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Sökning: WFRF:(Stegmayr Bernd) > (2000-2004)

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1.
  • Andersson, Christer, 1945-, et al. (författare)
  • Renal symtomatology in patients with acute intermitent porphyria
  • 2000
  • Ingår i: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 248, s. 319-325
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Can renal insufficiency in subjects with acute intermittent porphyria (AIP) be due solely to AIP?Design: A population-based study.Subjects: Subjects with AIP ≥ 18 years of age (n = 386) in the four most northerly counties of Sweden.Interventions: Screening with creatinine clearance at 24 h. Patients below the lower reference level underwent a repeat clearance test and, if still low, also chromEDTA clearance.Results: 286 (74%) subjects performed the creatinine clearance test and in 57 clearance was low; the second clearance proved normal in 23 who were then excluded. Eighteen subjects with other possible medical reasons for renal insufficiency, ethical reasons or refusing further examinations were also excluded. The 16 remaining subjects with no explanation for their renal insufficiency other than AIP were then studied in detail. All 14 women, mean age 52 years, and two uraemic men, 58 and 67 years, had manifest AIP. Twelve patients had hypertension (HT) and four were normotensive in spite of renal insufficiency. Histological findings of renal biopsies revealed diffuse glomerulosclerotic and interstitial changes with additional ischaemic lesions.Conclusion: Protracted vasospasm in attacks of AIP may be a cause of renal lesions. This is discussed.
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  • Jonsson, Per, et al. (författare)
  • Electrical current leakage during hemodialysis may increase blood-membrane interaction
  • 2001
  • Ingår i: International Journal of Artificial Organs. - : Wichtig Editore Srl. - 0391-3988 .- 1724-6040. ; 24:3, s. 136-139
  • Tidskriftsartikel (refereegranskat)abstract
    • During hemodialysis blood - membrane interaction causes complement activation. During dialysis there may be an electrical current leakage to the dialyzer, especially if there is a broken ground or a defect in another electrical device coupled to the patient.This study investigated whether an electric current of 1.5 mA DC could alter blood membrane interaction as measured by changes in C3d in the blood. Such a high current leakage could occur because there is no protection in the dialysis machine (Class 1B) against auxiliary current leakage. Such a current could come from a defective external device in contact with the patient during hemodialysis.Materials: A dialysis machine (Fresenius 2008C) with a filled blood-line system containing about 350 ml whole blood from each of 8 different donors was used in vitro. Each of the eight test-runs also contained 1000 U added heparin. The dialysis procedure was performed using hemophan membranes (GFS +12, Gambro) with bicarbonate and potassium 3.0 (D210, Gambro) as dialysate. Two electric poles were placed in the blood line, before and after the dialyzer (connected in parallel) and the ground was placed at entry and exit of the dialysate fluid coming from the machine to the dialysis filter. C3d was measured before the start of “dialysis” and at 15, 30, 45 and 60 min, during dialysis. Thereafter the 1.5 mA current was switched on and additional samples were drawn at 75 and 90 min. The mean C3d values were calculated. Paired non-parametric statistical analyses were performed.Results: There was a significant and continuous increase in C3d as compared to the “predialysis” level. The increase during 0 to 30 minutes was greater than that from 30 to 60 minutes (p=0.018); the increase in C3d during 60 to 90 min, was greater than that from 30 to 60 min (p=0.018) and there was no difference between the 0 to 30 and the 60 to 90 min increases.Conclusions: A current, used in this study, was able to induce a blood membrane interaction during in vitro dialysis. Even a weaker current leakage might have such adverse effects and similar interactions seem possible during regular dialysis depending on the extent of the leakage.
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  • Näsström, Birgit, et al. (författare)
  • Lipoprotein lipase during continuous heparin infusion : Tissue stores become partially depleted
  • 2001
  • Ingår i: Journal of Laboratory and Clinical Medicine. - : Elsevier BV. - 0022-2143 .- 1532-6543. ; 138:3, s. 206-213
  • Tidskriftsartikel (refereegranskat)abstract
    • Lipoprotein lipase (LPL) and hepatic lipase (HL) are located at vascular surfaces in extrahepatic tissues and in the liver, respectively. Heparin displaces the enzymes into the circulating blood. Animal studies have shown that the liver takes up and degrades LPL. To explore whether heparin leads to a depletion of tissue stores, we followed the lipase activities in plasma during an 8-hour primed infusion of heparin in 10 healthy subjects. After an initial peak, the HL activity decreased slowly after a time curve similar to that for activated partial thromboplastin time. The time curve for LPL was different. After the initial peak, the activity dropped by almost 80%, from 30 to 120 minutes, and then leveled off to a plateau that corresponded to about 15% of the peak level. A second bolus of heparin was given to 4 subjects after 4 hours. The plasma LPL activity increased, but only to about 35% of the original peak level. We conclude that when heparin releases LPL into plasma, the lipase becomes liable to be taken up and degraded by the liver. After less than 1 hour, the stores of LPL have been exhausted, and recruitment of lipase into plasma depends on a slow but stable delivery of newly synthesized molecules.
