186 research outputs found

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    Vancomycin Treatment of Infective Endocarditis Is Linked with Recently Acquired Obesity

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    BACKGROUND: Gut microbiota play a major role in digestion and energy conversion of nutrients. Antibiotics, such as avoparcin (a vancomycin analogue), and probiotics, such as Lactobacillus species, have been used to increase weight in farm animals. We tested the effect of antibiotics given for infective endocarditis (IE) on weight gain (WG). METHODOLOGY/PRINCIPAL FINDINGS: Forty-eight adults with a definite diagnosis of bacterial IE (antibiotic group) were compared with forty-eight age-matched controls without IE. Their body mass index (BMI) was collected at one month before the first symptoms and one year after hospital discharge. The BMI increased significantly and strongly in vancomycin-plus-gentamycin-treated patients (mean [+/-SE] kg/m(2), +2.3 [0.9], p = 0.03), but not in controls or in patients treated with other antibiotics. Seventeen patients had a BMI increase of >or=10%, and five of the antibiotic group developed obesity. The treatment by vancomycin-plus-gentamycin was an independent predictor of BMI increase of >or=10% (adjusted OR, 6.7; 95% CI, 1.37-33.0; p = 0.02), but not treatment with other antibiotics. Weight gain was particularly high in male patients older than 65 who did not undergo cardiac surgery. Indeed, all three vancomycin-treated patients with these characteristics developed obesity. CONCLUSIONS/SIGNIFICANCE: A major and significant weight gain can occur after a six-week intravenous treatment by vancomycin plus gentamycin for IE with a risk of obesity, especially in males older than 65 who have not undergone surgery. We speculate on the role of the gut colonization by Lactobacillus sp, a microorganism intrinsically resistant to vancomycin, used as a growth promoter in animals, and found at a high concentration in the feces of obese patients. Thus, nutritional programs and weight follow-up should be utilized in patients under such treatment

    The Transcriptional Programme of Human Heart Valves Reveals the Natural History of Infective Endocarditis

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    Infective endocarditis (IE) is an infectious disease that is mainly caused by Staphylococcus aureus and Streptococcus sp. It usually leads to valvular destruction and vegetation formation. Its pathophysiology is badly understood and likely involves immune and coagulation systems with close interactions with the microorganism. Our objective was to evaluate host response by comparing transcriptional profiles of cardiac valves from IE patients with controls. Hierarchical clustering revealed a signature of IE consisting of 146 genes. Among the 89 up-regulated genes, we identified two genes strongly associated with IE: metalloproteinase 12 (MMP-12) and aquaporin-9, a member of the aquaglyceroporin membrane channel family. The up-regulation of MMP-12 gene is strengthened by the down-modulation of the gene encoding its inhibitor TIMP3. In addition, MMP-12 was expressed in macrophages infiltrating EI valves. We also found that aquaporin-9 was expressed in endothelial cells lining neo-vessel lumen, suggesting that aquaporin-9 might be associated with neovascularization of infected valves leading to tissue oedema secondary to the inflammatory process. The Gene Ontology annotation and the resulting functional classification showed that most up-regulated genes account for recruitment of inflammatory cells in vegetations, angiogenesis and remodelling of endocardium tissue. A network analysis confirmed the involvement of molecules related to the remodelling of endocardium tissue and angiogenesis in IE. It also evidenced the role of caspases, especially that of caspase-9 and intrinsic apoptotic pathway in IE. Based on this study we propose a scenario for the natural history of IE in humans. Some parameters identified in this work could become tools for measuring the disease activity and should be tested as biomarkers for diagnosis or prognosis assessment in future studies
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