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)

The enzyme gamma-glutamyl transpeptidase is widely distributed throughout the body, notably kidney, seminal vesicles, pancreas, liver, spleen and brain. Being one of the enzymes of the gamma-glutamyl cycle, it is involved in aminoacid transport, catalysing a transpeptidation reaction between gamma-glutamyl peptides and most common amino acids. Methods of assay of the enzyme are based on its ability also to act on synthetic amides of glutamic acid; kinetic methods monitoring the release of p-nitroaniline from the substrate L-gamma-glutamyl p-nitroanilide are the most satisfactory. In diseases of the liver, the highest levels occur in association with cirrhosis, alcoholism, hepatic secondaries and cholestasis. As the enzyme is present in the endoplasmic reticulum of the hepatocyte, its activity is increased in situations leading to microsomal enzyme induction. Raised levels can also occur in pancreatitis, diabetes, myocardial infarction, congestive cardiac failure, chronic renal failure, cerebrovascular accidents, cerebral tumours and chronic obstructive pulmonary disease. Although the lack of specificity must be recognised, the estimation can be useful in the elucidation of some clearly defined problems arising during investigation of patients with suspected hepatic disease, especially where performed as part of a biochemical profile.
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PMID:Role of gamma-glutamyl transpeptidase activity in the diagnosis of hepatobiliary disease. 24 76

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.
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PMID:Magnesium deficiency and cardiac disorders. 80 29

Metolazone-induced acute pancreatitis and hypercalcemia are described in a 58-year-old woman with severe congestive cardiac failure. Her symptoms and laboratory abnormalities rapidly resolved upon discontinuation of metolazone. Both clinical and laboratory findings make other etiologies for the patient's pancreatitis extremely unlikely. The pathophysiology of thiazide-related hypercalcemia and pancreatitis is reviewed. To our knowledge, neither hypercalcemia nor the combination of acute pancreatitis with hypercalcemia has been reported previously in association with metolazone therapy, and the association of pancreatitis and metolazone has been noted previously only once.
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PMID:Case report: metolazone-associated hypercalcemia and acute pancreatitis. 192 34

Sonographic identification of thickening of the gallbladder wall that consists of multiple striations (alternate hypoechoic and hyperechoic layers) has been considered strong evidence of the presence of acute cholecystitis. We studied 27 patients in whom sonograms showed striated thickening of the gallbladder wall to determine the diagnostic significance of this finding. Striations were classified as focal or diffuse. Sonograms were correlated with pathologic findings in 16 patients and with clinical diagnoses and laboratory findings in 11. Patients were categorized as having cholecystitis with or without gangrene or edema of the gallbladder wall unrelated to gallbladder disease. Striated thickening of the gallbladder wall was due to cholecystitis in 10 patients, and all 10 had gangrenous changes at surgery or at pathologic examination. Striations were focal in eight of these patients and diffuse in two. Striated thickening of the gallbladder wall was due to edema of the wall unrelated to gallbladder disease in 17 patients. Causes included congestive heart failure (n = 4), renal failure (n = 5), liver disease (hepatic failure [n = 1], hepatitis [n = 6]), ascites (n = 2), hypoalbuminemia (n = 3), pancreatitis (n = 1), blockage of the lymphatic/venous drainage of the gallbladder (n = 2), and prominent Rokitansky-Aschoff sinuses (n = 1). More than one abnormality was present in five patients. Striations were focal in 11 of these patients and diffuse in six. The sonographic finding of striated gallbladder wall thickening is no more specific for cholecystitis than the observation of gallbladder wall thickening by itself, and it may occur in a variety of diseases. However, in the clinical setting of acute cholecystitis, the presence of striations suggests gangrenous changes in the gallbladder. The extent of the striations (focal or diffuse) is not useful in predicting the cause of the striated gallbladder wall thickening.
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PMID:Sonography of the gallbladder: significance of striated (layered) thickening of the gallbladder wall. 201 56

