular carcinoma with the abnormality. We conclude that the impaired vitamin K-dependent gamma-carboxylation observed in patients with hepatocellular carcinoma involves not only prothrombin, but also protein C, and that the impairment is not due to vitamin K deficiency.
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PMID:The acquired vitamin K-dependent gamma-carboxylation deficiency in hepatocellular carcinoma involves not only prothrombin, but also protein C. 283 89

We have investigated the effects of preoperative Lipiodol-Transcatheter arterial embolization (Lp-TAE) on both the nuclear DNA content of noncancerous liver cells by DNA-cytofluorometry (using NIKON SPM-RF1-D), and the histopathological findings of liver lesions. Lp-TAE through the hepatic artery was performed on ten primary hepatocellular carcinoma patients using Gelfoam in combination with adriamycin (40 mg) or mitomycin C (20 mg), emulsified in Lipiodol (10 ml) and 60% Urografin (2 ml). And hepatic resection was carried out after one or two months later in each case. Histologically, primary hepatocellular carcinoma lesions showed various patterns of necrosis, while the non-cancerous liver cells did not show hepatocellular infarction in the liver cirrhosis. The results of the nuclear DNA content showed an increase in the fractions of poliploid cells in the non-cancerous lesions treated with Lp-TAE compared with that in the normal age-matched controls. But we found no remarkable differences in the ploidy patterns between Lp-TAE treated patients and untreated patients with liver cirrhosis. In conclusion, preoperative Lp-TAE does not induce any remarkable histological hepatocellular damage of non-cancerous lesion and does not affect nuclear DNA content of non-cancerous liver cells.
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PMID:[Cytofluorometric and histopathological studies on non-cancerous liver lesions after lipiodol-transcatheter arterial embolization]. 284 9

The concentration of serum immunoreactive prolyl 4-hydroxylase (S-IRPH) was determined in patients with various liver diseases by the radioimmunoassay developed previously. S-IRPH values were elevated in acute hepatitis (p less than 0.01), hepatocellular carcinoma (p less than 0.05), metastatic liver neoplasm (p less than 0.01) and cholestatic diseases (p less than 0.001), but no significant elevation was seen in chronic hepatitis or liver cirrhosis. The mean value of S-IRPH was highest in cholestatic diseases, and next highest in acute hepatitis. In addition to acute hepatitis, S-IRPH was increased in other conditions of hepatocellular damage such as exacerbation of chronic hepatitis or immediately after transcatheter arterial embolization of hepatocellular carcinoma. In cases of hepatocellular damage S-IRPH varied concurrent with cytoplasmic enzyme (AST, ALT and LDH) levels and in cases of cholestatic diseases with biliary enzyme (Al-P and gamma GTP) levels. These properties appear to be unique among serum enzymes. The characteristics of S-IRPH were considered to be related to its unique subcellular localization within the cell, ie the membrane of rough endoplasmic reticulum.
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PMID:Studies on serum immunoreactive prolyl 4-hydroxylase in liver diseases--its elevation both in hepatocellular damage and cholestatic diseases. 284 41

Doppler ultrasound detection of the blood flow associated with liver tumours was studied in primary hepatocellular carcinoma as well as in metastatic liver cancer and haemangioma. Doppler signals were detected from 48 of 55 hepatocellular carcinomas (87.3%), seven of 25 metastatic liver cancers (28.0%) and four of 30 haemangiomas (13.3%). The waveforms of Doppler signals were divided into two types: the pulsatile wave, which was detected from hepatocellular carcinoma (in 35 of the 48 with Doppler signals) and metastatic liver cancer (in all seven with positive signals), and the continuous wave, which was seen from hepatocellular carcinoma (41 out of 48) and haemangioma (in all four with signals). In six patients with hepatocellular carcinoma who underwent transcatheter arterial embolization, the pulsatile wave detected before therapy disappeared immediately thereafter and it is possible that this type of wave originates from tumour vessels. In the study of small, hypoechoic, mass lesions appearing in liver cirrhosis, such signals were also demonstrated, even in eight of 10 small hepatocellular carcinomas less than 2 cm in diameter, whilst they were not detected from nine regenerative nodules related to cirrhotic change. In conclusion, the Doppler ultrasound method may be a useful technique in detecting blood flow within liver tumours and may offer the possibility of a differential diagnosis of small tumours.
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PMID:Pulsed Doppler in the diagnosis of small liver tumours. 284 47

