Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two studies investigating the association of liver disease with acute and chronic pancreatitis in alcoholics are presented. In a retrospective study of 50 patients, no clinical liver disease was found in 9 patients with acute pancreatitis, while 23 (56%) of 41 patients with chronic pancreatitis had liver disease by clinical criteria. Of this latter group, 8 were confirmed histologically; thus 19% of patients with chronic pancreatitis had biopsy-proven cirrhosis. Fifty alcoholic patients with pancreatitis were prospectively evaluated. All who had clinical evidence of liver disease were biopsied. No cases of liver disease were encountered in the 4 patients with acute pancreatitis. Although 28 (60%) cases of clinically diagnosed liver disease were present in 46 patients with chronic pancreatitis, only 20 of these seemed significant (cirrhosis, alcoholic hepatitis, severe fatty liver), for an incidence of 43%. Thus, clinically significant alcoholic liver disease occurs quite frequently in association with alcoholic pancreatitis. This association is meaningful in more effective management of these patients in general and in preoperative assessment of the risk of surgery in particular.
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PMID:Associated liver disease in alcoholic pancreatitis. 68 26

53 patients were controlled with CT after Whipple resection. The median age of the patients was 49 years, the median time after surgery nine years. Diagnostic criteria were the identification of the residual pancreas, signs of pancreatic atrophy and radiological signs of chronic pancreatitis. CT was performed with slice thickness of 4 mm and steps of 4 mm. The residual pancreas was visible in all 53 cases. Pancreatic atrophy was found in 26 cases, in four of these the residual pancreas was only 2 mm in size. Signs of chronic pancreatitis were found in 16 cases. By comparing preoperative and postoperative CT-scans, seven progresses of pancreatitis were detected. Signs of acute pancreatitis were not found in the 53 patients. Fatty liver degeneration was found in 7.5%. We found that CT is the most reliable technique to visualize the pancreas after Whipple resection. CT should be performed in all patients with clinical symptoms of an acute pancreatitis. CT should also be performed in patients with residual pancreas pseudocysts. There is no indication for CT in the routine examination of asymptomatic patients after Whipple resection.
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PMID:[Results of computerized tomography after Whipple operation of chronic pancreatitis]. 135 91

Opsonic glycoprotein, alpha 2-HS-glycoprotein concentration was studied in the serum of 753 patients with various hematological, malignant, immunological, metabolic, endocrine and liver diseases and 68 healthy controls. Decreased serum alpha 2-HS-glycoprotein levels were detected in patients with acute leukemias, chronic granulocyte and myelomonocyte leukemias, lymphomas, myelofibrosis, multiple myeloma, metastatizing solid tumors, systemic lupus erythematosus, rheumatoid arthritis, acute alcoholic hepatitis, fatty liver, chronic active hepatitis, liver cirrhosis, acute and chronic pancreatitis, and Crohn's disease. Elevated levels were measured in patients with B and NANB/C hepatitis. Further decreased levels were observed in some groups with secondary infections. Serum alpha 2-HS-glycoprotein levels are affected by many factors, influencing the synthesis and elimination of the protein. The detection of serum alpha 2-HS-glycoprotein concentration has no specific diagnostic value as a marker for tumors or other diseases, however, its determination can be useful for the assessment of a non-specific regulator of the host defence.
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PMID:[Diagnostic value of the determination of serum alpha2-HS-glycoprotein]. 140 55

The drinking behaviour of 95 consecutive men subjected to medicolegal autopsy in Helsinki was studied by interviewing a relative or friend of the deceased. Sufficient data for estimating the daily alcohol dose were obtained in 61 (64%) of the cases. Of these men, 21 (34%) were reported to drink at least an average of 80 g of alcohol daily. The validity of post-mortem alcohol reports was assessed by comparing the occurrence of alcohol-related diseases, toxicological data as well as the cause and manner of death with the reported alcohol consumption. Men whose reported daily alcohol consumption exceeded 80 g (mean 230 g) differed from men reported to drink less than 10 g (mean 3 g) in their more common incidence of positive post-mortem alcohol test (P less than 0.0005), fatty liver (P less than 0.001), enlarged liver (P less than 0.01), alcoholic hepatitis (P less than 0.05), chronic pancreatitis (P less than 0.01), and in their lower rate of death from cardiovascular diseases (P less than 0.05). The present results indicate that interviews with relatives or friends provide reliable data on the drinking behaviour of the deceased. At autopsy, the most sensitive tests coinciding with high consumption of alcohol in post-mortem alcohol reports but not with each other were positive post-mortem blood alcohol and the occurrence of fatty liver.
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PMID:Validity of post-mortem alcohol reports. 233 92

