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

A normal exocrine pancreatic function was demonstrated by the secretin-pancreozymin-test in five patients with Wilson's disease either without (n = 2) or with cirrhosis of the liver but without portal hypertension (n = 3). In another patient with cirrhosis of the liver without portal hypertension the pancreas was normal at post mortem examination. In two patients with cirrhosis of the liver and portal hypertension bicarbonate (n = 1) and amylase secretion (n = 2) were diminished. The regression of portal hypertension under therapy with penicillamine in one of the latter cases was paralleled by the return to normal of exocrine pancreatic function. It is concluded that exocrine pancreatic insufficiency in Wilson's disease is dependent on the development and the progression of chirrhosis of the liver and not due to a primary manifestation of the disease itself.
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PMID:[Involvement of the exocrine pancreas in Wilson's disease? (author's transl)]. 71 25

In cirrhosis of the liver induced in rats by administration of thioacetamide for 8 months, pancreatic amylase and protein concentration and the number of zymogen granules were found to exceed those of the controls. The finding is attributed to a deficient metabolism of enterohormones. The model seems to provide a suitable approach to the study of the hypersecretory state of the pancreas associated with cirrhosis of the liver.
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PMID:Pancreatic amylase- and protein-concentrations associated with thioacetamide-induced cirrhosis of the liver in rats. 75 13

A case of pancreatic ascites is reported and compared with 55 previously reported cases. A 42-year-old black male chronic alcoholic presenting with abdominal pain was found at operation to have chronic pancreatitis with no pseudocyst formation or overt duct disruption, in contrast to the majority of cases reported. The diagnosis and differentiation from cirrhosis of the liver were based on the operative findings, elevated serum amylase level, ascitic fluid amylase value, and protein content. Surgical exploration alone has proven beneficial--the patient has done well in the past 2 years with no recurrence of the ascites and continued weight gain. The clinical course was compatible with pancreatitis although the radiographic and angiographic studies were not diagnostic. It is suggested that the clinical entity of pancreatic ascites occurs more often than reported and a workup for it should be done even in the face of unconvincing radiographic and angiographic evidence.
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PMID:Pancreatic ascites. A case report and review of the literature. 120 11

Parotid saliva samples from 24 alcoholic subjects without evidence of cirrhosis were analyzed for changes in flow rate, composition, and epidermal growth factor (EGF) secretion. Mean (+/- SE) stimulated parotid saliva flow rate (ml/min/gland) was significantly (p less than 0.01) lower in alcoholic subjects than in matched control subjects. Reduction in parotid saliva flow rate was associated with significant (p less than 0.05) decrease in total protein and amylase secretion in this group of patients. In addition, secretion of immunoreactive EGF, a specific salivary protein, was also markedly reduced (p less than 0.05) in alcoholic patients. None of the parotid saliva samples from the alcoholic subjects had detectable bioactivity of EGF in saliva. These data suggest that chronic alcohol ingestion is associated with significant changes in parotid saliva secretion and its composition, which may perpetuate and compound ethanol-induced injury to the upper gastrointestinal tract.
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PMID:Ethanol and human saliva: effect of chronic alcoholism on flow rate, composition, and epidermal growth factor. 137 39

We have made a prospective study in alcoholic patients, with and without hepatic cirrhosis, in order to evaluate the presence of modifications in the composition of pancreatic juice (JPP) and in the pancreatogram that allows us to diagnose the existence of chronic pancreatitis associated with alcoholic cirrhosis (CE). The patients where 23 chronic alcoholics, 13 of them with CE and the other 10 with no hepatic injury (AC). In all, an endoscopic retrograde cholangiopancreatography (CPRE) was made and after having obtained a pancreatogram a intravenous infusion of secretin and cholecystokinin was performed. The total volume, the concentrations and the out-puts of bicarbonate, amylase, lipase and total proteins were measured in the pancreatic juice collected during 12 minutes. The pancreatogram was normal in the 92.3% of CE and in all the AC. Patients with CE had similar values of all the evaluated parameters to AC patients. In conclusion, there seems to be a good correlation between the pancreatogram and the analytic study of JPP, because the JPP has no qualitative and quantitative anomalies when the Wirsung duct is normal. In our opinion the study of JPP is not useful in the diagnostic of chronic pancreatitis associated with alcoholic hepatic cirrhosis.
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PMID:[Pancreatic function and morphology in chronic alcoholism with and without cirrhosis]. 141 27

A total of 164 patients with alcoholism-induced osteonecrosis were seen over a 22-year period, from 1962 to 1984. Twenty-three percent of patients were female and 30.5% were black. The average duration of alcohol abuse was 9.5 years, ranging from 8 to 20 years. The presence of femoral head necrosis was diagnosed in patients aged 21-67 years; 28% of patients were under 40 years of age and 76% were under 50 years. Bilateral hip necrosis was present in 44.5% of patients and, within three years of the diagnosis of FHN, the presence of multifocal necrosis became evident in 23 cases at sites away from the hip (shoulders and knees). Hyperlipidemia was found in 38.4% of cases, involving both cholesterol and triglycerides. Serum amylase was elevated in 33 patients; liver dysfunction was present in 50; hepatomegaly was found in 32; and biopsy-confirmed cirrhosis was present in 22 cases. Hyperuricemia was found in 22 patients, some of whom had received steroids. Disabling hip pain was the first manifestation of disability related to alcohol abuse in 158 patients, most of whom required total hip joint replacement. This study supports the hypothesis that alcoholism-induced bone necrosis is caused by fat embolism linked to co-existent hyperlipidemia. The treatment of hyperlipidemia by dietary means or lipotropic medication and the cessation of alcohol abuse is advised. Multi-center studies employing such treatment should provide evidence of its effect on the evolution of necrosis as well as the incidence of bilateral hip femoral head necrosis and multifocal lesions.
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PMID:Alcoholism-induced bone necrosis. 151 11

