[Prevalence of normal serum enzyme levels in acute pancreatitis. Importance of etiology].
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Biomedical subjects
Publications and source records attributed to M Elena.
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The value of the serum P3 amylase fraction in the prediction of the course of acute pancreatitis (AP) after the initial episode was studied prospectively. Eighty-eight patients with AP were included. Amylase, lipase, trypsin and the P3 amylase fraction were measured in serum obtained at the time of discharge. Patients were followed for 60 days after discharge and divided into two groups: 75 patients who did not have complications, of whom 22.6 per cent displayed elevation of one or more pancreatic enzymes at discharge (17.3 per cent hypertrypsinaemia, 9.3 per cent hyperlipasaemia and 6.6 per cent P3 fraction); and 13 patients who had an unsatisfactory outcome (4 died, 4 developed a pseudocyst and 5 presented with recurrent pancreatitis). All of the latter group had an increase in at least one enzyme at the time of discharge (92.3 per cent P3 fraction, 69.2 per cent trypsin, 15.3 per cent lipase, and 7.6 per cent amylase). Both the persistence of the P3 fraction and hypertrypsinaemia were significantly more frequent in patients with an unfavourable outcome than in those with an uncomplicated course (P less than 0.001). On the other hand, persistent elevation of total amylase and lipase were unrelated to outcome. The hospitalization time was similar in both groups (good outcome 21.4 +/- 1.9 days, unfavourable outcome 17.3 +/- 5.3 days). It is concluded that the presence of P3 amylase fraction or hypertrypsinaemia at the time of discharge from hospital in a patient with acute pancreatitis suggests a risk of a later complication. Careful surveillance until enzyme levels become normal is urged. It is suggested that isoamylase P3 determination is the most sensitive assay to screen for the complications of acute pancreatitis.
To characterize bleeding from gastric red spots in patients with cirrhosis, three groups of patients were studied: (a) 11 cirrhotic patients bleeding from gastric red spots, (b) 18 nonbleeding cirrhotic patients without gastric red spots, and (c) 13 noncirrhotic patients with endoscopic normal mucosa (controls). Histologic examination of antral biopsy specimens revealed a diffuse capillary ectasia without inflammation in 8 of the 11 cirrhotic patients with gastric lesions. Morphometric analysis disclosed a significantly greater mean mucosal capillary cross-sectional area in cirrhotic patients with gastric lesions (mean +/- SE, 1371 +/- 320 microns2) than in those without gastric lesions (541 +/- 61 microns2) (p less than 0.005) or controls (353 +/- 20 microns2) (p less than 0.001). Hypergastrinemia was detected in 8 of the 11 cirrhotic patients with lesions, in 2 of the 18 cirrhotic patients without gastric lesions, and in none of the controls (p less than 0.001). Gastrin serum levels correlated significantly (r = 0.80) with mean mucosal capillary cross-sectional area in patients with cirrhosis. Pepsinogen I serum levels below 20 ng/ml were observed in 7 of the 11 cirrhotic patients with lesions, in 1 of the 18 cirrhotic patients without lesions, and in none of the controls. These data indicate that bleeding from gastric red spots in patients with cirrhosis is a distinct entity characterized by vascular ectasia of the gastric mucosa. This condition seems to be associated with hypergastrinemia and low serum levels of pepsinogen I.
The main source of circulating immunoreactive somatostatin (IRS) seems to be the gastrointestinal tract. We therefore investigated plasma IRS in patients with various gastrointestinal diseases. Mean basal IRS oscillated between 46 and 73 pg/ml. A postprandial rise was observed in all patients and age-matched controls. However, the increment was significantly higher in patients with duodenal ulcer (159 +/- 20 pg/ml), active ulcerative colitis (176 +/- 17 pg/ml), and irritable bowel syndrome (194.4 +/- 20.4 pg/ml). Patients with duodenal ulcers who underwent vagotomy showed a decreased postprandial increment (107 +/- 10 pg/ml) when compared with active duodenal ulcer patients. No difference was demonstrable between controls and individuals with gastric ulcer, and patients with inactive ulcerative colitis. These results suggest that vagal innervation plays a role in postprandial IRS stimulation, whereas gastric hyperacidity, acute lesions of the colonic mucosa, and hypermotility of the gastrointestinal tract are associated with an exaggerated postprandial IRS response. Since somatostatin is known to influence many gastrointestinal functions, these variations in circulating IRS concentrations may be of pathophysiologic importance.
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In patients with chronic pancreatitis, the development of exocrine pancreatic failure is generally thought to be an irreversible process. We found evidence to the contrary in a prospective study of 70 patients who were evaluated by endoscopic retrograde cholangiopancreatography and sequential measurements of stool fat, percent urinary PABA excretion, and serum trypsin during a follow-up time period of 1-4 yr. Initial p-aminobenzoic acid (PABA) testing showed exocrine failure in 51 patients, 35 of whom had low serum trypsin levels while 14 (27%) disclosed unexpectedly high trypsin concentrations. Ductal morphology was similar in patients with low and high trypsin values. In 8 of the latter cases, steatorrhea improved and pancreatic function tests became normal after pancreaticojejunostomy in 4 patients, alcohol abstinence in 3 patients, and spontaneous resolution of a pseudocyst in 1 patient. Pancreatic cancer was present in a further 3 patients. Of the 37 patients with low PABA and low trypsin at the outset, there was no improvement of exocrine function in 17 of 18 who were surgically treated. Conservative treatment had a similar effect in another 6 patients who were available for follow-up in this group. The mean duration of symptomatic disease was shorter (p less than 0.001) in patients with low PABA and high trypsin levels (1.4 +/- 1.2 yr) than in those with low PABA and low trypsin levels (4.5 +/- 1.3 yr). The results show that up to 20% of patients with chronic pancreatitis have exocrine pancreatic failure, which is apparently due to early ductal obstruction of a gland with preserved function; this situation can be suspected when low urinary PABA excretion and high serum trypsin levels are simultaneously found; and (c) exocrine failure may be reversible in these patients by using a pancreatic drainage procedure or alcohol abstinence. Such a peculiar pattern of pancreatic function tests may also suggest pancreatic cancer.
