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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A comparative study of a new tumour marker, CA242, and CA19-9 was conducted with special reference to their diagnostic usefulness in pancreatic cancer. CA242 showed sensitivity similar to that of CA19-9 for overall cases and early cases (stage I tumour) of pancreatic cancer. For other malignancies, the positive rates of CA242 were lower than those of CA19-9 except for colorectal cancer. An important characteristics of CA242 was that it was only slightly and infrequently elevated in the sera of patients with benign diseases such as chronic pancreatitis, chronic hepatitis and liver cirrhosis. This characteristic was more apparent in the patients with benign obstructive jaundice, indicating that the serum level of this marker was scarcely affected by cholestasis. Using cut-off levels corresponding to a 90% specificity, the clinical results obtained with CA242 in the diagnosis of pancreatic cancer were similar to those obtained with CA19-9, except that CA19-9 was falsely negative in some patients with early-stage pancreatic cancer. These findings suggest the usefulness of this marker for screening pancreatic cancer in patients on their first hospital visit. However, CA242 was found to be influenced by the Lewis blood group system. This unfavourable result is attributed to the C241 catcher antibody of this assay system, which has almost the same epitope specificity as the C50 and the NS19-9 monoclonal antibodies. In conclusion, CA242 is superior to CA19-9 in diagnosing pancreatic cancer by virtue of its higher specificity.
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PMID:Comparative study of CA242 and CA19-9 for the diagnosis of pancreatic cancer. 808 Jul 34

The pathogenetic mechanism underlying glucose intolerance in pancreatic cancer is still unclear. We studied the pattern of three glucose regulating hormones (C-peptide, glucagon and GH) in pancreatic cancer patients with (N = 34) and without (N = 8) hyperglycemia, and compared the findings made with those from subjects with other hyperglycemic conditions of well-known origin [type I diabetes mellitus (8 cases) and diabetes mellitus secondary to chronic pancreatitis (13 cases) or liver cirrhosis (4 cases)]. In hyperglycemic pancreatic cancer patients, C-peptide was absent in 26% of the cases, reduced in 24%, elevated in 29% and within the normal range in the remaining 21%. In normoglycemic pancreatic cancer this hormone was reduced in two cases (25%) and within the normal range in all the others. GH was within the normal range in all cases: glucagon was below the normal range in some hyperglycemic pancreatic cancer patients (41%) or within the normal range in all the remaining patients. No correlations were found between the three hormones when findings from subjects were considered all together. However, in pancreatic cancer C-peptide and glucagon presented consensual variations. C-peptide, glucagon and GH levels were not related to tumor volume; glucagon was found to be associated with liver metastases. C-peptide was correlated with serum ALT and ALP. We may conclude that hyperglycemia associated with pancreatic cancer may be caused by different mechanisms. In some cases a reduced secretion of both insulin and glucagon was observed, as occurs in chronic pancreatitis. In the majority of patients, beta cell function appears normal, and the hyperglycemic state may depend on an altered peripheral sensitivity to insulin due to the pancreatic pathology itself or to consensual liver involvement.
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PMID:C-peptide pattern in patients with pancreatic cancer. 813 97

In a five year review of 648 patients with chronic pancreatitis, 446 (68.8%) were documented with regional complications consisting of biliary, duodenal or colonic obstruction, pseudocysts, haemorrhage, pancreatic ascites and gastric varices. Although the majority could be treated conservatively, surgical intervention was needed in 129 patients (28.9%). The commonest operations were choledocho-duodenostomy for distal bile duct obstruction, gastro-enterostomy for duodenal obstruction, local resection for colon obstruction, cyst-gastrostomy for pseudocysts, duct-enteric anastomosis for pancreatic ascites and splenectomy for gastric varices. Operative mortality was 8.5% and morbidity 27.9%. During 1-5 year follow-up, re-admission for pancreatitis was needed in 24%. No secondary biliary cirrhosis was encountered in long standing bile duct obstruction, but fibrosis was present in 73% of liver biopsies. Cholangitis occurred in 14%. Angiographic embolisation was useful in the control of massive bleeding from peri-pancreatic visceral arteries. Although relief of pain in chronic pancreatitis has generally been disappointing, regional complications, occurring in the majority of patients, can be corrected satisfactorily by surgical intervention.
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PMID:Surgical intervention for regional complications of chronic pancreatitis. 817 59

