N-acetyl-beta-glucosaminidase and beta 2-microglobulin in renal disease.
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Biomedical subjects
Publications and source records attributed to P Søgaard.
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The resistance types of Citrobacter freundii were investigated. The strains were divided into three groups according to susceptibility to penicillin derivatives. Group 1, comprising the ampicillin-carbenicillin sensitive strains (A-s/Ca-s), constituted 22%. Group 2 (ampicillin-resistant (A-r)/Ca-s) constituted 45% and group 3 (A-r/Ca-r) 32%. Two strains (1%) were recorded as A-s/Ca-r. Group 3 contained a higher proportion of multi-resistant strains than groups 1 and 2. The log2IC50 with ampicillin, carbenicillin, cephalothin and mecillinam in the tube-dilution method were determined for 32 strains. Groups 1 and 2 differed only as regards cephalothin resistance. The strains of group 3 were more A-r than the group 2 ones. The mecillinam susceptibility did not differ between the three groups. No strains in group 2 could transfer A-resistance. In group 3 ten out of 16 strains were able to transfer A-resistance. Resistance to sulphonamide, tetracycline, and streptomycin was also transferred, but with low frequency. The A-r/Ca-r strains could be divided into two subgroups, probably reflecting different modes of developing beta-lactam resistance. One group was very A- and Ca-r, less cephalothin-r, more mecillinam-r and could transfer A-resistance. The other group had very high cephalothin-resistance and could not transfer A-resistance. Citrobacter freundii and Enterobacter cloacae are very similar as regards resistance conditions.
The beta-lactamase activity with ampicillin (A) and cephalothin (Ce) as substrate was examined in 28 strains of Ent. cloacae and 24 strains of C. freundii by a micro-iodometric-(MIA) and an ultraviolet assay (UVA). Carbenicillin resistance (Ca-R) was present in 32 strains (16 of each species). All Ca-resistant (Ca-r) strains had elevated amounts of beta-lactamase. The conditions were very similar in the two species. The Ca-r strains could be divided into two subgroups. One group had very high ampicillinase activity and lower cephalothinase activity in MIA. In UVA the cephalothinase activity was equal to that in MIA. The strains could transfer their A- and Ca-R. The reaction velocity increased with time in MIA. The Ca-R was probably plasmid mediated. The other group had no or low ampicillinase activity in MIA. The cephalothinase activity in UVA was much higher than in MIA. Velocity decreased with time in MIA, probably due to inhibition by iodine. The strains were very Ce-r and could not transfer A-R. The Ca- and Ce-R was probably chromosomally mediated. The acquisition of Ca-R in Ent. cloacae and C. freundii was analogous to acquisition of A-R in E. coli. The fraction of strains with high ampicillinase activity (plasmid mediated among all strains with acquired beta-lactam resistance was the same in Ent. cloacae and C. freundii, viz. 0.63. In E. coli the corresponding value is 0.61. This fraction thus seems rather constant between the different genera.
The beta-lactamase activity with ampicillin (A) and cephalothin (Ce) as substrate was examined in 22 E. coli strains by a micro-iodometric - (MIA) and an ultraviolet assay (UVA). The strains were divided into three groups according to their sensitivity to A and carbenicillin (Ca). Group 1 contained 6 A-Ca sensitive (A-s/Ca-s) strains, group 2 contained 8 A-resistant (A-r)/Ca-s strains and group 3 eight A-r/Ca-r ones. MIA with A as substrate showed high activity in group 3. The activities in groups 1 and 2 did not differ and were very low. Group 1 had the lowest and group 3 the highest IC50 with A. UVA with Ce as substrate showed high activity in group 2, lower in group 3 and lowest in group 1. IC50 corresponded to this order. MIA with Ce as substrate showed high activity (measured 25 min after enzyme was added) in group 3, lower activity in group 2 and lowest in group 1. The initial velocity was highest in group 2, but decreased with time. In group 3 the velocity increased with time. Group 2 (A-r/Ca-s) strains contained cephalothinases that apparently were inhibited by iodine. The beta-lactam resistance was probably chromosomally mediated. Group 3 (A-r/Ca-r) strains contained beta-lactamases with predominantly ampicillinase activity and were not inhibited by iodine. The A-resistance was probably plasmid mediated.