108 patients who received tobramycin or amikacin could be evaluated for nephrotoxicity in a prospective randomized trial. Both groups had similar illnesses, and causative agents, concurrent drug administration, ages, sex ratios, initial serum creatinine and aminoglycoside levels and total dose and duration of therapy. Using urinary concentration of beta 2 microglobulin (beta 2m) as a marker, nephrotoxicity was detected in 13 (22.4%) of 58 patients given tobramycin and 13 (26%) of 50 given amikacin (n.s.). Using serum creatinine as a marker, nephrotoxicity was detected in 3 (5.2%) of 58 patients given tobramycin and in 7 (14%) of 50 given amikacin (n.s.). The whole group of 108 patients was used to compare the usefulness of serum creatinine levels versus urinary concentration of beta 2m. An elevation of serum creatinine was detected in 10 of 108 patients (9.3%). In 5 of these 10 patients the beta 2m remained normal, suggesting a functional renal failure. In 21 of the 108 patients (19.4%) the beta 2m increased while the serum creatinine remained normal, suggesting an aminoglycoside nephrotoxicity which would have remained undetected if only serum creatinine had been measured. In the remaining patients (77 of the 108; 71.3%) serum creatinine and urinary concentration of beta 2m both remained normal throughout the treatment. In conclusion no statistically significant differences were found between tobramycin and amikacin nephrotoxicity. Urinary beta 2m is more sensitive than serum creatinine and furthermore it allows one to differentiate aminoglycoside nephrotoxicity from functional renal failure.
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A total of 157 patients were treated with tobramycin or amikacin in a controlled prospective randomized trial. Dosages were adjusted to renal function according to a nomogram. Trough and peak aminoglycoside levels were available at the end of the trial. Of the above total, 113 recipients of nine or more doses of tobramycin or six or more doses of amikacin, without other apparent cause of renal failure, were evaluated for nephrotoxicity. Thirty-six patients were evaluated for auditory toxicity. The patients in groups evaluated for either nephrotoxicity or auditory toxicity were similar with respect to intensity and etiology of bacterial disease, concurrent exposure to other antimicrobial drugs, age and sex distribution, initial serum creatinine level, and total dose and duration of antimicrobial therapy. Nephrotoxicity of similar severity developed in 4 of 59 (6.8%) recipients of tobramycin and in 7 of 54 (13.1%) recipients of amikacin (P greater than 0.05). Mild auditory toxicity developed in 3 of 19 (15.7%) recipients of tobramycin and in 2 of 17 (11.7%) recipients of amikacin (P greater than 0.05). When patients with abnormally high mean trough or peak aminoglycoside levels were excluded from comparison, nephrotoxicity was 6.12 and 5.12% (P greater than 0.05) and auditory toxicity was 17.6 and 7.69% (P greater than 0.05) in the groups given tobramycin and amikacin, respectively. We conclude that the nephrotoxicity and auditory toxicity of amikacin and tobramycin are not significantly different and that such toxicities are indeed infrequent events when the dosages of these drugs are adjusted to hold blood levels within the safe boundaries suggested by the studies of others.
In order to discriminate between benign and malignant effusions, the value of carcinoembryonic antigen (CEA), alpha 1-acidglycoprotein (AGP), alpha-fetoprotein (AFP), phosphohexose isomerase (PHI), and beta 2-microglobulin (B2M) has been estimated in serous effusions in a group of 106 patients, 30 with a malignant and 76 with a benign effusion. Mean CEA and AGP levels in malignant effusions were significantly higher than in benign effusions; no significant differences of mean PHI, AFP and B2M levels of benign and malignant effusions were found. CEA level estimations were useful for confirming malignancy in 27% of malignant effusions but in only 7.5% of all effusions, and AGP and PHI for excluding it in 37.5 and 36.0% of all effusions, respectively. With the combination of CEA with AGP or PHI, a correct diagnosis was achieved in only 45 and 44% of all effusions, respectively. The combination of AFP or B2M with CEA, AGP or PHI did not improve the discriminative value for differentiating malignant and benign effusions.
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Morphologic and enzyme induction phenomena changes in the small bowel mucosa produced by excessive alcohol intake were studied. Both aspects may have nutritional repercussions in alcoholic patients. Three groups of patients were included in the study: group I made up of 20 healthy controls, group II with 30 alcoholic patients with active alcohol intake at the time of the study and group III made up of 30 alcoholics following abstinence. The nutritional status, possible existence of associated liver disease, intestinal morphology and the mucosal and serum gamma glutamyltranspeptidase (GGT) levels were evaluated. The morphologic changes observed under the study conditions, with normal levels of ingestion in alcoholic with active alcohol intake, were mild and could be related with the nutritional status and folate deficiency which some presented than being secondary to a direct toxic effect of the alcohol. Moreover, significant increases were observed in the GGT in the intestinal mucosa of alcoholics with active intake (3.97 +/- 1.37 mU/g of tissue) with respect to the control group (1.86 +/- 0.7 mU/g). The changes were rapidly reversible following abstinence and correlated with the changes observed in serum, thus suggesting an enzymatic induction mechanism.