By means of consecutive pancreatic stimulation, we have investigated the presence of changes of pancreatic function in alcoholic patients, with and without alcoholic liver disease, in order to detect functional alterations and possible association of hepatic and pancreatic disease. The patients were 49 chronic alcoholics (8 patients without liver disease, 11 hepatic steatosis, 9 alcoholic hepatitis and 21 alcoholic cirrhosis) and 15 non alcoholic subjects (8 normal controls and 7 cases of non alcoholic cirrhosis). In all the cases two consecutive stimulations were carried out: first with secretin and cholecystokinin (CCK) and second with CCK alone. The total volume and concentration as well as the output of bicarbonate, trypsin, amylase and total proteins were measured in the duodenal juice. Patients with alcoholic cirrhosis had larger volumes of duodenal juice and lower concentrations of bicarbonate, enzymes and proteins. There was also a tendency to larger volume and lower bicarbonate concentration as the hepatic lesion was more severe. Bicarbonate output was significatively higher in patients with alcoholic cirrhosis but for the remaining parameters the outputs were similar in all the groups. In conclusion, the alterations in pancreatic function parallel the severity of the liver disease. None of the patients had changes consistent with chronic pancreatitis.
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PMID:[Changes in pancreatic secretion in alcoholic liver disease]. 237 59

Pathogenetic associations between benign hepatic tumours and liver damage were studied in an autopsy series of 91 males with high incidence of alcoholism. Information on the consumption of alcohol was obtained by interviewing a family member or a close friend of the deceased. The reported use of alcohol correlated well with the increase of fatty and fibrotic changes and with the occurrence of liver cirrhosis, alcoholic hepatitis or pancreatitis. Benign bile duct tumours (bile duct adenomas and von Meyenburg's complexes) (n = 26) were associated with the occurrence of bridging (P less than 0.0005) and periportal (P less than 0.025) fibrosis of the liver and, independently from these, with chronic pancreatitis (P less than 0.05) and with non-parasitic liver cysts (n = 14) (P less than 0.01). The weight of the liver was greater (P less than 0.01) in males with focal nodular hyperplasia (n = 3). Cavernous hemangioma (n = 19) occurred independently of the parameters studied. None of the tumours showed significant correlation to liver cirrhosis, alcoholic hepatitis, fatty liver or diseases of the gallbladder. The results are in line with observations on the reactive nature and connections to fibropolycystic liver disease of benign bile duct tumours in laboratory animals and in man. Their presence in human liver specimens should be taken into account as a sign of liver damage, in this study related to heavy use of alcohol or to chronic inflammation of the pancreas.
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PMID:Benign bile duct tumours, non-parasitic liver cysts and liver damage in males. 395 Mar 64

Forty five cases of chronic pancreatitis have been diagnosed between January 1966 to July 1983 in the Hospital A. Posadas. The diagnosis was confirmed by the presence of one or more of the following data: pancreatic calcifications positive in 35, abnormal secretin test 37, ultrasonography and computed tomography pathological findings 10. Surgical operations were carried out in 25 patients and biopsy taken in 5. Thirty nine (86.6%) were males, 6 (13.3%) females, the mean age in each group was 47.4 and 39.8 years. Chronic alcoholism was certain in 41 (91.9) patients, in the remainder 4 no other etiologic factors were found. The main clinical data were: Weight loss 38 (84.4%) diabetes 34 (75.5%) pain 33 (73.3% in 7 as acute pancreatitis) Steatorrhea 23 (51.1%) jaundice 16 (35.5%- 11 by extrahepatic biliary tree obstruction, 5 by hepatic cirrhosis) pseudocysts 12 (26.6%). The more common associated diseases were: hepatic cirrhosis 6, fatty liver 2 (17.7%) gastroduodenal ulcer 6 (13.3%) cancer 4 (8.8%--gastric 1, pancreatic 3). In order to study the frequency of the clinical data the patients were grouped according to the presence or absence of calcifications and the etiologic factor Symptoms and signs were matched and statistic analysis (coefficient association phi) was made. Only a moderate association between acute pancreatitis in no calcified group and diabetes in calcified group were found. The chronologic study of certains clinical data shows that acute pancreatitis, jaundice, pseudo-cyst and surgical operations were significative more frequent in the first five years while diabetes has little more frequency in the second five year period. Twenty six surgical operations were carried out in 25 patients; 20 (76.9%) due to complications, 6 (23.1%) secondary to pain (pancreatic resection 3, pancreatoyeyunostomy 2, exploration 1). Twenty three patients were lost to follow-up, 12 died and 10 are still alive. This last group was followed at regular period, 8 remained asymptomatic and 2 have intermittent abdominal pain related to alcoholic ingestion.
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PMID:[Chronic calcified pancreatitis. Our experience]. 639 6