To confirm the respective influence of chronic alcoholism and liver disease on exocrine pancreatic function in cholecystokinin secretin (CS), tests were performed on patients with chronic liver cirrhosis (LC) and non-cirrhotic (nLC) disease of alcoholic (A) and nonalcoholic (nA) etiology. Results were compared in four subgroups (ALC, N = 26; AnLC, N = 45; nALC, N = 18; and nAnLC, N = 43). Volume of duodenal juice and bicarbonate output (BO) were increased and maximal bicarbonate concentration was decreased in ALC, compared with those in normal controls. Comparison of LC and nLC indicated that the volume, BO, and amylase output (AO) were greater in LC than in nLC of alcoholic etiology, but not in those of nonalcoholic etiology. The initial disappearance rate (KICG) of indocyanine green (ICG) excretion correlated with a parameter of CS test in alcoholic liver disease (vs. volume: r = -0.51, p less than 0.01 vs BO: r = -0.40, p less than 0.01), but not in nonalcoholic liver disease. Concurrent chronic pancreatitis with pain and definite exocrine insufficiency was observed in only one ALC patient and in four AnLC patients, but in none of the nonalcoholics. In alcoholic liver disease, exocrine pancreatic secretion tends to increase with severity of liver damage, but concurrence of definite chronic pancreatitis is not correlated with the severity.
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PMID:Exocrine pancreatic function in chronic liver diseases. 170 82

In order to assess the experimental level of enzymatic content in exocrine pancreas of cirrhotic rats, cirrhosis was induced with administration of thioacetamide (50 mg/kg) during ten weeks to male Wistar rats with an initial average weight of 350 g. Contents of amylase, lipase and trypsinogen were determined in pancreatic tissues and amylase, lipase and biliary salts in duodenal juice obtained by cannulation and perfusion with physiologic serum. A higher presence of trypsinogen and amylase was detected in pancreatic tissues, and of lipase in the duodenal juice, with a trend, although insignificant, towards a decrease in biliary salts among the cirrhotic group. No changes were observed in the morphologic study. The hypothesis that a deficit of biliary salts in experimental cirrhosis could be responsible of the enzymatic increase in the pancreatic tissue and, in particular, of the selective excretion of lipase, is discussed.
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PMID:[Modifications of the enzymatic content and morphology of the exocrine pancreas of rats with experimental hepatic cirrhosis induced by thioacetamide]. 172 29

Changes in the salivary glands, liver and pancreas in rats with experimentally induced liver injuries were examined. The injuries (experimental group) were induced by subcutaneous injections of carbon tetrachloride (0.01ml/kg body weight) in a 50% olive-oil solution. The injections were administered twice weekly for 10,20 and 40 weeks. Control animals received the same doses of olive oil during the same periods. 1. In the experimental group, serum glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) increased remarkably, whereas serum albumin decreased. 2. Swelling of the liver and multiple nodular formations occurred in the experimental group. Liver fibrosis with the formation of pseudolobules indicated a form of liver cirrhosis. 3. No significant histological changes were observed in the pancreases of animals in the 10- and 20-week experimental groups. Vacuolation in the acinar cells was observable in 3 of 8 cases in the 40-week experimental group. 4. In connection with histological findings of parotid glands, vacuolation of the acinar cells occurred in 7 of 12 cases in the 10-week experimental group, in 7 of 8 cases in the 20-week experimental group, and in all 8 cases in the 40-week experimental group. Vacuole numbers and sizes increased as the experimental period was prolonged. 5. Immunohistochemical investigation showed strong positive reactions to the anti-amylase antibody around vacuoles in acinar cells of parotid glands. In unvacuolated acinar cells, on the other hand, only slight positive reaction was observed. 6. Electronmicroscopic observation of the acini revealed greatly enlarged lumina and dilated intercellular canaliculi connected to the lumina. Small vacuoles were observed on the basement of the acini. 7. No such significant changes as fibrosis, vacuolation, and atrophy of acinar cells were observed in the submandibular and sublingual glands of the experimental animals. 8. Serum amylase activity increased more in the experimental than in the control rats. Electrophoretic patterns suggested that in the control group 95 percent of serum amylase was parotid type, and also in the experimental group 95 percent of serum amylase was parotid type. 9. Amylase activity in the parotid glands also increased more in the experimental than in the control animals.
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PMID:[A study on changes of liver and salivary glands in rats with experimentally induced liver injuries. Pathological and biochemical observations]. 172 65


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