Vancomycin Treatment of Infective Endocarditis Is Linked with Recently Acquired Obesity

Abstract

BackgroundGut 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 FindingsForty-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/m2, +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 ≥10%, and five of the antibiotic group developed obesity. The treatment by vancomycin-plus-gentamycin was an independent predictor of BMI increase of ≥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/SignificanceA 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.

MECHANISMS IN ENDOCRINOLOGY: Gut microbiota in patients with type 2 diabetes mellitus

“…Additionally, it has been shown that low-dose penicillin administration to mice from birth enhanced the effects of high-fat diet, that the timing of exposure to antibiotics was critical and that the metabolic effects could be transferred to germ-free mice, proposing a causal role of the gut microbiota (57). Decreased insulin sensivity following 1 week of vancomycin treatment was observed in humans following changes in gut microbiota and bile acids (34), whereas a retrospective study has reported increased adiposity following antibiotic treatment with vancomycin for infectious endocarditis (58). In contrast to these observations, exposure to antibiotics in early life among children of overweight mothers has been associated with a decreased risk of overweight in childhood (52) and studies of ob/ob, high-fat diet-fed and insulin-resistant mice have demonstrated improved glucose tolerance following antibiotic treatment (22,59).…”

The art of targeting gut microbiota for tackling human obesity

“…Bailey et al (2014) associated the exposure of antibiotics during infancy with early childhood obesity in a cohort study spanning 2001-2013 health records comprising 64.580 children. Another study, determining the impact of antibiotic therapy on BMI changes in adults with infective endocarditis (IE), observed that vancomycin-and gentamycin-treated patients increased significantly in their BMI values, while other patients treated with other antibiotics did not (Thuny et al 2010). A major effect was observed in male patients who did not have cardiac surgery and were older than 65 since they, indeed, developed obesity.…”

Changes in weight and body fat after use of tetracycline and Lactobacillus gasseri in rats

“…Studies show that increases in body weight caused by microbial antibiotics is becoming more frequent, particularly when the antibiotic has a broad spectrum of activity. Alternatively, the use of probiotics has been associated with weight loss and could presumably protect against the effect caused by antibiotics in the microbiota (Haight, Pierce, 1955;Saiman et al, 2010;Thuny et al, 2010;Saiman et al, 2012;Trasande et al, 2013).…”