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Abnormal macrophage response to microbial stimulus in a 43-year-old man with a severe form of atherosclerosis: a case report

Maria Conti1, Francesca Sanna2, Giulia AM Farci3, Sabrina Uda2, Giovanna Porcu2, Maria Collu4, Rosa R Bonatesta2 and Barbara Batetta2*

Author Affiliations

1 Department of Cardiovascular and Neurological Sciences, University Hospital, 09042 Monserrato, Italy

2 Department of Biomedical Sciences and Technologies, Institute of Experimental Pathology, Via Porcell, 09124 Cagliari, Italy

3 Department of Medicine, University Hospital, 09042 Monserrato, Italy

4 Department of Neuroscience, University Campus, 09042 Monserrato, Italy

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Journal of Medical Case Reports 2010, 4:183  doi:10.1186/1752-1947-4-183

Published: 18 June 2010



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.

Case presentation

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.