Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Of 1,153 patients with surgically confirmed primary hyperparathyroidism operated on at the Mayo Clinic between 1950 and 1975, only 17 (1.5%) had coexisting or prior pancreatitis. This frequency of association approximates the reported incidence of pancreatitis among general hospital patient populations. Other factors of possible etiologic significance in pancreatitis, such as gallstones or alcohol abuse, were present in 11 of the 17 patients. Cure of the hyperparathyroidism was usually not associated with amelioration of symptoms due to pancreatitis. A review of the available data, including experimental evidence, does not support a cause-and-effect relationship between primary hyperparathyroidism or hypercalcemia and pancreatitis.
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PMID:Hyperparathyroidism and pancreatitis. Chance or a causal association? 735 Mar 71

In the prospective clinical long-term study of 246 patients with chronic pancreatitis, 26 patients (24 men) developed 27 histologically proved malignant tumors (11%). Four additional patients with neoplasia were excluded (papilloma, two; Bowen's disease of the tonsils, one; and seminoma, one, occurring 8 years before onset of pancreatitis). In six patients pancreatic cancer was diagnosed (2.4%), which indicates a slightly increased risk over the general population. Interestingly, 21 patients developed extrapancreatic cancer (8.5%), including a very high incidence that has not been noted previously. The cancers were located in the oral cavity (in six), larynx (three), bronchus (eight), and gastrointestinal tract (four). The data suggest a causal relationship between chronic pancreatitis and cancer. As possible factors, smoking, alcohol abuse, diabetes, malnutrition, immune deficiency, and high dietary fat intake are discussed. There is, however, no definite evidence for any single known factor.
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PMID:High incidence of extrapancreatic carcinoma in chronic pancreatitis. 743

In this necropsy review of 37 cases of acute pancreatitis, evidence is presented that there are at least two different initiating mechanisms in acute necrotising pancreatitis in man. Firstly, there is primary duct inflammation, with subsequent inflammation and necrosis of the pancreatic parenchyma surrounding the excretory ducts. Included in this group are cases secondary to alcohol abuse and cholelithiasis. Secondly, there is necrosis confined to the microcirculatory periphery of the pancreatic lobule. These cases are usually secondary to some form of shock (septic or cardiogenic) and are thought to represent ischaemic pancreatitis. These patterns of necrosis are discussed in relation to the pancreatic anatomy and clinical findings.
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PMID:Histological evidence of initiating factors in acute necrotising pancreatitis in man. 745 60

Forty patients underwent total pancreatoduodenectomy for end-stage chronic pancreatitis. There were 34 men and six women of median age 39 (range 21-66) years. Alcoholism was the major aetiological agent (30 patients), and five patients had had previous acute idiopathic pancreatitis. The overwhelming indication for operation was severe abdominal pain, complicated by failing exocrine and endocrine function. Resection was performed in one (17 patients) or two (23) stages, following previous proximal (seven) or distal (16) pancreatectomy; progression from partial to total pancreatectomy occurred over an interval of 8-96 (median 15) months. A further six patients had undergone previous pseudocyst or duct drainage procedures. The pylorus was preserved in 28 patients and the spleen in ten. Median operating time was 6 (range 2.5-8.5) h and median blood loss 2000 (range 500-16,000) ml. There were two hospital deaths and three patients required reoperation. Of 38 survivors, 30 obtained complete or substantial relief of pain. There were 15 late deaths at 2.5-120.0 months after operation, 13 in the alcohol group and 11 disease-related. Total pancreatectomy can relieve the intractable pain of chronic pancreatitis at the cost of possible premature death from continuing alcohol abuse.
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PMID:Role of total pancreatectomy in the treatment of patients with end-stage chronic pancreatitis. 748 80

