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Träfflista för sökning "WFRF:(Hultberg Björn) srt2:(1990-1994)"

Search: WFRF:(Hultberg Björn) > (1990-1994)

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1.
  • Agardh, Carl-David, et al. (author)
  • Association between urinary N-acetyl-beta-glucosaminidase and its isoenzyme patterns and microangiopathy in type 1 diabetes mellitus
  • 1991
  • In: Clinical Chemistry. - 0009-9147. ; 37:10 Pt 1, s. 1696-1699
  • Journal article (peer-reviewed)abstract
    • Urinary N-acetyl-beta-glucosaminidase (NAG) and its isoenzymes (NAG A and NAG B) in samples from 87 type 1 diabetic patients and 40 apparently healthy reference subjects were studied with enzyme immunoassays. The diabetic patients had higher concentrations of urinary NAG than did the control subjects (P less than 0.01), but the isoenzyme pattern did not differ. There was a positive correlation between metabolic control (Hb A1c concentrations) and total NAG (P less than 0.01), NAG A (P less than 0.01), and NAG B (P less than 0.001). The diabetic patients were divided into three groups, depending on the degree of retinopathy. Subjects with severe forms of retinopathy did not have increased concentrations of urinary NAG unless they had concomitant nephropathy. The isoenzyme pattern was similar irrespective of degree of retinopathy or nephropathy. The results indicate that concentrations of urinary NAG are positively correlated to the degree of nephropathy, whereas there is no such correlation to the degree of retinopathy.
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2.
  • Agardh, Carl-David, et al. (author)
  • Lack of association between plasma homocysteine levels and microangiopathy in type 1 diabetes mellitus
  • 1994
  • In: Scandinavian Journal of Clinical & Laboratory Investigation. - : Informa UK Limited. - 1502-7686 .- 0036-5513. ; 54:8, s. 637-641
  • Journal article (peer-reviewed)abstract
    • The reactive vascular-injuring amino acid homocysteine was previously shown to be increased in plasma in diabetic patients with clinical signs of nephropathy. In this study, plasma homocysteine was measured in type 1 diabetic patients with normoalbuminuria (n = 22), microalbuminuria (n = 40) and proteinuria (n = 14) in order to investigate whether plasma homocysteine levels are increased already at the stage of incipient nephropathy, i.e. microalbuminuria. Furthermore, patients were characterized according to the degree of retinopathy. Plasma homocysteine in the whole population (n = 76) was related to B-Folate (r = 0.38, p < 0.01), S-Creatinine (r = 0.55, p < 0.001), S-Urea (r = 0.37, p < 0.01), U-Albumin (r = 0.46, p < 0.001), urinary N-acetyl-beta- glucosaminidase (r = 0.40, p < 0.001), systolic blood pressure (r = 0.36, p < 0.01) and diabetes duration (r = 0.44, p < 0.001). There were no differences in plasma homocysteine levels between patients with normoalbuminuria (8.0 +/- 1.7 mumol l-1; mean +/- SD) and those with microalbuminuria (9.1 +/- 3.4 mumol l-1). However, patients with clinical signs of nephropathy had higher plasma homocysteine levels (12.9 +/- 5.7 mumol l-1, p < 0.01) compared to the other two groups. There was no association between plasma homocysteine levels and different degrees of retinopathy. Thus, the present study does not show any relation between plasma homocysteine levels and early stages of diabetic nephropathy or retinopathy indicating that elevated concentrations of plasma homocysteine does not explain the increased risk for atherosclerosis observed in patients with microalbuminuria.
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3.
  • Hultberg, Björn, et al. (author)
  • Enzyme immunoassay of urinary beta-hexosaminidase isoenzymes in patients with renal transplants
  • 1990
  • In: Clinica Chimica Acta. - : Elsevier BV. - 0009-8981. ; 192:2, s. 107-114
  • Journal article (peer-reviewed)abstract
    • beta-Hexosaminidase (NAG) and percent of NAG B were studied in twenty patients following renal transplantation. Median urinary NAG for twenty reference individuals was 0.26 U/mmol creatinine and NAG B was 24%. Urinary NAG decreased rapidly from a median of 3.7 U/mmol on the third day, to 1.2 U/mmol on the 15th day after transplantation in the patients with no major complications. The percentage of NAG B did not change significantly during this period and did not differ from the reference population. Rejection and cyclosporine toxicity were diagnosed on 17 occasions. Urinary NAG rose more than twofold in 15 of these episodes. The percentage of NAG B was slightly increased in 6 of these. Six months after discharge 17 of the renal transplants functioned well. They exhibited a marked decrease (almost normalized) of urinary NAG with no change in the percentage of NAG B.
