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)

Ascites occurring in patients with a history of alcoholism is usually due to cirrhosis but clinically significant ascites also occurs in association with pancreatic disease. We reviewed 265 cases of pancreatitis over a five-year period. There were 129 blacks and 136 Caucasians. Ages ranged from 19-86 years with a mean of 46.2 years. Eight of these cases (3%) were found to have pancreatic ascites. The initial serum and urinary amylase had no prognostic value regarding the subsequent development of pancreatic ascites. The mean ascitic fluid amylase was 14,426 Somogyi units (range 1,279-67,774). The mean ascitic fluid protein was 4.6 gm./100ml. (range 1.4-7.2). High enzyme and protein concentration in the ascitic fluid are characteristic of pancreatic ascites. Out of eight cases, two were associated with a pseudocyst, three with hemorrhagic pancreatitis and three with acute edematous pancreatitis. Four of these eight (50%) died. Pancreatic ascites is a distinct clinical entity which should be differentiated from cirrhotic, tuberculous or malignant ascites.
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PMID:Pancreatic Ascites. 43 2

The new method for continuous reinfusion of sterilized, cell-free and concentrated ascitic fluid is described, and utilized in 72 patients with intractable ascites in both malignancy as well as liver cirrhosis and is described with satisfactory results. The management by repeated ascites reinfusion of patients with benign massive ascites has been possible. This method is capable of being applied to patients with malignant ascites. Symptomatic relief and prolonged survival time is anticipated. The method described in this study is simple and free of adverse effects.
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PMID:Treatment of intractable ascites by continuous reinfusion of the sterilized, cell-free and concentrated ascitic fluid. 91 Apr 2

Activity of adenosine deaminase (ADA) in serum and peritoneal fluid was studied prospectively in 24 aetiologically proved cases of ascites and 10 age-matched controls. Patients were divided into 3 groups according to causes of ascites, viz. malignant ascites (11), tubercular peritonitis (7) and cirrhosis of liver (6). Serum ADA values and peritoneal: serum ADA ratio did not show any consistent pattern in any group. But in patients with tubercular peritonitis ADA activity in ascitic fluid was significantly higher (P < .001) than in the other groups. An ascitic ADA level of 30 units/L had a sensitivity of 100% and specificity of 94.1% for tubercular peritonitis. These findings suggest that the ascitic fluid ADA activity is useful for the diagnosis of tubercular peritonitis; this method is simple and least invasive.
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PMID:Diagnostic evaluation of ascitic adenosine deaminase activity in tubercular peritonitis. 145 64

Human chorionic gonadotropin (hCG) is a clinically relevant marker of trophoblastic and nontrophoblastic malignancies. In the present studies, in addition to determining serum hCG, we investigated the presence and properties of hCG immunoreactivity in ascites of patients with nontrophoblastic malignant tumors and, for comparison, in ascites caused by cirrhotic liver disease. Total hCG immunoreactivity [hCG (+hCG-beta)] was found to be elevated above the reference value (greater than 5 IU/liter) in the serum of 2 of 20 patients with cirrhosis and 11 of 20 patients with malignant tumors. For comparison, in ascites, hCG (+hCG-beta) concentrations were frequently higher than in the corresponding serum samples and exceeded 10 IU/liter in 0 of 20 cirrhotic samples and in 16 of 20 malignant samples. In order to elucidate the nature of the hCG immunoreactive material, all samples were then assessed by immunoradiometric assays specific for the intact hCG molecule (holo-hCG) and the free hCG-beta subunit, respectively. In the holo-hCG assay, elevated values were detected in 0 of 20 (0 of 20) cirrhotic ascites (serum) samples and 0 of 20 (1 of 20) malignant ascites (serum) samples. In the free hCG-beta assay, on the other hand, no positive results were obtained in the ascites or serum of 20 patients with liver cirrhosis; however, 8 of 20 serum samples and 16 of 20 ascites samples derived from tumor patients were positive. In accord with the immunological data, gel chromatographical studies of malignant ascites revealed the abundance of free hCG-beta subunit rather than that of holo-hCG. In contrast to malignancy-related ascites, in ascites of patients receiving hCG injections for treatment of infertility, holo-hCG was more abundant than free hCG-beta immunoreactivity. Incubation experiments of purified holo-hCG in ascites for 24 h at -20, 20, or 37 degrees C showed no substantial dissociation of the hCG molecule and release of free hCG-beta immunoreactivity, thus arguing against production of free hCG-beta by degradation of holo-hCG and in favor of its tumor-related secretion. In conclusion, hCG-beta immunoreactivity is frequently elevated in malignancy-related ascites and appears to be related to the presence of free beta subunit of hCG rather than that of the intact hCG molecule. Interestingly, hCG-beta determination in ascites proved to be clearly superior to serum measurement in discriminating between tumor and cirrhosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunoreactive human chorionic gonadotropin and its free beta subunit in serum and ascites of patients with malignant tumors. 154 Sep 61

