83 research outputs found

    Influence of Skin Commensals on Therapeutic Outcomes of Surgically Debrided Diabetic Foot Infections-A Large Retrospective Comparative Study

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    In diabetic foot infections (DFI), the clinical virulence of skin commensals are generally presumed to be low. In this single-center study, we divided the wound isolates into two groups: skin commensals (coagulase-negative staphylococci, micrococci, corynebacteria, cutibacteria) and pathogenic pathogens, and followed the patients for ≥ 6 months. In this retrospective study among 1018 DFI episodes (392 [39%] with osteomyelitis), we identified skin commensals as the sole culture isolates (without accompanying pathogenic pathogens) in 54 cases (5%). After treatment (antibiotic therapy [median of 20 days], hyperbaric oxygen in 98 cases [10%]), 251 episodes (25%) were clinical failures. Group comparisons between those growing only skin commensals and controls found no difference in clinical failure (17% vs. 24 %, p = 0.23) or microbiological recurrence (11% vs. 17 %, p = 0.23). The skin commensals were mostly treated with non-beta-lactam oral antibiotics. In multivariate logistic regression analysis, the isolation of only skin commensals was not associated with failure (odds ratio 0.4, 95% confidence interval 0.1-3.8). Clinicians might wish to consider these isolates as potential pathogens when selecting a targeted antibiotic regimen, which may also be based on oral non-beta-lactam antibiotic agents effective against the corresponding skin pathogens

    Parsonage-Turner Syndrome rather than Zoster Neuritis?

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    We report the case of an 86-year-old man with acute left shoulder pain, followed by left limb monoparesis and a herpetic rash on the left upper limb and thoracic region. This situation presented a diagnostic challenge because of the simultaneity of symptoms attributable to Parsonage-Turner syndrome and herpes zoster neuropathy. A detailed clinical history, physical examination and electroneuromyography were essential to distinguish the neurological structures involved and to ascertain the diagnosis

    Pseudomonal Diabetic Foot Infections: Vive la Différence?

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    Objective To assess the outcomes of diabetic foot infections (DFIs) due to Pseudomonas aeruginosa. Patients and Methods From April 24, 2013 to July 31, 2016, we analyzed data from patients prospectively enrolled in our clinical pathway of DFIs, comparing those with infection due to Pseudomonas with those without infection due to Pseudomonas. Results Overall, we assessed 1018 cases of DFIs: 392 with osteomyelitis and 626 with only soft tissue infections. The prevalence of P aeruginosa in deep wound cultures was 10% (104/1018); of the 1018 cultures, 22 were monomicrobial, 82 were polymicrobial, and 46 were with osteomyelitis. Overall, the patients were treated with a median of 1 surgical debridement and a total of 20 days of antibiotic therapy. In a comparison of crude groups, the proportion of clinical failures was significantly higher with Pseudomonas than with other pathogens (36/104 [35%] vs 218/914 [24%], respectively; P=.02). A multivariate analysis showed that pseudomonal DFIs did not recur more often than nonpseudomonal DFIs (hazard ratio, 1.0; 95% confidence interval, 0.6-1.7). Among the 104 cases of pseudomonal DFIs, there was no association between failure of treatment and the total duration of antibiotic therapy, duration of intravenous therapy, duration of combined antibiotic therapy with more than 1 agent, or duration of oral (fluoroquinolone) therapy. Among 15 cases of pseudomonal recurrence, 2 (13%) developed resistance to the antibiotic agent used for the index episode. Conclusion For DFIs caused by P aeruginosa, other than choosing an antibiotic agent that is active against the organism, it does not appear necessary to treat with a different therapeutic regimen compared with the treatment of nonpseudomonal DFIs. There is no difference

    Moderate to Severe Soft Tissue Diabetic Foot Infections: A Randomized, Controlled, Pilot Trial of Post-Debridement Antibiotic Treatment for 10 versus 20 days

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    Background: The optimal duration of antibiotic therapy for soft-tissue infections of the diabetic foot (ST-DFI) remains unknown. Objective: We determine if antibiotic therapy after debridement for a short (10 days), compared with a long (20 days), duration for ST-DFI results in similar rates of clinical remission and adverse events (AE). Summary Background Data: The optimal duration of systemic antibiotic therapy, after successful debridement, for soft tissue infections of diabetic patients is unknown. Because of the high recurrence risk, overuse is commonplace. Methods: This was a randomized, controlled, non-inferiority pilot trial of cases of diabetic foot infection (excluding osteomyelitis) with the primary outcome of “clinical remission at two-months follow-up”. Results: Among 66 enrolled episodes (17% females; median age 71 years), we randomized 35 to the 10-day arm and 31 to the 20-day arm. The median duration of the parenteral antibiotic therapy was 1 day, with the remainder given orally. In the intention-to-treat (ITT) population, we achieved clinical remission in 27 (77%) patients in the 10-day arm compared to 22 (71%) in the 20-days arm (p = 0.57). There were a similar proportion in each arm of AE (14/35 versus 11/31; p = 0.71), and remission in the per-protocol (PP) population (25/32 vs. 18/27; p = 0.32). Overall, eight soft tissue DFIs in the 10-day arm and five cases in the 20-day arm recurred as a new osteomyelitis (8/35 [23%] versus 5/31 [16%]; p = 0.53). Overall, the number of recurrences limited to the soft tissues was 4 (6%). By multivariate analysis, rates of remission (ITT population, hazard ratio 0.6, 95%CI 0.3-1.1; PP population 0.8, 95%CI 0.4-1.5) and AE were not significantly different with a 10-day compared to 20-day course. Conclusions: In this randomized, controlled pilot trial, post-debridement antibiotic therapy for soft tissue DFI for 10 days gave similar (and non-inferior) rates of remission and AEs to 20 days. A larger confirmatory trial is under way

