DermKnowledgeBASE: Arteriosclerosis Obliterans

Arteriosclerosis Obliterans

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The text is the summary of recent articles on Arteriosclerosis Obliterans at 75 thresold from National Library of Medicine (NLM). This information is subject to NCBI's Disclaimer and Copyright notice.


The aim of the present study was to investigate circulating OLFM2 levels in lower Extremity arteriosclerosis obliterans (LEASO) patients and the association of OLFM2 with postoperative restenosis in patients [1]. Whether miR-31 is involved in the pathological processes of arteriosclerosis obliterans (ASO) remains to be elucidated, as does the mechanism of miR-31 regulation of arterial smooth Muscle cells (ASMCs) [2]. A 58-year-old male patient with Progressive forefoot Gangrene caused by arteriosclerosis obliterans was presented [3]. The study endpoint was major amputation within 3 months after PB-MNC [4]. The collected data were evaluated for correlation between patients with and without major amputation within 3 months after PB-MNC [5].

As a response to cholesterol crystal accumulation, the NLRP3 inflammasome is activated to produce IL-1β which eventually leads to atherosclerotic lesions [6]. Currently, many guidelines recommend endovascular therapy as the first choice for arteriosclerosis obliterans [7]. The test indices with nitroglycerine in patients with obliterating atherosclerosis have reduced step by step [8]. Graft patency and major amputation (MA) were examined as primary endpoints and the predictor of each outcome was estimated by multivariate analysis [9]. She had undergone intravascular treatment of lower limb arteriosclerosis obliterans 3 times [10].

Binary logistic regression analysis was used to evaluate related risk factors [11]. The serum endothelial cell injury model with ASO BSS was prepared [12]. Bilateral vitrectomy has been especially associated with a poor visual prognosis in patients with PDR [13]. Here we report the case of 50-year-old Woman with ESKD and systemic lupus erythematosus who developed calciphylaxis after anti-thrombotic therapy, including warfarin, for ischemic skin Ulcers due to arteriosclerosis obliterans and anti-phospholipid Antibody syndrome [14]. Cumulative patency and limb salvage in collagen disease were significantly worse compared to arteriosclerosis obliterans [15].

References: 1 , 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 , 11 , 12 , 13 , 14 , 15 ,

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