Spread of extended-spectrum beta-lactamase-producing Klebsiella pneumoniae: are beta-lactamase inhibitors of therapeutic value?

Because of recurrent colonization by Klebsiella pneumoniae strains producing type SHV-4 extended-spectrum beta-lactamases (ESBLs), a case-control study was conducted in an intensive care unit to investigate the risk of acquisition, with special reference to antibiotic therapy and resuscitation procedures. Fifty-one patients colonized or infected by ESBL-producing K. pneumoniae (cases) were matched with 51 noncolonized patients (controls). Duration of intubation was significantly longer for cases than for controls, while duration of beta-lactamase inhibitor therapy was significantly shorter. By means of multivariate analysis, intubation was the only risk factor identified (odds ratio [OR] = 1.19), while beta-lactamase inhibitor therapy was shown to be a protective factor (OR = 0.849). During outbreaks of SHV-4 type ESBL-producing K. pneumoniae in intensive care units, preferential use of beta-lactamase inhibitors may help control the emergence and spread of these pathogens even if essential hand washing and isolation procedures are adhered to.

Plasma iron status and lipid peroxidation following thrombolytic therapy for acute myocardial infarction.

Free radical species have been implicated as important agents involved in myocardial ischemic and reperfusion injuries. Superoxide is capable of mobilizing iron from ferritin and the released iron can cause hydroxyl formation from H2O2. The aim of this study was to evaluate the time-dependent increase in lipid peroxidation assessed by plasma thiobarbituric acid reactive substances (TBARS) and the relationship between lipid-peroxidation and the iron status. Peripheral venous blood samples were obtained from 17 men with acute myocardial infarction (AMI) before thrombolytic treatment (T0) and 1, 2, 3, 4, 8, 12, 16, 20, 24 and 48 hours after commencing fibrinolytic treatment. The concentration of TBARS, the parameters of iron metabolism, serum myoglobin, creatine kinase, and creatine kinase-MB were measured. Early reperfusion was judged by regression of sinus tachycardia (ST) elevation and reduction of chest pain. Recanalization of coronary artery was evaluated by a late coronary angiography 24-96 hours after thrombolysis. After thrombolytic therapy, the TBARS level was raised from 2.98 +/- 0.80 (T0) to 4.57 +/- 1.24 (peak), and decreased to 2.96 +/- 0.40 nmol/mL plasma at T48 (T0 vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.7 +/- 7.5 hours. The iron increased significantly from 0.67 +/- 0.34 (T0) to 1.15 +/- 0.52 mg/L (peak), and returned to the pre-reperfusion to levels: 0.53 +/- 0.28 UI/L at T48 (TO vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.4 +/- 7.3 hours. In return, no correlation was found between the increase of plasma creatine-kinase activity, myoglobin and iron or between the biochemical markers and time of fibrinolytic therapy. The results confirmed the importance of the temporal relationship between lipid peroxidation and iron status after thrombolytic therapy. Our results are in agreement with the concept that antioxidant agents used in association with thrombolytic therapy might be useful.