[Nitroxoline - an option for the antibiotic treatment of urinary tract infections]. / Nitroxolin ­ eine Option zur antibiotischen Therapie von Harnwegsinfektionen.

BACKGROUND: Resistance of uropathogenic bacteria against the common antibiotics is considerable-especially in the elderly. OBJECTIVES: In Germany nitroxoline is licensed for the treatment of acute urinary tract infections and for prophylaxis of recurrent infections. What is the actual resistance pattern of uropathogenic bacteria? MATERIALS AND METHODS: The in vitro susceptibility of 477 uropathogenic bacteria from patients in 2015 was determined by means of the agar diffusion method. RESULTS: Obviously, this agent is still active against the vast majority of uropathogenic bacteria and in particular against strains of Escherichia coli (E. coli). Pseudomonas aeruginosa and enterococci are not really within the spectrum of nitroxoline. One has to keep in mind, however, that even among E. coli and other enterobacteriaceae there are single resistant isolates. This applies in particular to problem strains resistant to many other antibiotics. DISCUSSION: Nitroxoline is a reasonable alternative and a promising option for calculated treatment of urinary tract infections-especially of the elderly, although this drug is not recommended in the current guideline. Laboratory testing of clinical isolates should be requested-at least when treatment fails.

Reduction of CK and CK-MB indexes of infarct size by intravenous nitroglycerin.

The effect of i.v. nitroglycerin administration on indexes of infarct size was examined in 31 patients with acute myocardial infarction. Serial creatine kinase (CK) and CK-MB isoenzyme determinations were used to calculate infarct size. Twenty-nine patients served as controls. Two subgroups of the study group were formed to evaluate differences between early and late intervention. In the first group (n = 22), continuous infusion of nitroglycerin over 48 hours was initiated within 8 hours (mean 4.5 hours) after the onset of symptoms. Peak CK activity for the nitroglycerin-treated patients (n = 9) in this subgroup was 544 U/1 vs 871 U/1 for the controls (n = 13) (p less than 0.05). The rate of CK release was reduced from 79 to 33 U/1.hr (58%), as was total CK and CK-MB release (p less than 0.02). Calculated infarct size was 69 gEq in the controls and 48 gEq in patients receiving nitroglycerin (CK-MB: 69 vs 43 gEq, p less than 0.05). In the late intervention subgroup, nitroglycerin therapy was begun more than 8 hours (mean 12.8 hours) after the onset of symptoms. Here, too, use of the agent was associated with lower peak CK and CK-MB levels as well as a reduction in calculated infarct size (p less than 0.05). Hemodynamic measurements, recorded every 4 hours, showed that nitroglycerin also reduced left ventricular filling pressure significantly and cardiac output increased. Blood pressure fell slightly, and systemic vascular resistance declined. The results indicate that i.v. nitroglycerin reduces CK and CK-MB release and thus calculated infarct size in both early and late intervention.

[Reduction of CK and CK-MB enzyme levels as indicators of infarct size by intravenous nitroglycerin (author's transl)]. / XI. Reduktion der CK- und CK-MB-Enzymaktivität und der Infarktgrösse durch intravenöses Nitroglyzerin.

Intravenous nitroglycerin has beneficial effects on hemodynamics and on myocardial ischemia. The aim of the present study was to investigate whether it also reduces final infarct size. In 60 patients with myocardial infarction serial blood samples were tested for creatine kinase (CK) and its isoenzyme CK-MB activity for infarct size calculations. Hemodynamic parameters were measured every 4 hours. Patients were randomized to a control (n = 29) and a nitroglycerin group (n = 31). In the early intervention group continuous perfusion of nitroglycerin for 48 hours was started < 8 hours (mean 4.5 hours) after onset of symptoms, and in the late intervention group > 8 hours (mean 12.8 hours) after onset of symptoms. In early intervention (n = 22) peak CK activity was 871 U/l in control patients and 544 U/l (p < 0.05) in the nitroglycerin group. The rate of CK release was reduced from 79 to 33 U/l x h, i.e. by a total of 58%, as was total CK and CK-MB release (p < 0.02). Calculated CK infarct size was 69 g equiv. in controls and 48 g equiv. in the nitroglycerin group. (CK-MB: 68 versus 43 g equiv., p < 0.05). In late intervention (n = 28) the differences were less pronounced. Nitroglycerin reduced left ventricular filling pressure significantly and increased cardiac output. Blood pressure changed insignificantly and peripheral vascular resistance decreased. In conclusion, nitroglycerin reduces CK and CK-MB release and hence calculated infarct size, particularly when treatment is begun within the first 8 hours after onset of symptoms.