A retrospective study was undertaken of 41 patients diagnosed as having suffered spontaneous liver rupture over a 4-year period to identify the clinical features, treatment and outcome of this complication in an area in which hepatocellular carcinoma is endemic. Two patients were excluded with a revised diagnosis of haemorrhagic malignant ascites. Of the remaining 39 patients, 37 bled from ruptured hepatocellular carcinoma, one from peliosis hepatis and multiple liver cell adenomas, and one from a malignant hepatic epithelioid haemangioendothelioma. Analysis showed that 59 per cent of patients were in shock on admission and that all but two of the 37 patients with ruptured hepatocellular carcinoma were men with cirrhosis. The association with cirrhosis was significantly higher than in a series of 45 patients with hepatocellular carcinoma undergoing elective resection during the same period (P less than 0.05). Treatment consisted of supportive care only in two patients, angiographic embolization in four, emergency liver resection in 11 of whom six died, hepatic artery ligation in 12 of whom eight died, and suture and/or packing in eight of whom six died. One patient died at laparotomy and in another patient bleeding was successfully arrested by intratumoural injection of absolute alcohol. Because of the high operative mortality of emergency surgery in these poor risk patients, prospective evaluation of emergency angiographic embolization is required.
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PMID:Management of bleeding liver tumours in Hong Kong. 185 53

99 patients with ascites (60 patients with liver cirrhosis and 39 patients with peritoneal carcinosis) were examined by ultrasound tomography of the gall bladder. In most of the cirrhotic patients a thick gall bladder wall was found (7.7 +/- 3.4 mm) often with a three-layer structure. The gall bladder wall of the patients with peritoneal carcinosis was most often not thickened (2.5 +/- 1.6 mm). The difference is statistically significant (p less than 0.1). Thickening of the gall bladder wall was found in both groups of patients by a decreased serum albumin level. The ultrasound tomography of the gall bladder could help in the differentiation of cirrhotic from malignant ascites, especially in combination with determination of the serum albumin level.
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PMID:[The differentiation of cirrhotic from malignant ascites by ultrasonic tomography of the gallbladder]. 189 13

A terminal case of giant cell hepatocellular carcinoma, subsequent to Hepatitis B-associated macronodular cirrhosis is presented, illustrated and discussed. The uncommon finding of malignant ascites, in itself atypical of hepatocellular carcinoma, with an almost exclusive content of giant cells as the cellular component, was a feature of this unusual variant of hepatocellular carcinoma.
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PMID:Giant cell hepatocellular carcinoma. 196 67