Among a total of 634,440 autopsy cases in "The Annuals of Pathological Autopsy Cases in Japan" from 1958 to 1984, 929 cases with nonspecific myocarditis were registered. The average incidence was 0.15%, fluctuating around 3- to 5-year intervals with a remarkable rise observed after 1974. The major complications in cases of myocarditis were pneumonitis, hepatitis or hepatic cirrhosis, pancreatitis, malignancies, lymphatic or thymic involvements. A clinicopathological study of 36 cases of myocarditis and 27 cases of postmyocarditic cardiomegaly indicated a classification of acute, subacute, healing and chronic or recurrent stages as well as dilatation-hypertrophy- and right ventricle-dominant types. Acute myocarditis was characterized by diffuse inflammatory cell infiltration and showed various types of arrhythmias and shock. Subacute myocarditis showed ventricular dilatation, edematous interstitium and severe congestive heart failure. Chronic myocarditis with dilatation and/or hypertrophy and irregular fibrosis included right ventricular involvement, endomyocardial disease, sick sinus syndrome in selected cases, congestive heart failure in most cases, and showed a male predominancy. Postmyocarditic cardiomegaly was similar to chronic myocarditis but showed more hypertrophy, preexcitation waves and prominent negative T waves in electrocardiography and sudden death.
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PMID:Nonspecific myocarditis: a statistical and clinicopathological study of autopsy cases. 252 82

The value of ascitic fluid adenosine deaminase activity in distinguishing tuberculosis from other causes of ascites was examined in a retrospective study of 41 patients with bacteriologically confirmed tuberculous peritonitis and 41 control patients, matched for age and sex, with ascites of other causes (12 alcoholic cirrhosis, 5 cryptogenic cirrhosis, 12 malignant disorders, 3 pancreatitis, and 9 miscellaneous causes). The mean ascites adenosine deaminase activity was 99.8 (SD 49.1) in tuberculous patients and 14.8 (8.4) U/l in control patients (p less than 0.0001). A cutoff of 32.3 U/l had a sensitivity of 95% and specificity of 98% in distinguishing between the two groups. In a subsequent prospective study of 64 patients with ascites, 11 were found to have tuberculosis. Of the others, 23 had cirrhosis (18 alcoholic, 5 cryptogenic), 17 malignant disorders, 3 pancreatitis, 5 cor pulmonale, 3 congestive cardiac failure, 1 systemic mastocytosis, and 1 renal failure and hypothyroidism. The mean ascites adenosine deaminase activity was 112.6 (45.0) U/l in the patients with tuberculous ascites and 16.3 (36.7) U/l (p less than 0.0001) in those with ascites of other causes. In this study, adenosine deaminase had a sensitivity of 100% and specificity of 96% in discriminating tuberculosis from other causes of ascites. These findings suggest that the ascitic fluid adenosine deaminase activity may be used to identify patients in whom the diagnosis of abdominal tuberculosis must be pursued.
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PMID:Diagnostic value of ascites adenosine deaminase in tuberculous peritonitis. 256 65

Corticosteroids are widely used as therapy for the adult respiratory distress syndrome (ARDS) without proof of efficacy. We conducted a prospective, randomized, double-blind, placebo-controlled trial of methylprednisolone therapy in 99 patients with refractory hypoxemia, diffuse bilateral infiltrates on chest radiography and absence of congestive heart failure documented by pulmonary-artery catheterization. The causes of ARDS included sepsis (27 percent), aspiration pneumonia (18 percent), pancreatitis (4 percent), shock (2 percent), fat emboli (1 percent), and miscellaneous causes or more than one cause (42 percent). Fifty patients received methylprednisolone (30 mg per kilogram of body weight every six hours for 24 hours), and 49 received placebo according to the same schedule. Serial measurements were made of pulmonary shunting, the ratio of partial pressure of arterial oxygen to partial pressure of alveolar oxygen, the chest radiograph severity score, total thoracic compliance, and pulmonary-artery pressure. We observed no statistical differences between groups in these characteristics upon entry or during the five days after entry. Forty-five days after entry there were no differences between the methylprednisolone and placebo groups in mortality (respectively, 30 of 50 [60 percent; 95 percent confidence interval, 46 to 74] and 31 of 49 [63 percent; 95 percent confidence interval, 49 to 77]; P = 0.74) or in the reversal of ARDS (18 of 50 [36 percent] vs. 19 of 49 [39 percent]; P = 0.77). However, the relatively wide confidence intervals in the mortality data make it impossible to exclude a small effect of treatment. Infectious complications were similar in the methylprednisolone group (8 of 50 [16 percent]) and the placebo group (5 of 49 [10 percent]; P = 0.60). Our data suggest that in patients with established ARDS due to sepsis, aspiration, or a mixed cause, high-dose methylprednisolone does not affect outcome.
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PMID:High-dose corticosteroids in patients with the adult respiratory distress syndrome. 331 54

