Tuttolomondo Antonino, Maida Carlo, Pinto Antonio
Antonino Tuttolomondo, Carlo Maida, Antonio Pinto, Dipartimento Biomedico di Medicina Interna e Specialistica, U.O.C di Medicina Interna e Cardioangiologia, Università degli Studi di Palermo, 90127 Palermo, Italy.
World J Orthop. 2015 Jan 18;6(1):62-76. doi: 10.5312/wjo.v6.i1.62.
Diabetic foot ulcerations have been extensively reported as vascular complications of diabetes mellitus associated with a high degree of morbidity and mortality. Diabetic foot syndrome (DFS), as defined by the World Health Organization, is an "ulceration of the foot (distally from the ankle and including the ankle) associated with neuropathy and different grades of ischemia and infection". Pathogenic events able to cause diabetic foot ulcers are multifactorial. Among the commonest causes of this pathogenic pathway it's possible to consider peripheral neuropathy, foot deformity, abnormal foot pressures, abnormal joint mobility, trauma, peripheral artery disease. Several studies reported how diabetic patients show a higher mortality rate compared to patients without diabetes and in particular these studies under filled how cardiovascular mortality and morbidity is 2-4 times higher among patients affected by type 2 diabetes mellitus. This higher degree of cardiovascular morbidity has been explained as due to the observed higher prevalence of major cardiovascular risk factor, of asymptomatic findings of cardiovascular diseases, and of prevalence and incidence of cardiovascular and cerebrovascular events in diabetic patients with foot complications. In diabetes a fundamental pathogenic pathway of most of vascular complications has been reported as linked to a complex interplay of inflammatory, metabolic and procoagulant variables. These pathogenetic aspects have a direct interplay with an insulin resistance, subsequent obesity, diabetes, hypertension, prothrombotic state and blood lipid disorder. Involvement of inflammatory markers such as IL-6 plasma levels and resistin in diabetic subjects as reported by Tuttolomondo et al confirmed the pathogenetic issue of the a "adipo-vascular" axis that may contribute to cardiovascular risk in patients with type 2 diabetes. This "adipo-vascular axis" in patients with type 2 diabetes has been reported as characterized by lower plasma levels of adiponectin and higher plasma levels of interleukin-6 thus linking foot ulcers pathogenesis to microvascular and inflammatory events. The purpose of this review is to highlight the immune inflammatory features of DFS and its possible role as a marker of cardiovascular risk in diabetes patients and to focus the management of major complications related to diabetes such as infections and peripheral arteriopathy.
糖尿病足溃疡作为糖尿病的血管并发症已被广泛报道,其具有高度的发病率和死亡率。世界卫生组织定义的糖尿病足综合征(DFS)是“足部溃疡(位于踝关节远端,包括踝关节),伴有神经病变以及不同程度的缺血和感染”。能够导致糖尿病足溃疡的致病因素是多方面的。在这条致病途径最常见的原因中,可以考虑周围神经病变、足部畸形、足部压力异常、关节活动异常、创伤、外周动脉疾病。多项研究报告称,与非糖尿病患者相比,糖尿病患者的死亡率更高,特别是这些研究还充分表明,2型糖尿病患者的心血管死亡率和发病率要高出2至4倍。这种较高的心血管发病率被解释为是由于糖尿病患者中主要心血管危险因素、心血管疾病无症状表现以及心血管和脑血管事件的患病率和发病率较高所致。在糖尿病中,大多数血管并发症的一个基本致病途径已被报道与炎症、代谢和促凝变量的复杂相互作用有关。这些致病因素与胰岛素抵抗、随后的肥胖、糖尿病、高血压、血栓前状态和血脂紊乱直接相互作用。正如图托洛蒙多等人所报道的,糖尿病患者中炎症标志物如白细胞介素-6血浆水平和抵抗素的参与证实了“脂肪-血管”轴的致病问题,这可能导致2型糖尿病患者的心血管风险。据报道,2型糖尿病患者的这种“脂肪-血管轴”的特征是脂联素血浆水平较低,白细胞介素-6血浆水平较高,从而将足部溃疡的发病机制与微血管和炎症事件联系起来。本综述的目的是强调糖尿病足综合征的免疫炎症特征及其作为糖尿病患者心血管风险标志物的可能作用,并聚焦于糖尿病相关主要并发症如感染和外周动脉病变的管理。