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Biomedical subjects

M Panteghini

Publications and source records attributed to M Panteghini.

At least 91 records · Page 5Linked to original sources
PubMed1989

Time course of changes in serum activity of the P3 isoform of pancreatic amylase isoenzyme in patients with acute pancreatitis.

We studied the temporal sequence of serum P3 isoamylase changes in patients with acute pancreatitis, in comparison with serum pancreatic lipase (LPS) activity. Twenty-four hospitalized patients with acute pancreatitis, the onset not more than 12 h previously, were admitted to the study. Serum samples were collected daily for 6 days after onset for enzyme determinations. Measurements in the 48-h period after the onset of acute pancreatitis showed clinical sensitivities of total amylase, P3 isoform and LPS of 100%. During the following period, LPS and P3 isoform activities decreased with time with parallel changes, still showing diagnostic sensitivity significantly higher than total amylase. P3 isoform and LPS appear to be interchangeable markers of pathological release of pancreatic enzymes into the bloodstream during acute pancreatitis. However, LPS determination is more convenient because of its simplicity and shorter turnaround time.

Acute Disease↗
PubMed1989

Diagnostic value of measuring pancreatic lipase and the P3 isoform of the pancreatic amylase isoenzyme in serum of hospitalized hyperamylasemic patients.

We assayed amylase (AMY) isoenzymes by cellulose acetate electrophoresis and determined pancreatic lipase (LPS) activity by a turbidimetric colipase-supplemented method in 54 hospitalized hyperamylasemic patients (32 men and 22 women; mean age 61.5, SD 16, years). In AMY isoenzyme analysis, use of a value for P3 isoform greater than 14 U/L as a positive test for acute pancreatitis gave a diagnostic efficiency of 92.6%, a predictive value of a positive test result of 90.5%, and a predictive value of a negative test of 100%. Four of 12 patients with other, nonpancreatic abdominal diseases had false-positive test results. LPS activity (cutoff limit, 700 U/L) was as effective as P3 isoform in distinguishing patients with acute pancreatitis (sensitivity, 100%) from those without acute pancreatitis (specificity, 81.3%). Thus, P3 isoform and LPS appear to be interchangeable markers of pathological release of pancreatic enzymes into the bloodstream during acute pancreatitis. This finding decreases the need for the expensive radiological procedures currently required to confirm this diagnosis. In particular, negative results virtually exclude acute pancreatitis.

Acute Disease↗
PubMed1989

Effects of therapeutic coronary reperfusion on aspartate aminotransferase isoenzymes in sera of patients with acute myocardial infarction.

We examined the kinetics of the catalytic activities of aspartate aminotransferase (AST, EC 2.6.1.1) isoenzymes in serum of 28 patients with myocardial infarction who were to receive either intracoronary urokinase--reperfusion angiographically proved--or conventional therapy (control group). Cytosolic (soluble) AST (s-AST) activity in serum increased rapidly immediately after recanalization, reaching a maximum 12 h after the onset of infarction. In the control group, this peak was reached 28 h after the onset (P less than 0.001). Peak s-AST activity was similar in the two groups. Peak activity and peak time for mitochondrial AST (m-AST) were the same for the two groups of patients; intervention that affects myocardial perfusion caused only a slight additional increase in m-AST activity in the early post-infarct period. There may be advantages to measuring m-AST, which is briefly influenced by reperfusion, instead of the usual cytosolic enzymes for assessment of myocardial damage in patients with myocardial infarction treated with thrombolytic therapy.

Adult↗
PubMed1988

Serum isoforms of creatine kinase isoenzymes.

The CK-2 and CK-3 isoenzymes of human serum creatine kinase (CK) can be further subdivided into five isoforms (subforms derived from the same isoenzyme). Three are derived from CK-3 and two from CK-2. The formation of these isoforms is a postsynthetic phenomenon brought about by a serum carboxypeptidase that acts on the M monomer of the enzyme. Sera from healthy subjects contain CK-3(1) as the dominant isoform with lesser amounts of CK-3(2) and CK-3(3). Following damage of muscle tissue, the serum isoform distribution changes as a result of the increased release of CK enzyme. This provides more diagnostic information concerning acute myocardial infarction and other muscle diseases than is available from routine CK isoenzyme analysis.