An investigation of the resistance types in Enterobacter cloacae is presented. The frequency of the different resistance types was determined. The strains were divided into three groups according to sensitivity to penicillin derivatives. The ampicillin-carbenicillin-sensitive (A-s/Ca-s) group 1 comprised 20% of the E. cloacae strains received in this laboratory. The ampicillin resistant-carbenicillin-sensitive (A-r/Ca-s) group 2 comprised 38.5% of the strains and the A-r/Ca-r group 3 comprised 41.5% of the strains. Group 3 contained a high proportion of multi-resistant strains. The log 2 IC50 against ampicillin, carbenicillin, cephalothin and mecillinam was determined for 28 strains. The group 3 strains were more ampicillin-resistant than the group 2 ones. Group 1 and 2 did not differ as regards carbenicillin sensitivity. The cephalothin resistance increased from group 1 to group 2 and further on to group 3. Mecillinam sensitivity did not differ between the three groups. The ability to transfer ampicillin resistance was investigated in the 24 A-r strains. The 8 group 2 strains were not able to transfer resistance, while 9 of 16 strains in groups 3 could transfer A-resistance with frequencies ranging from 10-0.2 to 10-5.7. Resistance to sulphonamide, tetracycline and streptomycin was also transferred, often with the same frequency as the ampicillin resistance.
The ability to transfer resistance traits was investigated in 49 E. coli strains isolated from clinical specimens. The strains were divided into the three groups according to sensitivity to penicillin derivatives. Group 1 contained 8 ampicillin-carbenicillin sensitive (A-s/Ca-s) strains, group 2 contained 16 ampicillin resistent-carbenicillin sensitive (A-r/Ca-s) strains and group 3 contained 25 ampicillin-carbenicillin resistant strains. In group 3, 17 strains could transfer A-resistance (range of transfer frequency was 10(0.0) to 10(-7.5). The 16 strains in group 2 that did not transfer A-resistance more often than mutants arose from the recipient (10(-8.8). The mutants of the recipient selected on A-plates were A-r/Ca-s/cephalothin-resistant, exactly as the strains in group 2. The A-resistance in group 3 was probably based on plasmids, and that of group 2 was based on mobilizable plasmids and/or chromosomal resistance. The frequencies of transfer of sulphonamide-, tetracycline- and streptomycin resistance of the strains in groups 1 and 2 did transfer, were in the same range as the frequencies of transfer in group 3.
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In November-December 1977 an epidemic of bacteraemia due to P. cepacia was observed in Odense, Denmark (nine patients), and in Nijmegen, Holland (seven patients). All patients recovered. The epidemic was traced to intrinsic contamination of two batches of the anaesthetic fentanyl. All isolates from the patients and from the two batches belonged to the same biotype, had identical sensitivity patterns, and identical antigens. The P. cepacia strain differed from stock strains in being able to grow in two passages in methyl-p-hydroxi-benzoate, 0.5 mg/ml, which promoted the growth of the microorganism: inocula of 2-20 cfu were sufficient to initiate growth in the drug or preservative. These facts indicate the inadvisability of using p-hydroxi-benzoates as preservatives in vials. The strain was inhibited at temperatures above 38.5 degrees C, corresponding to the recovery of the patients after a period with fever above 39 degrees C. Fourteen out of 15 patients examined had agglutinin titres greater than or equal to 320, while 36 blood donors had titres less than 40. Of 12 patients with postoperative fever in the same period whose blood cultures did not yield P. cepacia, three had titres greater than 320.
From Nov. 15 to Dec. 17, 1977, Pseudomonas cepacia was isolated from the blood of 16 patients in Odense, Denmark, and Nijmegen, Holland, 2--5 days after an operation with general anaesthesia. The fever started 14--70 h after operation and lasted 2--4 days. All patients recovered. 14/15 patients examined 7--51 days later had agglutinating antibody titres of 400-3,200 against the epidemic strain. Ps. cepacia with identical biochemical characters and sensitivity pattern was isolated from unbroken vials containing the anaesthetic fentanyl, which had been given to all 16 patients. Two batches were contaminated, one heavily so (10(4)--10(5) cfu/0.1 ml). Seven other batches examined yielded no growth. The preservative added to the vials was a mixture of methyl- and propyl-p-hydroxybenzoates which not only allowed growth of the Ps. cepacia strain but could also serve as a carbon source as did citric and malonic acids. The concentration of preservative was not reduced in contaminated vials. The vials had not been sterilized after closure; too much reliance had been placed on an aseptic technique and insufficient preservatives.
An investigation of the resistance types in lactose fermenting E. coli is presented. The frequency and sensitivity to beta-lactam antibiotics of different resistance types was investigated. The strains were divided into three groups according to sensitivity to penicillin derivatives. Group 1 contained the ampicillin-carbenicillin sensitive (A-s/Ca-s), group 2 the ampicillin resistant-carbenicillin sensitive (A-r/Ca-s) and group 3 the ampicillin-carbenicillin resistant (A-r/Ca-r). A-s/Ca-r were not observed. One third of the A-r strains were sensitive to carbenicillin. The distribution of resistance types was different in the three groups. Group 1 was dominated by the usual sensitive E. coli. Group 3 contained a very high proportion of multiresistant types. The IC50 against ampicillin, carbenicillin and cephalothin of 55 strains was determined. Group 3 (A-r/Ca-r, 25 strains) was much more ampicillin resistant than group 2 (A-r/Ca-s, 16 strains). Group 2 was less sensitive to carbenicillin than group 1 (A-s/Ca-s, 14 strains). Group 3 did not differ significantly from group 1 with respect to cephalothin sensitivity, while group 2 was much more resistant than the others.