Review of the literature presented deals with the state of connective tissue and some aspects of its metabolism in ulcer disease, chronic gastritis, chronic hepatitis, hepatic cirrhosis, acute and chronic pancreatitis. Disorders of synthesis and degradation of collagen, changes in metabolism of glycosaminoglycans, glycoproteins and aminoglycans are described, their pathogenetical role in development end exacerbation of diseases of digestive organs is demonstrated.
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PMID:[Connective tissue function in diseases of the digestive organs (a review of the literature)]. 820 30

In the course of alcoholic chronic pancreatitis, increased serum alkaline phosphatase level is usually caused by common bile duct stenosis but may also be due to alcoholic liver disease. The aims of this prospective study were to investigate whether clinical, biochemical and radiological factors could predict liver histopathological appearance. The study comprised 48 patients with chronic alcoholic pancreatitis, common bile duct stenosis and increased serum alkaline phosphatase levels; clinical, biochemical, radiological and histological data were recorded in all cases. Liver biopsy examination (surgical [n = 45] or intercostal [n = 3]) showed (a) biliary obstructive liver abnormalities (n = 33), which were severe in 20 cases (biliary fibrosis in 15, secondary biliary cirrhosis in 3, secondary sclerosing cholangitis in 2) and moderate in 13 cases; (b) alcoholic liver disease in 9; and (c) normal liver in 6. Clinical, biochemical and radiological data were not statistically different between patients with biliary obstructive liver disease and those with alcoholic liver disease. Forty-five patients underwent surgery; two patients with alcoholic hepatitis died after surgery, at the beginning of this study. We conclude that in chronic alcoholic pancreatitis with common bile duct stenosis and increased serum alkaline phosphatase levels, clinical, biochemical and radiological data cannot be used to predict the type of liver lesions. Therefore liver biopsy is warranted to identify (a) alcoholic hepatitis, which increases operative risk; and (b) biliary obstructive liver disease, frequent and often severe, in which surgical biliary decompression should be considered.
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PMID:Factors predictive of liver histopathological appearance in chronic alcoholic pancreatitis with common bile duct stenosis and increased serum alkaline phosphatase. 822 11

A simple, reliable, and reproducible fluorometric method for measuring thiobarbituric acid-reactive substances (TBARS) in serum is proposed, based on the reaction between malondialdehyde (MDA) and thiobarbituric acid. Formation of TBARS was complete at pH 2.4-2.6, but extraction with n-butanol proved complete only at lower pH, i.e., 1.6-1.7. Analytical recoveries of MDA added to serum were 94%-101%; within- and between-run CVs were 2.4-3.6% and 4.6-5.5%; and the detection limit for TBARS in serum was 0.10 mumol/L. Optimized conditions included: (a) collection of either serum or heparinized plasma, (b) preservation from in vitro autoxidation by glutathione and EDTA, and (c) storage at -20 degrees C up to 35 days. The mean (+/- SD) TBARS concentration in 47 healthy adults was 1.01 (0.21) mumol/L; no sex-related difference was observed. Higher concentrations were measured in patients with renal insufficiency undergoing hemodialysis and in patients with insulin-dependent diabetes, chronic pancreatitis, or liver cirrhosis.
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PMID:Optimized steps in fluorometric determination of thiobarbituric acid-reactive substances in serum: importance of extraction pH and influence of sample preservation and storage. 825 25