Measurement of fibronectin in ascites has been proposed for the differentiation of ascites either due to malignant growth in the peritoneal cavity or liver cirrhosis with portal hypertension. The high ascitic fibronectin concentration in patients with peritoneal carcinomatosis was thought to be due to the synthesis of this protein by neoplastic cells. Therefore in ascites of malignant origin cellular fibronectin should be present as it is synthesized by neoplastic cells. On the other side the transsudative ascites due to liver cirrhosis with portal hypertension should mainly contain plasma-fibronectin, which is secreted by hepatocytes into the bloodstream. With the aid of two different monoclonal antibodies and immunoblotting of partially digested or intact ascitic fibronectin, cellular fibronectin could be demonstrated in ascitic fluid of 10 patients with peritoneal carcinomatosis, 13 patients with liver cirrhosis, one patient with right-sided heart failure and one patient with Budd-Chiari-Syndrome. As determined by a specific ELISA 8 out of 10 samples of malignant ascites contained more than 30 mg/l of cellular fibronectin, whereas 10 out of 13 samples of ascites due to liver cirrhosis contained less than 10 mg/l. Whereas in ascites of malignant origin cellular fibronectin represented about 20% of total fibronectin, in portal ascites fibronectin represented sometimes more than 50% of total fibronectin. Cellular fibronectin of non-malignant origin is probably produced by mesothelial cells or peritoneal macrophages. Therefore, fibronectin accumulating in peritoneal carcinomatosis is only to some extent locally produced, but mainly caused by an unhindered exsudation of plasma-fibronectin.
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PMID:[Genesis of fibronectin in ascites--detection of cellular and plasma fibronectin in portal and malignant ascites]. 205 24

Ascitic fluid alpha 1-antitrypsin (AF-AAT) was compared with ascitic fluid total protein (AF-TP) and the serum-ascites albumin gradient (SAAG) in the differential diagnosis of ascites. The study included 82 consecutive patients of which 42 had cirrhosis, 8 hepatoma (with cirrhosis), and 27 malignant ascites (peritoneal 18, liver 9). The concentration of AF-AAT (milligrams per deciliter) was significantly elevated (P less than 0.001) in hepatoma (174 +/- 123), malignant liver disease (232 +/- 119) and peritoneal neoplasms (376 +/- 106) in comparison with cirrhotics (66 +/- 33). In separating ascites caused by cirrhosis or malignancy, AF-AAT (discriminating limit of 120 mg/dl) had a 96% sensitivity, 95% specificity, and 96% diagnostic efficacy, which was superior to the 87% observed for AF-TP and 86% for the SAAG. Similar results were obtained for the A/S AAT ratio but this test was not available in all patients. AF-AAT was particularly useful in patients with malignancy causing portal hypertension as assessed by SAAG (hepatoma, malignant liver disease). We conclude that AF-AAT may be a valuable parameter in the differential diagnosis of ascites.
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PMID:Ascitic fluid alpha 1-antitrypsin. 216 27

Several studies performed in alcoholics with advanced liver disease have demonstrated a positive correlation between the serum-ascites albumin gradient (SAAG) and measured portal venous pressure. A single study performed in 15 patients with exudative malignant ascites and 29 patients with alcoholic liver disease demonstrated that a SAAG of less than 1.1 was essentially diagnostic of a malignant origin of the ascites. In an effort to confirm and extend these observations to individuals with nonalcoholic liver disease, 24 patients with nonalcoholic liver disease and 11 with alcoholic liver disease undergoing orthotopic liver transplantation (OTLx) were studied. At the time of liver transplantation, each had their serum and ascitic fluid albumin levels determined, the gradient calculated, and their portal venous pressure (PVP) as well as the corrected portal venous pressure (PPc) measured directly. A significant correlation (r = 0.624) between the PPc and the SAAG was found in the 11 alcoholics (P less than 0.05). No such correlation existed for those with nonalcoholic liver disease (r = 0.398). Moreover, a SAAG less than 1.1 was found in three of nonalcoholics with cirrhosis in the absence of an abdominal malignancy. We conclude that (1) the SAAG and PPc are statistically related to each other in individuals with alcoholic liver disease but not in those with a nonalcoholic cause for cirrhosis, and (2) SAAG less than 1.1 is not diagnostic of abdominal malignancy but can occur in those with advanced nonmalignant hepatic disease.
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PMID:Serum-ascites albumin gradients in nonalcoholic liver disease. 229 91


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