Creatine Kinase↗
PubMed1988

An alternative approach to the prevention of succinyldicholine-induced apnoea.

Succinyldithiocholine was utilized as a substrate analogue of succinyldicholine to study normal and atypical serum pseudocholinesterase (EC 3.1.1.8). In the method, the enzyme acts on succinyldithiocholine to release thiocholine, which reacts with 5,5'-dithio-bis-(2-nitrobenzoic acid) to produce a coloured compound with maximal absorbance at 410 nm. The procedure appears to be precise (between-day analysis gives a coefficient of variation between 1.1 and 3.7%) and amenable to automation, permitting routine use in any laboratory. The reference interval for 300 healthy adults with "usual" cholinesterase genotype was estimated to be 34-77 U/l, with a significant difference between males and females (40-78 U/l for men and 33-76 U/l for women, p less than 0.01). The median activity in 105 individuals with "heterozygous" cholinesterase genotype was 22 U/l (range 5-35 U/l), and for 14 "atypical" homozygotes 1.5 U/l (range 1-4 U/l). The assay with succinyldithiocholine may offer a direct procedure for preoperative screening of individuals with an abnormal response to the muscle relaxant succinyldicholine, thus avoiding the determination of genotype by measurement of inhibitor numbers.

Apnea↗
PubMed1988

Comparison of catalytic activity and mass concentration of serum creatine kinase MB isoenzyme in the detection of coronary reperfusion in acute myocardial infarction after therapeutic thrombolysis.

Serum creatinine kinase MB isoenzyme time-activity curves are useful for the assessment of coronary reperfusion after acute myocardial infarction. The purpose of this study was to compare serum creatine kinase MB catalytic activity with mass concentration for the determination of coronary reflow after therapeutic thrombolysis. Creatine kinase MB mass was determined immunoenzymometrically. Creatinine kinase MB catalytic activity concentration was determined by electrophoresis. Serum was collected every 4 hours for 96 hours in two groups of myocardial infarction patients: A (n = 10), urokinase induced reperfusion; B (n = 10), conventional therapy without urokinase. Peaks of mass and activity occurred at similar times in groups A and B. Both were significantly earlier in the urokinase treated patients. The maximal rate of increase of creatine kinase MB (based on either mass or catalytic activity) was threefold greater in the urokinase group. There are no important differences between the behaviour of creatine kinase measured as catalytic concentration or as mass concentration. Mass concentration is therefore equally useful as an indicator of coronary reperfusion.

Adult↗
PubMed1987

Serum isoforms of creatine kinase MM and MB in myocardial infarction. An appraisal of quantitative, clinical and pathophysiological information.

Using an electrophoretic method, the changes in the catalytic activities of three CK-MM isoforms (MM1, MM2, MM3) and two CK-MB isoforms (MB1, MB2) in the serum of 13 patients with acute myocardial infarction (AMI) have been monitored for 3 days after the onset of chest pain. In post-AMI period, MM3 reaches a peak first, 17 h after infarction (394 U/l), followed by MB2 (17.3 h, 190 U/l), MB1 (20.6 h, 82 U/l), MM2 (28.7 h, 637 U/l), and MM1 (32 h, 780 U/l). According to their faster decay from circulation, MB2 and MM3 have higher fractional disappearance rates (-0.035 and -0.026 per hour, respectively). The MM3/MM1 activity ratio rises beyond the upper limit found in healthy subjects within about 3 h after onset of symptoms and peaks 9.3 h after AMI, even earlier than peaks of isoforms. These characteristics make the ratio an earlier and more sensitive indicator of acute enzyme release from necrotic myocardium.