A computer model was developed with decision analysis software to explore the long-term clinical and economic outcomes of alcohol abstinence maintenance with either standard counselling therapy or standard therapy plus 48 weeks of adjuvant acamprosate in detoxified alcoholic patients. Important complications of alcoholism were modelled using Markov processes, and included relapse (return to drinking), alcohol-related hepatic disease, acute and chronic pancreatitis, acute and chronic gastritis, oropharyngeal carcinoma, oesophageal carcinoma, alcoholic cardiomyopathy, alcohol-related peripheral neuropathy, alcoholic psychosis, accidental death, and suicide. Probabilities of developing complications were dependent on whether the patients within the cohort remained abstinent or had relapsed. Relapse rates, probabilities, and costs for acamprosate therapy and treatment of complications were taken from published literature. The analysis was performed from the German health insurance perspective. Life expectancy and total lifetime costs (costs of initial abstinence maintenance therapy plus costs of complications) were calculated for a typical male cohort with average age of 41 years, 80% with fatty liver, 15% with cirrhosis, 22% with chronic pancreatitis, and 1% with alcoholic cardiomyopathy at baseline. Life expectancy with and without acamprosate therapy was 15.90 and 14.70 years respectively, and discounted (5% per annum) average total lifetime costs per patient were DEM 46 448 and DEM 49 549 respectively. We conclude that, despite the acquisition costs of DEM 2177, adjuvant acamprosate therapy was both clinically and economically attractive under conservative assumptions.
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PMID:The long-term cost-effectiveness of improving alcohol abstinence with adjuvant acamprosate. 1102 23

Chronic inflammatory processes produce an excess of ROS and DNA-reactive aldehydes from lipid peroxidation (LPO), such as trans-4-hydroxy-2-nonenal (HNE) and malondialdehyde (MDA), which can modify cellular macromolecules and drive to malignancy. Etheno-modified DNA bases are generated inter alia by reaction of DNA with the major LPO product, HNE. We are investigating steady-state levels of etheno-DNA adducts in organs with diseases related to persistent inflammatory processes that can lead to malignancies. We have developed ultrasensitive and specific methods for the detection of etheno-DNA base adducts in human tissues and in urine. Etheno-DNA adduct levels were found to be significantly elevated in the affected organs of subjects with chronic pancreatitis, ulcerative colitis and Crohn's disease. When patients with alcohol abuse-related hepatitis, fatty liver, fibrosis and cirrhosis were compared with asymptomatic livers, excess hepatic DNA damage was seen in the three latter patient groups. Etheno-deoxyadenosine excreted in urine was measured in HBV-infected patients diagnosed with chronic hepatitis, cirrhosis and hepatocellular carcinoma. As compared to controls, these patients had up to 90-fold increased urinary levels. Impaired or imbalanced DNA-repair pathways may influence the steady-state levels of etheno-DNA adducts in inflamed tissues. In conclusion, etheno-DNA adducts may serve as potential lead markers for assessing progression of inflammatory cancer-prone diseases. If so, the efficacy of human chemopreventive interventions for malignant disease prevention could be verified.
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PMID:Accumulation of lipid peroxidation-derived DNA lesions: potential lead markers for chemoprevention of inflammation-driven malignancies. 1609 77

An 11-year-old male developed systemic calciphylaxis during induction therapy for acute lymphoblastic leukemia. His predisposing conditions were hypercalcemia, supplements for pamidronate-induced hypocalcemia and hypophosphatemia and renal insufficiency. He died of cardiorespiratory arrest on the 20th day of induction treatment. Autopsy revealed extensive calcium deposits in the heart, lungs and kidneys. He had diffused alveolar damage, acute tubular necrosis, chronic pancreatitis and marked hepatic steatosis. Systemic calcium deposition may progress rapidly in children with hypercalcemia of malignancy. Since pamidronate reduces mineral resorption from tissues, calcium and phosphate replacements increase systemic mineral deposits. Thus, mineral supplements should be considered only to combat symptoms.
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PMID:Systemic calciphylaxis. 1849 73


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