Long-term treatment of survivors of an acute myocardial infarction with angiotensin-converting enzyme inhibitors has a beneficial impact on their long-term outcome. We tested the hypothesis that captopril could reductively cleave the lipoprotein(a) molecule and in addition act as a scavenger of oxygen free radicals. In a double-blind trial, 20 patients were randomized to receive either captopril 50 mg daily or corresponding placebo. patients were followed for a period of 30 days. Blood samples were drawn prior to randomization and after 30 days of treatment. Plasma concentrations of lipoprotein(a) and malondialdehyde were evaluated. Captopril treatment produced a significant reduction in plasma content of lipoprotein(a) ( < 0.05) and at day 30 the plasma content of lipoprotein(a) was also significantly lower than that in the placebo group (p < 0.05). furthermore, on day 30 plasma concentrations of malondialdehyde, an indicator of oxidative damage, were significantly lower in the captopril group when compared to baseline values and corresponding placebo group values (p < 0.05). The observed effect of captopril treatment on lipoprotein(a) and malondialdehyde might be ascribed to the sulfhydryl group in the captopril molecule.
The study comprised 83 patients, mean (+/-SD) age 47 +/- 8 years, with essential hypertension. Systolic and diastolic blood pressure at inclusion were 171 +/- 16 and 110 +/- 7 mm Hg, respectively. Two small resistance arteries were dissected from a subcutaneous gluteal biopsy and mounted in an isometric small vessel myograph for measurement of the media:lumen ratio. Left ventricular mass (LVM) was estimated by echocardiography, and the occurrence of ventricular arrhythmias was assessed by ambulatory ECG for 48 h. Left ventricular hypertrophy (LVH) occurred in 67% of the patients. Systolic function was generally unimpaired. ST depression was found in 75%, and ventricular arrhythmias in 45%. Twenty-two patients had permanent ST depression, and they had also greater LVM and more frequent ventricular arrhythmias than those without permanent ST depression. The area under the ST trend curve of all significant ST depressions was correlated to the LVM (r = 0.42, p < 0.001). Patients with arrhythmias had significantly greater area under the ST trend curve of all significant ST depressions than patients without arrhythmias (p < 0.05). In patients with LVH and permanent ST depression, the media:lumen ratio of the peripheral vessels was greater than that of patients with LVH but without permanent ST depression (11.6 +/- 2.9 vs. 9.8 +/- 2.0, p < 0.01). This suggests that hypertensive structural changes similar to those observed in peripheral vessels might occur in the walls of myocardial resistance arteries.
The objective of this study was to evaluate the relationship between early hemodynamic instability and myocardial ischemia and the effect of early intravenous enalapril therapy on this relationship. In patients with myocardial infarction (MI), early treatment with angiotensin-converting enzyme inhibitors is controversial. In hypotensive patients, initiation of treatment may exacerbate myocardial ischemia and thereby affect the clinical outcome. Therefore, in the CONSENSUS II study, a total of 60 patients randomly allocated to either intravenous enalapril or placebo treatment commenced within 24 h after the onset of MI were evaluated by repeated blood pressure measurements, ambulatory ST-segment monitoring before discharge and exercise testing. Significant ST-depression was present in 34 patients. Patients with ST-depression before discharge (residual ischemia) during either exercise testing or ambulatory monitoring or both had a decrease in initial mean arterial blood pressure (MAP) of 20 vs. 9 mm Hg in those without ST-depression (n = 24), (p < 0.00001). However, patients (n = 13) with long-lasting ST-depression during Holter monitoring, (> 60 min of ST-depression) presented with the most severe fall in MAP of 29 mm Hg (p < 0.00001) and a lower systolic blood pressure at inclusion (p < 0.01) compared to the remainder of patients. Furthermore, the number of recurrent acute ischemic events during follow-up was higher in these patients (7 vs. 1; p < 0.01). Ten of the patients treated with enalapril showed a long-lasting ST-depression versus only 3 in the placebo group (p = 0.08), and the average duration of all significant ST-depressions during Holter monitoring was significantly longer in the enalapril group compared to the placebo group (p < 0.05). Finally, 7 enalapril patients (20%) suffered an acute ischemic event in contrast to 1 patient (4%) in the placebo group (p = 0.07). In conclusion, early administration of enalapril had a potential proischemic effect in hypotension-prone patients mediated through exacerbation of the hemodynamic response, inasmuch as initial blood pressure fall after MI is related to residual myocardial ischemia and recurrent acute ischemic syndromes.