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  • Näsström, Birgit, et al. (författare)
  • Lipoprotein lipase during heparin infusion : lower activity in hemodialysis patients
  • 2003
  • Ingår i: Scandinavian Journal of Clinical and Laboratory Investigation. - 0036-5513 .- 1502-7686. ; 63:1, s. 45-53
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: [corrected] Patients on hemodialysis often have a moderate hypertriglyceridemia in combination with low HDL cholesterol. A contributing factor may be a derangement of the lipoprotein lipase (LPL) system. During dialysis, with heparin as anticoagulant, the enzyme is released into the circulating blood. METHODS: We have followed LPL activity and triglycerides during ordinary heparin administration in nine hemodialysis patients and controls matched for age and gender. Blood samples were drawn before heparin administration and at 15, 30, 60, 120, 180 and 240 min. RESULTS: LPL activity peaked at 15 or 30 min and then decreased to a plateau that was only 20%, of the peak. The activity was reduced in the patients by about 50% during the peak, and about 20% during the following plateau. During the peak of lipase activity the triglycerides decreased in both groups, but the change was less pronounced in patients, as was expected from the lower circulating lipase activity. During the plateau phase with low lipase activity, the triglycerides increased towards baseline values. CONCLUSIONS: During hemodialysis with heparin, there is a peak in LPL activity as well as a reduction in triglycerides during the first hour. Thereafter LPL activity decreases towards a plateau, while triglycerides increase towards baseline. The peak activity of LPL in the patients was only half that in controls, while the plateau was comparable. The data indicate that during and following each dialysis there is a period when LPL activity becomes depleted to a level that is limiting for normal lipoprotein metabolism.
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9.
  • Näsström, Birgit, et al. (författare)
  • Lipoprotein lipase in hemodialysis patients : indications that low molecular weight heparin depletes functional stores, despite low plasma levels of the enzyme.
  • 2004
  • Ingår i: BMC Nephrology. - : Springer Science and Business Media LLC. - 1471-2369. ; 5:1, s. 17-
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Lipoprotein lipase (LPL) has a central role in the catabolism of triglyceride-rich lipoproteins. The enzyme is anchored to the vascular endothelium through interaction with heparan sulphate proteoglycans and is displaced from this interaction by heparin. When heparin is infused, there is a peak of LPL activity accompanied by a reduction in triglycerides (TG) during the first hour, followed by a decrease in LPL activity to a stable plateau during the remaining session while TG increase towards and beyond baseline. This suggests that tissue stores of LPL become depleted. It has been argued that low molecular weight (LMW) heparins cause less disturbance of the LPL system than conventional heparin does. METHODS: We have followed LPL activity and TG during a dialysis-session with a LMW heparin (dalteparin) using the same patients and regime as in a previous study with conventional heparin, i.e. a primed infusion. RESULTS: The shape of the curve for LPL activity resembled that during the earlier dialyses with conventional heparin, but the values were lower during dialysis with dalteparin. The area under the curve for LPL activity during the peak period (0-180 minutes) was only 27% and for the plateau period (180-240 minutes) it was only 36% of that observed with conventional heparin (p < 0.01). These remarkably low plasma LPL activities prompted us to re-analyze LPL activity and to measure LPL mass in frozen samples from our earlier studies. There was excellent correlation between the new and old values which rules out the possibility of assay variations as a confounding factor. TG increased from 2.14 mmol/L before, to 2.59 mmol/L after the dialysis (p < 0.01). From 30 minutes on, the TG values were significantly higher after dalteparin compared to conventional heparin (p < 0.05). CONCLUSION: These results indicate that LMW heparins disturb the LPL system as much or more than conventional heparin does.
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10.
  • Näsström, Birgit, et al. (författare)
  • Lower plasma levels of lipoprotein lipase after infusion of low molecular weight heparin than after administration of conventional heparin indicate more rapid catabolism of the enzyme
  • 2003
  • Ingår i: Journal of Laboratory and Clinical Medicine. - 0022-2143 .- 1532-6543. ; 142:2, s. 90-99
  • Tidskriftsartikel (refereegranskat)abstract
    • The functional pool of lipoprotein lipase (LPL) is anchored to heparan sulfate at the vascular endothelium. Injection of heparin releases the enzyme into the circulating blood. Animal experiments have shown that the enzyme is then extracted and degraded by the liver. Low molecular weight (LMW) heparin preparations are widely used in the clinic and are supposed to release less LPL. In this study, we infused a LMW heparin into healthy volunteers for 8 hours. The peak of LPL activity was only about 30% and the subsequent plateau of LPL activity only about 40% compared with those seen with conventional heparin. When a bolus of heparin was given after 4 hours' infusion of LMW or conventional heparin, only relatively small, and similar, amounts of LPL entered plasma. This suggests that the difference between LMW and conventional heparin lay in the ability to retain LPL in the circulating blood, not in the ability to release the lipase. Triglycerides (TGs) decreased when the heparin infusion was started, as expected from the high circulating LPL activities. After 1 to 2 hours, TG levels increased again, and after 8 hours they were about twice as high as before the heparin infusion. This indicates that the amount of LPL available for lipoprotein metabolism had become critically low in relation to TG transport rates. This study indicates that LMW heparin compared with conventional heparin causes as much or more depletion of LPL and subsequent impairment of TG clearing.
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