Conti Maria, Sanna Francesca, Farci Giulia Am, Uda Sabrina, Porcu Giovanna, Collu Maria, Bonatesta Rosa R, Batetta Barbara
Department of Biomedical Sciences and Technologies, Institute of Experimental Pathology, Via Porcell, 09124 Cagliari, Italy.
J Med Case Rep. 2010 Jun 18;4:183. doi: 10.1186/1752-1947-4-183.
New evidence indicates infections are emerging as risk factors for atherosclerosis although their specific role in the development and progression of atherosclerosis is still unclear.
A 43-year-old Caucasian man who had been treated for four years for multiple sclerosis progressively manifested systemic hypertension, polycythemia, peripheral arterial occlusion with intermittent claudication, and persistent headaches. In 2006, an instrumental analysis (magnetic resonance imaging) of our patient revealed widespread fibrocalcific atherosclerotic lesions which accounted for all his current symptoms, including those related to microbial stimulus. Two particular aspects were of interest, namely a lack of conventional cardiovascular risk factors and a negative family history for cardiovascular events. His chemical blood tests all yielded negative findings although a low positive hepatitis C virus-ribonucleic acid titer was detected. The titer had progressively increased and worsening atherosclerosis threatened the life of our patient. Interferon therapy was not appropriate for our patient due to the severe adverse effects observed shortly after its administration.
The reaction of individual cells to infections may provide an explanation as to why individuals with a similar microbial burden, corrected for the presence of other risk factors, display a different susceptibility to developing or worsening atherosclerosis. The identification of susceptible individuals and the treatment even of silent infections may provide an additional tool against atherosclerosis and its clinical complications. The evaluation of cell susceptibility before and after the correction of risk factors may contribute to the assessment of the efficacy of drug therapy.
新证据表明感染正成为动脉粥样硬化的危险因素，尽管其在动脉粥样硬化发生和发展中的具体作用仍不明确。
一名43岁的白种男性，因多发性硬化症接受了四年治疗，逐渐出现系统性高血压、红细胞增多症、伴有间歇性跛行的外周动脉闭塞以及持续性头痛。2006年，对该患者进行的仪器分析（磁共振成像）显示广泛的纤维钙化性动脉粥样硬化病变，这些病变解释了他目前所有的症状，包括与微生物刺激相关的症状。有两个特别值得关注的方面，即缺乏传统的心血管危险因素以及心血管事件的家族史阴性。他的血液化学检测均呈阴性结果，尽管检测到丙型肝炎病毒核糖核酸滴度呈低阳性。该滴度逐渐升高，且不断恶化的动脉粥样硬化威胁着患者的生命。由于在给予干扰素治疗后不久观察到严重不良反应，所以该治疗对我们的患者不合适。
单个细胞对感染的反应可能解释了为什么在校正其他危险因素后，具有相似微生物负荷的个体对动脉粥样硬化的发生或恶化表现出不同的易感性。识别易感个体并治疗甚至是隐匿性感染可能为对抗动脉粥样硬化及其临床并发症提供一种额外的手段。在校正危险因素前后评估细胞易感性可能有助于评估药物治疗的疗效。
