| 1. |
- Ahnström, Josefin, et al.
(författare)
-
Plasma concentrations of apolipoproteins A-I, B, and M in patients with abdominal aortic aneurysms.
- 2010
-
Ingår i: Clinical Biochemistry. - : Elsevier BV. - 1873-2933 .- 0009-9120. ; 43:4-5, s. 407-410
-
Tidskriftsartikel (refereegranskat)abstract
- Objectives: Apolipoproteins play important roles in the development of atherosclerosis but their involvement in the pathogenesis of abdominal aortic aneurysm (AAA) is poorly understood. The aim was to investigate whether apoA-I, apoB and apoM are independently associated with AAA. Design and methods: Plasma apoA-I, apoB and apoM were measured in 343 patients with AAA and in 214 elderly apparently healthy control individuals from the background population. Results: AAA patients had lower apolipoprotein levels, as compared to healthy individuals; apoA-I, 1.62 vs. 2.08 g/l; apoB, 0.91 vs. 1.04 g/l; apoM, 0.72 vs. 0.91 mumol/l (p<0.0001 for all three). In multivariate analyses, apoA-I and apoB were associated with AAA, odds ratios (95% confidence intervals) being 0.53 (0.43-0.64) and 0.86 (0.75-0.998), respectively. Conclusions: ApoA-I, apoB and apoM levels were significantly lower in patients with AAA than in the control individuals, but only apoA-I and apoB were independently associated to AAA.
|
|
| 2. |
- Ahnström, Josefin, et al.
(författare)
-
Plasma concentrations of apolipoproteins A-I, B, and M in patients with critical limb ischemia.
- 2010
-
Ingår i: Clinical Biochemistry. - : Elsevier BV. - 1873-2933 .- 0009-9120. ; 43, s. 599-603
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: Apolipoproteins affect development of atherosclerosis, but their involvement in the pathogenesis of critical limb ischemia (CLI), a severe form of atherosclerosis, has not previously been examined. DESIGN AND METHODS: ApoA-I, apoB, and apoM were measured in plasma from 196 CLI subjects and 214 control individuals from the background population. RESULTS: Cases had lower levels of the apolipoproteins, as compared to controls; apoA-I, 1.23 vs. 2.08 g/L; apoB, 0.93 vs. 1.04 g/L; apoM, 0.75 vs. 0.91 mumol/L (p<0.0001 for all three). ApoA-I and apoM correlated negatively with inflammatory markers and positively to 1- and 3-year survival rates, whereas apoB did not. In multivariate analyses, apoA-I, but not apoB and apoM, was independently associated with CLI, the odds ratio being 0.015. CONCLUSIONS: In subjects with CLI, plasma concentrations of apoA-I, apoB and apoM were significantly lower than in control individuals, but only apoA-I was independently associated to CLI.
|
|
| 3. |
- Arkblad, Eva L, et al.
(författare)
-
Two cases of 5-fluorouracil toxicity linked with gene variants in the DPYD gene.
- 2010
-
Ingår i: Clinical biochemistry. - : Elsevier BV. - 1873-2933 .- 0009-9120. ; 43:3, s. 331-4
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: Dihydropyrimidine dehydrogenase (DPD) is the initial rate-limiting enzyme in endogenous pyrimidine catabolism and is responsible for the reduction of the pyrimidine analog 5-fluorouracil (5-FU). DPD deficiency is known to cause potentially lethal toxicity in patients receiving 5-FU. We here report a frequency analysis of one of the major splice-site mutations in the DPDY gene, and further two new DPYD gene variants. DESIGN AND METHODS: Restriction fragment length polymorphism (RFLP) and DNA sequence analysis were performed on genomic DNA and mRNA. RESULTS: In 400 patients that were diagnosed with cancer and were eligible for 5-FU treatment, 14 patients were found to be heterozygous for the splice-site mutation DPYD IVS14+1G>A, which corresponds to a population frequency of 3.5%. Two novel variants in the DPYD gene were identified. The first case was heterozygous for DPYD c.1796T>C (p.M599T). In the second case, we observed heterozygosity for the splice-site mutation DPYD IVS14+17A>G. CONCLUSIONS: We report two new DPYD gene variants, of which DPYD c.1796T>C is potentially pathogenic, whereas DPYD IVS14+17A>G is suggested as a variant without clinical significance.
|
|
| 4. |
|
|
| 5. |
- Eggers, Kai M., et al.