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4.
  • Hultberg, Björn, et al. (author)
  • Increased levels of plasma homocysteine are associated with nephropathy, but not severe retinopathy in type 1 diabetes mellitus
  • 1991
  • In: Scandinavian Journal of Clinical & Laboratory Investigation. - : Informa UK Limited. - 1502-7686 .- 0036-5513. ; 51:3, s. 277-282
  • Journal article (peer-reviewed)abstract
    • The reactive vascular-injuring amino acid homocysteine was measured in plasma samples from 79 well-characterized type 1 diabetic patients and 46 control subjects. Patients with proliferative retinopathy had higher homocysteine levels (15.0 +/- 6.3 mumols l-1; mean +/- SD, p less than 0.001; n = 42) than those with progressive retinopathy during a two-year period (10.4 +/- 1.6 mumols l-1; n = 12), no or minimal retinopathy (10.7 +/- 4.3 mumols l-1; n = 25), and the control subjects (11.0 +/- 3.4 mumols l-1). Within the group of patients with proliferative retinopathy increased homocysteine levels were confined to those patients that had serum creatinine levels greater than 115 mumols l-1 and/or an albumin:creatinine clearance ratio greater than or equal to 0.02 x 10(-3) (17.0 +/- 5.9 mumols l-1; n = 23), whereas those with no or only minimal nephropathy had levels (12.1 +/- 5.5 mumols l-1; n = 18) that were not different from the control group. We conclude that neither type 1 diabetes mellitus nor diabetic retinopathy per se is associated with increased plasma homocysteine levels. In contrast, homocysteine accumulates, probably owing to reduced glomerular filtration, in diabetic patients with advanced nephropathy. This suggests that homocysteine might contribute to the accelerated development of macroangiopathy seen especially in this subgroup of diabetic patients.
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5.
  • Hultberg, Björn, et al. (author)
  • The association between plasma beta-hexosaminidase and its isoenzyme patterns and retinopathy in type 1 diabetes mellitus
  • 1991
  • In: Clinica Chimica Acta. - 0009-8981. ; 196:2-3, s. 177-183
  • Journal article (peer-reviewed)abstract
    • beta-Hexosaminidase and its isoenzyme patterns were investigated in plasma from patients with Type 1 diabetes mellitus. The patients were divided into three main groups matched for duration of diabetes: (a) proliferative retinopathy (b), progress of retinopathy within a two-year period (c) and with no background retinopathy. When all patients were compared to a reference group, a significant increase of plasma beta-hexosaminidase activity was found. Patients with proliferative retinopathy had significantly increased activity of plasma beta-hexosaminidase compared to the reference group but not compared to the other diabetic patients. The isoenzyme distribution was not different in any of the diabetic subgroups compared to the reference group. It was also shown that various degrees of diabetic nephropathy did not influence total plasma Hex or the isoenzyme pattern.
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6.
  • Sterner, Gunnar, et al. (author)
  • Determination of urinary N-acetyl-beta-glucosaminidase in patients with hypertension and renal artery stenosis
  • 1993
  • In: Journal of Internal Medicine. - : Wiley. - 1365-2796 .- 0954-6820. ; 234:3, s. 281-285
  • Journal article (peer-reviewed)abstract
    • The purpose of the study was to measure the urinary excretion of N‐acetyl‐beta‐glucosaminidase (U‐NAG) in patients suspected of having renovascular hypertension and to compare the enzyme excretion before and after active intervention with operation or percutaneous transluminal renal angioplasty (PTRA). Eighty‐one patients with severe, therapy‐resistant hypertension were examined with regard to renal artery stenosis (RAS). At least one significant renal artery stenosis was found in 61 patients, whilst the remaining 20 patients were classified as having essential hypertension. Enzyme levels were found to be significantly higher in RAS patients as compared with patients with severe hypertension lacking significant renal artery stenosis, 0.66 (0.41–0.91, median value, 1st and 3rd quartiles) versus 0.35 (0.27–0.54); P < 0.01. Both groups of patients had significantly higher U‐NAG values than a healthy reference population (0.2, 0.13–0.27; P < 0.01). Forty of the RAS patients were randomized to surgery or PTRA and followed prospectively for 2 years. After either renal vascular surgery or PTRA a significant rise in U‐NAG excretion was observed 7–10 days after treatment. Urinary NAG excretion remained elevated during long‐term follow‐up. It is suggested that U‐NAG should be determined in patients with therapy‐resistant hypertension with suspicion of renal artery stenosis.
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