| 1. |
|
|
| 2. |
- Elgzyri, T, et al.
(författare)
-
Can duplex arterial ultrasonography reduce unnecessary angiography?
- 2008
-
Ingår i: Journal of Wound Care. - : Mark Allen Group. - 0969-0700 .- 2052-2916. ; 17:11, s. 497-500
-
Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To assess the value of arterial duplex ultrasound, which assesses the location and severity of arterial disease, in determining whether invasive vascular intervention is required.METHOD: A total of 166 consecutive diabetic patients presenting at a multidisciplinary foot clinic with severe peripheral vascular disease, with or without a foot ulcer, were included in this prospective study. The choice of vascular intervention was based on the results of a duplex ultrasound examination. Subjects were followed up for two years, and their clinical management, vascular assessments and interventions given, and patient outcomes were recorded in a specially designed protocol.RESULTS: Based on findings of the duplex ultrasound, it was recommended that 55 patients (33%) should undergo angioplasty (percutaneous transluminal angioplasty [PTA] and/or subintimal recanalisation), 64 patients (39%) diagnostic angiography and 47 patients (28%) medical treatment only, thereby avoiding unnecessary angiography and its potential complications. Diagnostic angiography was recommended when the duplex ultrasound results were inconclusive. Fifty-two of the 55 patients recommended angiography with simultaneous angioplasty had an angiography; of these, 42 (81%) then had an angioplasty. Fifty-seven of the 64 patients with inconclusive results had an angiography. Of these, 23 (40%) subsequently had angioplasty, only 10 (18%) had reconstructive surgery and 24 (42%) had a diagnostic angiography only.CONCLUSION: Arterial duplex ultrasound may assist evaluations of the need for and type of invasive vascular intervention in patients with an ischaemic diabetic foot. It can thus help avoid diagnostic angiographies that do not result in vascular intervention. However, such decision-making remains at the discretion of the vascular surgeon and radiologist.
|
|
| 3. |
- Keildson, Sarah, et al.
(författare)
-
Expression of phosphofructokinase in skeletal muscle is influenced by genetic variation and associated with insulin sensitivity.
- 2014
-
Ingår i: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 63:3
-
Tidskriftsartikel (refereegranskat)abstract
- Using an integrative approach in which genetic variation, gene expression, and clinical phenotypes are assessed in relevant tissues may help functionally characterize the contribution of genetics to disease susceptibility. We sought to identify genetic variation influencing skeletal muscle gene expression (expression quantitative trait loci [eQTLs]) as well as expression associated with measures of insulin sensitivity. We investigated associations of 3,799,401 genetic variants in expression of >7,000 genes from three cohorts (n = 104). We identified 287 genes with cis-acting eQTLs (false discovery rate [FDR] <5%; P < 1.96 × 10(-5)) and 49 expression-insulin sensitivity phenotype associations (i.e., fasting insulin, homeostasis model assessment-insulin resistance, and BMI) (FDR <5%; P = 1.34 × 10(-4)). One of these associations, fasting insulin/phosphofructokinase (PFKM), overlaps with an eQTL. Furthermore, the expression of PFKM, a rate-limiting enzyme in glycolysis, was nominally associated with glucose uptake in skeletal muscle (P = 0.026; n = 42) and overexpressed (Bonferroni-corrected P = 0.03) in skeletal muscle of patients with T2D (n = 102) compared with normoglycemic controls (n = 87). The PFKM eQTL (rs4547172; P = 7.69 × 10(-6)) was nominally associated with glucose uptake, glucose oxidation rate, intramuscular triglyceride content, and metabolic flexibility (P = 0.016-0.048; n = 178). We explored eQTL results using published data from genome-wide association studies (DIAGRAM and MAGIC), and a proxy for the PFKM eQTL (rs11168327; r(2) = 0.75) was nominally associated with T2D (DIAGRAM P = 2.7 × 10(-3)). Taken together, our analysis highlights PFKM as a potential regulator of skeletal muscle insulin sensitivity.
|
|