The aim of this study was to evaluate the serum behavior of human pancreas-specific protein/procarboxypeptidase B (hPASP/PCPB) in the early phases of acute pancreatitis, and to calculate its sensitivity and specificity in comparison with those of serum amylase and lipase in the diagnosis of this illness. Twenty-six acute pancreatitis patients were studied; the pancreatitis was of biliary origin in 11, due to alcohol abuse in 8, and due to other causes in 7. Sixteen patients had mild pancreatitis and 10 the severe form of the disease. Thirty-one patients with nonpancreatic acute digestive diseases were also studied. Serum concentrations of hPASP/PCPB, amylase and lipase were determined in all subjects on admission to the study as well as daily for the following 5 days in acute pancreatitis patients. All patients with acute pancreatitis had abnormally high serum hPASP/PCPB, amylase and lipase concentrations on the first day of admission. On the sixth day of the disease, 76% of acute pancreatitis patients had abnormally high serum concentrations of hPASP/PCPB, whereas only 48% (p < 0.05) had elevated serum amylase and lipase. No differences in serum levels of hPASP/PCPB, amylase or lipase were found between patients with alcoholic pancreatitis and those with other etiological forms of the disease, or between those with mild and severe forms of pancreatitis. The specificity of the three serum pancreatic protein assays, calculated on the 31 patients with nonpancreatic acute digestive diseases, was 90% for both hPASP/PCPB and lipase, 75% for amylase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human pancreas-specific protein/procarboxypeptidase B: a useful serum marker of acute pancreatitis. 751 50

Ethanol abuse is a well-known association of pancreatitis. The effects of chronic ethanol consumption on pancreatic digestive and lysosomal enzymes may be relevant to the pathogenesis of alcoholic pancreatitis, because pancreatic enzymes play an important role in the development of pancreatic injury. The aims of this study were to determine the effects of ethanol on gene expression and glandular content of pancreatic digestive enzymes and on gene expression of the lysosomal enzyme cathepsin B (known to be capable of activating trypsinogen). Pancreatic content and mRNA levels for lipase, trypsinogen, and chymotrypsinogen were determined in rats that were pair-fed a nutritionally adequate liquid diet with or without ethanol for 4 weeks. mRNA levels for the lysosomal enzyme cathepsin B were also assessed in this model. Ethanol significantly increased the content of lipase in the pancreas. There was a trend toward an increase in trypsinogen and chymotrypsinogen levels; however, these differences were not statistically significant. mRNA levels for lipase, trypsinogen, and chymotrypsinogen were raised in ethanol-fed rats. Ethanol feeding also increased mRNA levels for the lysosomal enzyme cathepsin B. Furthermore, there was a close, statistically significant correlation between changes in mRNA levels and tissue activities of pancreatic digestive and lysosomal enzymes after ethanol consumption. These results suggest that ethanol increases the capacity of the pancreatic acinar cell to synthesize digestive and lysosomal enzymes, thereby increasing the susceptibility of the gland to enzyme-related injury.
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PMID:Ethanol-induced alterations in messenger RNA levels correlate with glandular content of pancreatic enzymes. 773 27

We analyzed the molecular defects in the lipoprotein lipase gene of a patient with type I hyperlipidemia suffering from recurrent pancreatitis, indicative for lipoprotein lipase deficiency. Postheparin lipoprotein lipase activity in the patient was decreased by 70%. Direct genomic sequencing revealed compound heterozygosity for two mutation: the well-known Gly188-->Glu and a new Val69-->Leu substitution. Val69 is situated in a conserved hydrophobic region of the lipoprotein lipase protein, and the substitution with leucine gives rise to a 80% decrease in specific catalytic activity, as supported by site-directed mutagenesis experiments, followed by expression in COS-cells. The combination of both defects in the lipoprotein lipase gene was incidentally associated with severe clinical expression of disease, and triglyceride levels of more than 30 mmol/l were measured. In our patient, triglyceride levels wer usually below 10 mmol/l. We, therefore, postulate that the residual LPL activity in our patient is usually sufficient to keep the triglyceride level within bounds and expression of disease occurred only when conditions such as alcohol abuse or poor compliance to diet were present.
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PMID:A compound heterozygote for lipoprotein lipase deficiency, Val69-->Leu and Gly188-->Glu: correlation between in vitro LPL activity and clinical expression. 791 54

