Context: Advanced Glycation End-Products (AGEs) are signaling proteins associated to several vascular and neurological complications in diabetic and non-diabetic patients. AGEs proved to be a marker of negative outcome in both diabetes management and surgical procedures in these patients. The reported role of AGEs prompted the development of pharmacological inhibitors of their effects, giving rise to a number of both preclinical and clinical studies. Clinical trials with anti-AGEs drugs have been gradually developed and this review aimed to summarize most relevant reports. Evidence Acquisition: Evidence acquisition process was performed using PubMed and ClinicalTrials.gov with manually checked articles. Results: Pharmacological approaches in humans include aminoguanidine, pyridoxamine, benfotiamine, angiotensin converting enzyme inhibitors, angiotensin receptor blockers, statin, ALT-711 (alagebrium) and thiazolidinediones. The most recent promising antiAGEs agents are statins, alagebrium and thiazolidinediones. The role of AGEs in disease and new compounds interfering with their effects are currently under investigation in preclinical settings and these newer anti-AGEs drugs would undergo clinical evaluation in the next years. Compounds with anti-AGEs activity but still not available for clinical scenarios are ALT-946, OPB-9195, tenilsetam, LR-90, TM2002, sRAGE and PEDF. Conclusions: Despite most studies confirm the efficacy of these pharmacological approaches, other reports produced conflicting evidences; in almost any case, these drugs were well tolerated. At present, AGEs measurement has still not taken a precise role in clinical practice, but its relevance as a marker of disease has been widely shown; therefore, it is important for clinicians to understand the value of new cardiovascular risk factors. Findings from the current and future clinical trials may help in determining the role of AGEs and the benefits of anti-AGEs treatment in cardiovascular disease.
Introduction:
Lactic acidosis is a rare but life-threatening complication associated with prolonged linezolid therapy. No specific treatment is suggested, except for antibiotic therapy interruption.
Case Report:
A 70-years-old woman faced severe linezolid intoxication after antibiotics therapy initiation for infection of a surgical sternal wound. The patient suffered from a severe increment of blood lactate and thrombocytopenia. The patient underwent double ICU admission, and, thanks to dialytic treatment, linezolid and lactate serum levels came back to normality.
Conclusion:
More studies should be done to evaluate the human tissue storage sites of linezolid and the influence of various factors on its clearance and plasma concentrations in critically ill patients.
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