There are four factors that govern fluid movement to or from the pleural space: hydrostatic pressure, colloid osmotic pressure, filtration coefficient, and lymphatic function. When any of these factors are altered, fluid accumulates within the pleural space. Congestive heart failure, pancreatitis, neoplasia, hypoalbuminemia, and pulmonary thromboembolism can evoke pleural effusions by altering normal fluid transport mechanisms. This approach to pleural effusion helps to explain fluid accumulation. Chylothorax, hemothorax, and empyema are also covered in the article.
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PMID:Pleural effusions and diseases of the pleura. 390 7

The CT scan of 100 patients with ascites were reviewed to assess the relative distribution of fluid in the greater and lesser peritoneal sacs. Discordant fluid accumulations were found in most cases. Patients with benign, transudative ascites (e.g., peritoneal dialysis, cirrhosis, congestive heart failure) had large greater sac collections with little fluid in the lesser sac. Those patients with diseases of organs bordering the lesser sac (e.g., pancreatitis, posteriorly penetrating gastric ulcer) had larger lesser sac fluid collections with little in the greater sac. Cytologically positive carcinomatosis of the abdomen was associated with concordant fluid volumes in these two spaces. These findings suggest that fluid within the lesser sac is not a typical manifestation of generalized peritoneal ascites and that its presence should direct a search for pathology in neighboring organs and for peritoneal malignancy.
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PMID:Lesser sac fluid in predicting the etiology of ascites: CT findings. 697 68

Anatomical variations in aortic root pathology, including combinations of dissection, aneurysmal dilatation, annuloaortic ectasia, and valve disease, defy standardized repair and mandate application of various surgical reconstructions. To examine these techniques, and their influence on morbidity and mortality, we reviewed 53 consecutive patients undergoing aortic root procedures. Thirty-two patients underwent total root reconstruction. Of these, 21 underwent Bentall procedures, 9 had a modification thereof, and 2 underwent a Cabrol reconstruction. Less extensive pathology was corrected in 21 patients with a partial root reconstruction. These included aortic valve replacement (AVR) and a separate tube graft in 14 patients, AVR and primary aortic repair +/- wrapping in 4 individuals, and AVR and patch aortic root enlargement in 3 patients. Mean age was 53.2 years (range 20 to 79). Nearly 20% had undergone previous cardiac surgery and 7.5% were emergencies. Early mortality was 4%. Complications included dysrhythmias (48%), myocardial infarction (4%), stroke (4%), pneumonia (14%), and pancreatitis (2%). There were no reoperations for bleeding. Three late complications, one pseudoaneurysm and two perivalvular leaks, were successfully repaired. Late deaths (13.7%) were caused by congestive heart failure (3), myocardial infarction (MI) (1), cancer (1), stroke (1), and accidental fall (1). Kaplan-Meier analysis reveals 1-, 5-, and 10-year survivals of 98%, 81%, and 66%. Survival and mortality data did not differ between groups, and except for the incidence of atrial dysrhythmias, complication rates also were not significantly different. This series illustrates the need for and the successful application of a selective approach to aortic root reconstruction.
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PMID:Selectivity in aortic root reconstruction. 799 93


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