When activated, lymphocytes secrete glycoproteins related to particular surface proteins, including soluble forms of the interleukin-2 receptor (sIL-2R) and of the surface proteins CD4 (sCD4) and CD8 (sCD8). We evaluated the release of these glycoproteins in order to assess the activation of the cellular immune system during the course of acute pancreatitis. Thirty-five patients with acute pancreatitis (22 M, 13 F, mean age 64 years, range 16-97) were studied. The diagnosis was based on typical abdominal pain associated with a twofold increase of serum lipase as well as morphological abnormalities compatible with acute pancreatitis seen at computed tomography and/or ultrasonography. The pancreatitis was of biliary origin in 22 patients, due to alcohol abuse in 8, due to pancreas divisum in 1, due to type IV hyperlipoproteinemia in 1 and of unknown origin in 3. Based on clinical outcome, 22 patients had mild pancreatitis, whereas 13 had severe disease. In all patients serum sIL-2R, sCD4 and sCD8 were determined on admission and daily for the following 5 days using enzyme immunoassay (EIA) techniques. Serum concentrations of sIL-2R and sCD8 were significantly higher in acute pancreatitis patients relative to healthy controls during the entire observation period, whereas sCD4 levels were significantly lower in acute pancreatitis patients than in the control group from the 2nd to the 6th day of observation. Serum sIL-2R concentrations were significantly higher in patients with severe pancreatitis than in those with the mild form of the disease, whereas no differences in serum concentrations of sCD8 and sCD4 were found between patients with mild pancreatitis and those with severe disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Behavior of serum soluble interleukin-2 receptor, soluble CD8 and soluble CD4 in the early phases of acute pancreatitis. 806 32

Pancreatic fibrosis in patients with alcoholic dependence syndrome was studied histopathologically. In 30 of 41 autopsied patients with alcoholic dependence syndrome, fibrosis was observed despite the absence of clinical pancreatitis. The fibrosis was categorized into three types, according to Martin's classification: intralobular sclerosis in 15 cases, perilobular sclerosis in seven cases, and a mixed intralobular and perilobular sclerosis in the remaining eight cases. The type of the fibrosis was not related to the duration of alcohol abuse. Alcoholic liver cirrhosis was coexistent in 23 of the 30 cases of pancreatic fibrosis. These cases were also divided into categories according to the three types, as follows: intralobular sclerosis in 12 (80%) of 15 cases, perilobular sclerosis in four (57%) of seven cases, and mixed sclerosis in seven (88%) of eight cases. That is, intralobular and mixed sclerosis were frequently coexistent with alcoholic liver cirrhosis. When the pancreases from the 19 subjects with intralobular sclerosis and mixed sclerosis coexistent with liver cirrhosis in alcoholic dependence syndrome were compared with 20 pancreases from patients with nonalcoholic liver cirrhosis, periacinar (or intralobular) fibrosis was found in all cases of the former, but in none of the latter. Hence, it was concluded that periacinar fibrosis occurred as a result of alcohol abuse. Pancreatic fibrosis in patients with alcoholic dependence syndrome was distributed mainly in the intralobular areas and was frequently coexistent with alcoholic liver cirrhosis.
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PMID:Pancreatic fibrosis in patients with alcoholic dependence syndrome. 821 22

A patient with a history of alcohol abuse and pancreatitis presented with a pleural effusion resulting from a fistula between the pancreatic duct and left pleural space. Two weeks into her hospitalization, fever and persistent bloodstream infection with Erysipelothrix rhusiopathiae and Candida albicans developed. The patient had no history of exposure to animals. To our knowledge this is the first report of an E. rhusiopathiae infection presenting during hospitalization. This case suggests the possibility of a carrier state of infection and illustrates that a high index of suspicion is necessary for identification of unusual pathogens in hospitalized patients.
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PMID:Persistent bacteremia with Erysipelothrix rhusiopathiae in a hospitalized patient. 826 64


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