    Effectiveness of Therapeutic Patient Education Interventions in Obesity and Diabetes: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

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    Diabetes mellitus (DM) and obesity account for the highest burden of non-communicable diseases. There is increasing evidence showing therapeutic patient education (TPE) as a clinically and cost-effective solution to improve biomedical and psychosocial outcomes among people with DM and obesity. The present systematic review and meta-analysis present a critical synthesis of the development of TPE interventions for DM and obesity and the efficacy of these interventions across a range of biomedical, psychosocial and psychological outcomes. A total of 54 of these RCTs were identified among patients with obesity and diabetes and were thus qualitatively synthesized. Out of these, 47 were included in the quantitative synthesis. There was substantial heterogeneity in the reporting of these outcomes (I2 = 88.35%, Q = 317.64), with a significant improvement noted in serum HbA1c levels (standardized mean difference (SMD) = 0.272, 95% CI: 0.118 to 0.525, n = 7360) and body weight (SMD = 0.526, 95% CI: 0.205 to 0.846, n = 1082) in the intervention group. The effect sizes were comparable across interventions delivered by different modes and delivery agents. These interventions can be delivered by allied health staff, doctors or electronically as self-help programs, with similar effectiveness (p < 0.001). These interventions should be implemented in healthcare and community settings to improve the health outcomes in patients suffering from obesity and DM

    Genetic Regulation of Plasma Lipid Species and Their Association with Metabolic Phenotypes.

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    The genetic regulation and physiological impact of most lipid species are unexplored. Here, we profiled 129 plasma lipid species across 49 strains of the BXD mouse genetic reference population fed either chow or a high-fat diet. By integrating these data with genomics and phenomics datasets, we elucidated genes by environment (diet) interactions that regulate systemic metabolism. We found quantitative trait loci (QTLs) for approximately 94% of the lipids measured. Several QTLs harbored genes associated with blood lipid levels and abnormal lipid metabolism in human genome-wide association studies. Lipid species from different classes provided signatures of metabolic health, including seven plasma triglyceride species that associated with either healthy or fatty liver. This observation was further validated in an independent mouse model of non-alcoholic fatty liver disease (NAFLD) and in plasma from NAFLD patients. This work provides a resource to identify plausible genes regulating the measured lipid species and their association with metabolic traits

    The therapeutic role of NAD+ modulation in fatty liver disease

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    NAFLD encompasses a disease spectrum ranging from hepatic steatosis to nonalcoholic steatohepatitis (NASH), fibrosis, and finally cirrhosis, which predisposes to the development of hepatocellular carcinoma. With no approved pharmacological treatment, NAFLD is currently the most common etiology of chronic liver disease in western countries and its prevalence continues to growth concurrent to the rising obesity epidemic. SIRT1 may prove to be a critical target for the treatment of NAFLD since it has been demonstrated to induce transcription of genes involved in mitochondrial metabolism and antioxidant protection, while also inhibiting inflammatory and death signaling. In my PhD thesis projects, we aimed to explore the effect of SIRT1 activation through NAD+ modulation in the treatment of NAFLD. Protection against NAFLD by NAD+ repletion. In this study we evaluated the potential of Nicotinamide Riboside (NR) as a therapeutic agent against the development of NAFLD. First, we observed a positive correlation between gene sets for β-oxidation and genes involved in NAD+ biosynthesis in two distinct data sets of healthy human liver samples supporting the function of NAD+ as a coenzyme in key metabolic processes. Then we showed that NAD+ repletion using NR, an NAD+ booster, attenuated mitochondrial dysfunction and prevented and reversed fatty liver development in a several mouse models of NAFLD. Inhibiting PARPs protects against NAFLD development. We hypothesized that overactivation of PARP proteins, NAD+ consuming enzymes that are involved in various cell stress responses, promotes NAD+ depletion in NAFLD. To evaluate this hypothesis, we tested the therapeutic effect of a PARP inhibitor, olaparib in two mouse models of NAFLD. We found that PARP inhibition repletes NAD+ levels, protects against NAFLD and reduces ER-stress and fibrosis. The beneficial effect of PARP was dependent on Sirt1. In summary, our studies demonstrated a major role for NAD+ levels and PARP activity in the development of NAFLD. Repletion of NAD+, by NR administration, or PARP inhibition may therefore represent attractive strategies to counteract the development of NAFLD
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