IMAGES
IN THE
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Bacterial Endocarditis Complicated by Leukocytoclastic Vasculitis Hisham Salahuddin, MD, Faraz Khan Luni, MD, Nauman Siddiqui, MD, Micheal Rohs, MD, Dinkar Kaw, MD and Nezam Altorok, MD* *Department of Internal Medicine, University of Toledo Medical Center, Toledo, Ohio (E-mail: [email protected]) The authors have no financial or other conflicts of interest to disclose.
FIGURE 1
A
29-year-old woman who underwent dental extraction 1 month before her presentation with painful purpuric skin lesions that progressed to necrotic ulcers over the buttocks and lower extremities (Figure 1A). Physical examination demonstrated new pansystolic murmur grade IV/VI at the apex of the heart and splinter hemorrhages. Initial laboratory testing was pertinent for elevated inflammatory markers, low C3 and C4 levels, positive Rheumatoid factor, positive p-ANCA (titer 1:5120) and positive anti-serine proteinase 3. Blood cultures grew Staphylococcus epidermidis. A transesophageal echocardiogram confirmed the presence of large vegetation on the mitral valve associated with severe mitral regurgitation (Figure 1B). Skin biopsy demonstrated small- and medium-sized vessels with reactive endothelium and surrounding acute inflammatory cells as depicted between the arrows in Figure 1C, on background of fibrinoid necrosis and focal extravasated red blood cells and nuclear dust, all suggestive of leukocytoclastic vasculitis. Endocarditis is one of the vasculitis mimickers that should remain in the differential diagnosis of systemic vasculitis because
500
clinically and pathologically it may be hard to differentiate between the 2 entities, as both diseases can present with peripheral ischemic/embolic phenomena, splinter hemorrhages, low complements and positive rheumatoid factor. Moreover, positive testing for ANCA, anti-proteinase 3 and/ or anti-myeloperoxidase is not uncommon in endocarditis,1 which further complicates the clinical picture. Although the treatment for vasculitis is immunosuppressive therapy, the treatment for vasculitis driven by infective endocarditis is eradication of the infection. Therefore, it is important to recognize and distinguish vasculitis mimickers from true vasculitis to avoid unnecessary treatment with immunosuppressive agents. REFERENCE 1. Mahr A, Batteux F, Tubiana S, et al. Brief report: prevalence of antineutrophil cytoplasmic antibodies in infective endocarditis. Arthritis Rheumatol 2014;66:1672–7.
The American Journal of the Medical Sciences
Volume 350, Number 6, December 2015
IN THE
MEDICAL SCIENCES
Bacterial Endocarditis Complicated by Leukocytoclastic Vasculitis Hisham Salahuddin, MD, Faraz Khan Luni, MD, Nauman Siddiqui, MD, Micheal Rohs, MD, Dinkar Kaw, MD and Nezam Altorok, MD* *Department of Internal Medicine, University of Toledo Medical Center, Toledo, Ohio (E-mail: [email protected]) The authors have no financial or other conflicts of interest to disclose.
FIGURE 1
A
29-year-old woman who underwent dental extraction 1 month before her presentation with painful purpuric skin lesions that progressed to necrotic ulcers over the buttocks and lower extremities (Figure 1A). Physical examination demonstrated new pansystolic murmur grade IV/VI at the apex of the heart and splinter hemorrhages. Initial laboratory testing was pertinent for elevated inflammatory markers, low C3 and C4 levels, positive Rheumatoid factor, positive p-ANCA (titer 1:5120) and positive anti-serine proteinase 3. Blood cultures grew Staphylococcus epidermidis. A transesophageal echocardiogram confirmed the presence of large vegetation on the mitral valve associated with severe mitral regurgitation (Figure 1B). Skin biopsy demonstrated small- and medium-sized vessels with reactive endothelium and surrounding acute inflammatory cells as depicted between the arrows in Figure 1C, on background of fibrinoid necrosis and focal extravasated red blood cells and nuclear dust, all suggestive of leukocytoclastic vasculitis. Endocarditis is one of the vasculitis mimickers that should remain in the differential diagnosis of systemic vasculitis because
500
clinically and pathologically it may be hard to differentiate between the 2 entities, as both diseases can present with peripheral ischemic/embolic phenomena, splinter hemorrhages, low complements and positive rheumatoid factor. Moreover, positive testing for ANCA, anti-proteinase 3 and/ or anti-myeloperoxidase is not uncommon in endocarditis,1 which further complicates the clinical picture. Although the treatment for vasculitis is immunosuppressive therapy, the treatment for vasculitis driven by infective endocarditis is eradication of the infection. Therefore, it is important to recognize and distinguish vasculitis mimickers from true vasculitis to avoid unnecessary treatment with immunosuppressive agents. REFERENCE 1. Mahr A, Batteux F, Tubiana S, et al. Brief report: prevalence of antineutrophil cytoplasmic antibodies in infective endocarditis. Arthritis Rheumatol 2014;66:1672–7.
The American Journal of the Medical Sciences
Volume 350, Number 6, December 2015