To determine the relationship between nutritional status and ethanol consumption, 250 chronically alcoholic men (mean age 41 +/- 11 years) entering an alcoholism treatment program were studied. A control group of 100 male volunteers (mean age 40 +/- 10 years) was also evaluated. Detailed clinical history, laboratory analysis and nutritional status assessment were carried out in each case and control. In addition, ethanol-related diseases such as liver disease, chronic pancreatitis, cardiomyopathy, myopathy and peripheral neuropathy were ruled out in all patients. The mean daily ethanol consumption of the alcoholics was 235 +/- 62 g over an average of 19 years. All of them belong to a very stable, middle-class working group of men. Only 25 (10%) alcoholics showed evidence of energy malnutrition, 15 (6%), of protein malnutrition, and 6 (2%) of both. In the multivariate analysis, the only independent factors for the development of malnutrition were the total lifetime dose of ethanol and calorie intake (ethanol excluded) (P < 0.01; both), as well as cirrhosis (P < 0.01) when protein malnutrition was considered. Alcoholic cirrhosis was diagnosed in 20 cases, skeletal myopathy in 117, dilated cardiomyopathy in 20 and peripheral neuropathy in 41. When patients with ethanol-related diseases were excluded, no significant differences in nutritional parameters were observed between chronic alcoholics and controls. We conclude that malnutrition is not as frequent as previously thought in middle socioeconomic class male alcoholics and its existence may be considered as another consequence of ethanol intake or secondary to the alcohol-related diseases.
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PMID:Nutritional status in chronically alcoholic men from the middle socioeconomic class and its relation to ethanol intake. 827 79

Pancreatic phospholipase A2 (PLA2) is secreted into the pancreatic juice by pancreatic acinar cells as a proenzyme (proPLA2), which is activated by trypsin. Radioimmunoassays with monoclonal antibodies to PLA2 and proPLA2 were used to examine the serum PLA2 and proPLA2 levels simultaneously in patients with various pancreatic diseases. In healthy subjects, proPLA2 proved to be the major form of the enzyme. The serum PLA2 level were found to be significantly increased in patients with acute pancreatitis, the active phase of chronic relapsing pancreatitis, and the early stage of pancreatic cancer. In the terminal stage of pancreatic cancer the serum PLA2 level became low. In patients with chronic pancreatitis, significant correlations were observed between the levels of factors evaluated by the secretin test and the serum total PLA2 and proPLA2 level, but not the PLA2 level. The serum PLA2 and proPLA2 concentrations, and the proportion of proPLA2 in the total, were within normal ranges in patients with liver cirrhosis, hepatocellular carcinoma, and chronic renal failure. These results suggest that simultaneous measurements of serum PLA2 and proPLA2 are clinically useful for diagnosis and monitoring of the active phase of pancreatitis.
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PMID:Simultaneous determinations of pancreatic phospholipase A2 and prophospholipase A2 in various pancreatic diseases. 844 83

Chylous ascites is mainly due to malignant abdominal disease or cirrhosis. We report the case of chylous ascites associated with protein losing enteropathy caused by fibrotic compression of abdominal lymphatic vessels and superior mesenteric vein complicating alcohol-related chronic pancreatitis. This is the second case published in the literature.
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PMID:[A case of chylous ascites associated with exudative enteropathy complicating chronic pancreatitis of alcoholic origin]. 846 71

Major arterial hemorrhage associated with pancreatic pseudocysts represents a formidable complication with high mortality rates. This study was undertaken to analyze presentation and outcome and to assess the role of angiography in diagnosis and management of this complication. A retrospective review of 180 patients referred for surgical management of pancreatic pseudocysts from 1964 to 1991 identified 13 patients (7.2%) with arterial hemorrhage. Eight patients presented with intracystic hemorrhage, 4 with upper gastrointestinal bleeding, and 1 with intra-abdominal bleeding. Six patients had gastroduodenal artery bleeding, 4 splenic, and 1 each left gastric, right colic, and left gastroepiploic. The site of bleeding was identified with selective visceral angiography in 9 patients; evidence of pseudocyst bleeding was seen in 5 of 7 patients who had contrast-enhanced computerized tomography (CT) scans. Angiographic embolization for control of hemorrhage was used in 6 patients and operative control in 7. Over the past decade, bleeding has been controlled with angiographic embolization in all patients except 1 with massive bleeding due to splenic artery erosion. Average blood loss was less in patients treated with angiographic embolization (6.8 vs 17.5 units, packed red cells, P < .05, Wilcoxon rank sum test). The sole mortality was a patient with cirrhosis treated in 1969. Clinical presentation of pseudocyst bleeding is variable; the underlying cause is usually related to chronic pancreatitis due to alcohol abuse. The dynamic contrast-enhanced CT scan is valuable in demonstrating evidence of pseudocyst bleeding. Accurate diagnosis with dynamic CT scan and angiography and control of bleeding with angiographic embolization has improved the outcome in patients with this complication.
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PMID:Arterial hemorrhage complicating pancreatic pseudocysts: role of angiography. 847 74


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