Adult↗
PubMed1987

Isoforms of creatine kinase isoenzymes in serum in acute myocardial infarction after intracoronary thrombolysis.

Kinetics of the catalytic activities of creatine kinase (CK;EC 2.7.3.2) for three CK-3 and two CK-2 isoforms in serum were studied in 20 patients with myocardial infarction randomly assigned to receive either intracoronary urokinase (group A) or conventional therapy (group B). The temporal characteristics of isoform changes described were (a) time at which the isoform activities are significantly greater than initial values, (b) maximal rate (Ka) at which isoforms are released into blood, (c) time lag from onset of pain until maximum activity value, (d) peak value of each serum isoform, and (e) rate (Kd) at which each isoform is cleared from serum. Thrombolytic treatment induced earlier peak times in group A: for CK-3(3), 7.4 vs 20.0 h; for CK-3(2), 11.6 vs 24.8; for CK-3(1), 18.6 vs 34.3; for CK-2(2), 9.1 vs 17.8; and for CK-2(1), 11.8 vs 26.8 (numbers given are medians; for all isoforms, P less than 0.05). Ka values were at least twofold greater and the first increase was significantly earlier in the urokinase group. Consequently, the ratio for CK-3(3) to CK-3(1) activities peaked significantly earlier in group A. Isoform peak activities and Kd were not significantly different between the two groups.

Adult↗
PubMed1987

Activity of serum aspartate aminotransferase isoenzymes in patients with acute myocardial infarction.

Activities of aspartate aminotransferase (AST) isoenzymes were determined in serial serum samples from 40 cases of acute myocardial infarction, and compared with activities of creatine kinase, CK-MB isoenzyme, lactate dehydrogenase, and alpha-hydroxybutyrate dehydrogenase for temporal changes. Cytosolic (soluble) AST (s-AST) and mitochondrial AST (m-AST) respectively increased 6.6 and 9.0 h after onset of chest pain. The median time at which serum m-AST activity peaked (15.8 U/L, range 6.4-53.5 U/L) was 47.8 h after the onset of infarction, 19.8 h later than the peak s-AST activity (171 U/L, range 53-517 U/L) and m-AST also disappeared from the serum more slowly than s-AST (p less than 0.001). Serum m-AST values were above normal for at least six days after the infarct. The ratio of m-AST to total AST in serum increased after myocardial infarction, being greatest (20%, range 11-32%) on the third day after onset. For individuals, peak activities of s-AST correlated well with total CK (r = 0.91) and CK-MB (r = 0.86) peak activities, indicating that s-AST also reflects the infarct size. However, m-AST correlated poorly with the enzymes commonly used in infarct diagnosis; it apparently provides different biological information.

Adult↗
PubMed1986

Isoforms of creatine kinase MM and MB in acute myocardial infarction: a clinical evaluation.

Serum creatine kinase (CK, EC 2.7.3.2) isoenzymes MM and MB were resolved, respectively, into three (MM1, MM2, MM3) and two (MB1, MB2) isoforms (subforms derived from the same isoenzyme) by electrophoresis and the isoform patterns were determined in multiple sequential serum samples, timed from the onset of chest pain, from 58 patients with acute myocardial infarction (AMI). During the first 3 h after the onset of chest pain, the serum isoform activity resembled the pattern seen in normal volunteers. Specimens obtained 6 h after AMI showed predominantly MM3 and MB2 (45% and 11% of the total CK activity, respectively). Between 10 and 72 h, there was a gradual shift in which MM3, MM2 and MB2 decreased, while MM1 and MB1 increased. MB2 and MB1 disappeared from the pattern for samples collected after 24-48 h, while MM1 was always the most prominent band at the end of the observation period (66%, range 41-77%, at 48 h). These data suggest that a single determination of CK isoform pattern, drawn between 6 and 48 h after AMI, may provide an effective means of predicting the time of onset of necrosis. There were no significant differences in the CK isoform patterns according to infarct location and functional status of patients.

Adult↗