Transcatheter arterial embolization (TAE) for unresectable hepatocellular carcinoma (HCC) was performed in cirrhotic patients with nonoccluded main portal trunk and total bilirubin levels less than 5 mg/dl. In 48 patients with tumor response to TAE, its benefit was evaluated by comparing their survival with that in 28 patients after conservative treatments, matched by clinical data. In TAE-treated patients, tumor findings on computerized tomography and angiogram were significantly different between those dying within 3 months and those surviving over 18 months. In cases of tumors occluding the first- or second-order portal branches or occupying more than 20% of the liver, or relatively hypovascular tumors with unclear boundaries, survival was not different between TAE- and non-TAE-treated patients, whereas it was significantly improved by TAE in cases without these findings. These results suggest that TAE is beneficial in cases of unresectable HCC complicating liver cirrhosis, but its benefit is limited under certain conditions.
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PMID:Transcatheter arterial embolization for hepatocellular carcinoma. Benefits and limitations for unresectable cases with liver cirrhosis evaluated by comparison with other conservative treatments. 298 26

In 6 patients with spontaneous rupture of hepatocellular carcinoma complicating liver cirrhosis, but with no occlusion of the main portal trunk, transcatheter arterial embolization was performed within 7 days of the rupture. All 6 patients were thought to be inoperable because of shock state or severe hepatic dysfunction. In all 6 patients, the progressive decrease in the hematocrit ceased soon after the embolization. Five patients survived for 31-168 days after the embolization; 1 patient who developed septicemia died 10 days later. We conclude that transcatheter arterial embolization is beneficial as a procedure of first choice for ruptured hepatocellular carcinoma when the portal blood flow is maintained.
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PMID:Benefit of transcatheter arterial embolization for ruptured hepatocellular carcinoma complicating liver cirrhosis. 298 72

Twenty-two patients with hepatocellular carcinoma were treated with transcatheter arterial embolization therapy. In the six who died within about a month, serum albumin and Ch-E were lower, and total bilirubin and ICG R15 were higher than in the other cases. In four of them, more than 50% of the liver was occupied by tumor, and tumor thrombosis were found in the portal trunk or bilateral first portal branch. Five patients died of hepatic failure followed by upper gastrointestinal bleeding. One died of cachexia. The causes of short survival were 1) severe liver cirrhosis, 2) portal obstruction, 3) large tumor, 4) widespread TAE, 5) retrograde flow of gelfoam.
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PMID:[Retrospective study of short survival cases in hepatocellular carcinoma after transcatheter arterial embolization therapy]. 298 79

A total of 850 patients with hepatocellular carcinoma seen during the last 8 years were analyzed retrospectively for survival in relation to treatment and disease stage. A new staging scheme based on tumor size, ascites, jaundice and serum albumin was used. Clearly, the prognosis depended on disease stage. The median survival of 229 patients who received no specific treatment was 1.6 months, 0.7 month for Stage III patients, 2.0 months for Stage II, and 8.3 months for Stage I. The median survival of Stage I patients who had hepatic resection (n = 115) was 25.6 months and Stage II patients with resection (n = 42) was 12.2 months. In patients who had a small cancer (less than or equal to 25% of liver area in size) the median survival was 29.0 months. Survival of the surgically treated patients, which represented a highly selected group, was better than that of medically treated patients of a comparable stage. Median survival of Stage I medically treated patients (n = 124) was 9.4 months, for Stage II (n = 290) 3.5 months, and for Stage III (n = 50) 1.6 months. Medical treatment prolonged survival in Stage II and III patients, but not in Stage I. Transcatheter arterial embolization gave a better survival compared with chemotherapy, whether intra-arterial bolus administration of mitomycin C, systemic mitomycin C, or oral/rectal tegafur, in Stage II. Among various chemotherapeutic modalities, intra-arterial bolus injection was superior to systemic chemotherapy in survival in Stage II. In Stage III, chemotherapy improved survival as compared with no specific treatment. The major causes of death were hepatic failure and gastrointestinal bleeding, probably due to the coexistent advanced cirrhosis. These results in survival are much improved over the past reports, and the differences are probably a result of earlier diagnosis and frequent hepatic resections.
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PMID:Natural history of hepatocellular carcinoma and prognosis in relation to treatment. Study of 850 patients. 299 Jun 61


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