(författare)
-
Clinical and prognostic implications of circulating pentraxin 3 levels in non ST-elevation acute coronary syndrome
- 2013
-
Ingår i: Clinical Biochemistry. - : Elsevier BV. - 0009-9120 .- 1873-2933. ; 46:16-17, s. 1655-1659
-
Tidskriftsartikel (refereegranskat)abstract
- Objectives: Pentraxin 3 (PTX3) is the prototype of the long pentraxin family. PTX3 is involved in inflammatory processes affecting the cardiovascular system, and PTX3 levels have been shown to be elevated and independently prognostic in ST-elevation myocardial infarction. Data on PTX3 levels in non-ST-elevation acute coronary syndrome (NSTE-ACS), in contrast, are limited. The aim of the present analysis was to investigate the implications of PTX3 levels in a fairly large sample of NSTE-ACS patients and in comparison to levels of C-reactive protein (CRP). Design and methods: We measured levels of PTX3 and CRP in both 82 healthy controls and 401 NSTE-ACS patients from the GUSTO IV study, and studied the associations of these biomarkers to clinical data and 1-year mortality. Results: NSTE-ACS patients had significantly higher median PTX3 levels compared to healthy controls (3.8 vs. 1.9 mu g/L; p < 0.001). PTX3 levels in patients with NSTE-ACS were independently related to female sex and cardiac troponin T levels, but not to age or cardiovascular risk factors. PTX3 levels were higher in patients who died within 1 year but did not emerge as an independent predictor of 1-year mortality (adjusted OR 1,2 [95% Cl 0.6-2.31). This was in contrast to CRP (adjusted OR 1.5 [95% Cl 1.1-2.3]). Neither PTX3 nor CRP yielded significant discriminative value regarding mortality prediction. Conclusions: PTX3 levels are elevated in NSTE-ACS. However, the prognostic information provided by PTX3 levels is limited and inferior compared to CRP. Our data, thus, do not support the measurement of PTX3 in patients with NSTE-ACS.
|
|
| 6. |
- Eggers, Kai M., 1962-, et al.
(författare)
-
Myeloperoxidase is not useful for the early assessment of patients with chest pain
- 2010
-
Ingår i: Clinical Biochemistry. - : Elsevier BV. - 0009-9120 .- 1873-2933. ; 43:3, s. 240-245
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Myeloperoxidase (MPO) has been listed as a potentially useful risk marker in acute coronary syndrome. However, its clinical utility in patients with acute chest pain is not yet defined. DESIGN AND METHODS: MPO (Architect, Abbott Diagnostics) was measured in 120 healthy controls and 303 chest pain patients who had been admitted to the coronary care units of three Swedish hospitals. RESULTS: Chest pain patents had significantly higher median MPO levels compared to healthy controls (120.6 vs. 78. 9 pmol/L; p<0.001). However, MPO was not useful for the diagnosis of myocardial infarction (c-statistics 0.61 [95% CI 0.54-0.67]), and Cox regression analysis revealed no independent association between MPO and mortality (adjusted hazard ratio 1.3 [95% CI 0.8-2.0]) or the composite endpoint (adjusted hazard ratio 1.1 [95% CI 0.8-1.5]) after a median follow-up of 4.9 years. CONCLUSIONS: MPO provided no clinically relevant information in the present population of chest pain patients.
|
|
| 7. |
- Ekman, Carl, et al.
(författare)
-
Plasma concentrations of Gas6 and soluble Axl correlate with disease and predict mortality in patients with critical limb ischemia.
- 2010
-
Ingår i: Clinical Biochemistry. - : Elsevier BV. - 1873-2933 .- 0009-9120. ; May 4, s. 873-876
-
Tidskriftsartikel (refereegranskat)abstract
- INTRODUCTION: Critical limb ischemia (CLI) is a severe peripheral arterial disease, characterized by rest pain, ulcers and gangrene in the legs. Gas6 is a vitamin K-dependent protein, which binds and activates the tyrosine kinase receptor Axl. Gas6-mediated Axl-signaling influences endothelial activation, neointima formation and immune regulation. Axl can be cleaved and soluble Axl (sAxl) is detectable in circulation. DESIGN AND METHODS: We quantified plasma concentrations of Gas6 and sAxl in 189 CLI patients and 204 controls. RESULTS: Gas6 and sAxl concentrations were increased in the CLI patients (p<0.0001) and correlated to C-reactive protein, interleukin-6, tumor necrosis factor alpha and neopterin. Patients who died within three years of sampling (n=84) had increased concentrations of Gas6 and sAxl as compared to survivors (p=0.0009 and p=0.0011). CONCLUSIONS: Plasma concentrations of Gas6 and sAxl correlate to inflammation and predict survival. This indicates that Gas6 and sAxl have a role in CLI, presumably connected to the inflammatory process.
|
|
| 8. |
- Ekman, Carl, et al.
(författare)
-
Plasma concentrations of growth arrest specific protein 6 and the soluble form of its tyrosine kinase receptor Axl as markers of large abdominal aortic aneurysms.
- 2010
-
Ingår i: Clinical Biochemistry. - : Elsevier BV. - 1873-2933 .- 0009-9120. ; 43, s. 110-114
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: The tyrosine kinase receptor Axl is expressed in the vasculature and Gas6 is the ligand. The extracellular part of Axl (sAxl) can be found in circulation. The aim of this study was to determine plasma concentrations of Gas6 and sAxl in patients with abdominal aortic aneurysms (AAA) and to evaluate if Gas6 and sAxl can be used as biomarkers. DESIGN AND METHODS: Immunoassays for sAxl and Gas6 were used to investigate plasma from AAA patients. Patients with large (n=123) or small AAA (n=122) were compared with healthy controls (n=141). RESULTS: Gas6 correlated positively and sAxl correlated negatively with AAA size. As a consequence, the calculated Gas6/sAxl ratios correlated even better to AAA size. Forty percent of all patients with a large AAA had higher Gas6/sAxl ratio than any in the control group. DISCUSSION: The Gas6/Axl system might be involved in AAA pathogenesis, and the Gas6/sAxl ratio may be useful as a biomarker.
|
|
| 9. |
- Garwicz, Daniel, et al.
(författare)
-
Early recognition of reverse pseudohyperkalemia in heparin plasma samples during leukemic hyperleukocytosis can prevent iatrogenic hypokalemia
- 2012
-
Ingår i: Clinical Biochemistry. - : Elsevier BV. - 0009-9120 .- 1873-2933. ; 45:18, s. 1700-1702
-
Tidskriftsartikel (refereegranskat)abstract
- Objectives: To investigate the cause of apparent hyperkalemia in leukemic heparin plasma. Design and methods: Lithium heparin plasma and serum samples from a patient with chronic lymphocytic leukemia (CLL) with hyperleukocytosis were transported by either a pneumatic tube system or manual transport and analyzed either immediately or after 4 h. Results: Pneumatic tube transported samples resulted in higher plasma potassium levels than manually transported samples. Serum potassium was lower than plasma potassium, confirming the suspicion of "reverse" pseudohyperkalemia. Letting the pneumatic tube transported samples stand on the bench for 4 h before centrifugation surprisingly resulted in decreased or unchanged plasma potassium. Conclusions: The reverse pseudohyperkalemia in heparin plasma samples from a CLL patient was caused by pneumatic tube transport. Our results suggest extracellular leakage of potassium, followed by active transport of potassium into intact leukemic cells. This is the first Swedish case of reverse pseudohyperkalemia in a CLL patient, where clinical suspicion of false hyperkalemia and awareness of the phenomenon lead to a rapid laboratory diagnosis. The demonstration of reverse pseudohyperkalemia prevented potentially dangerous medical interventions, such as potassium lowering treatment.
|
|
| 10. |
|
|
