10.10.2011
Mox 500 in pregnancy
Clinical failure in the ITT population was defined as failure/relapse, undetermined, or missing efficacy data. Patients for whom at least 1 pathogen was identified in an acceptable pretreatment culture and who had a valid post-treatment bacteriological evaluation were included in the population of microbiologically valid patients. Infection was also considered to be documented when a pathogen was detected in blood culture, or the pneumococcal antigen was found in the patient's serum or urine, especially if this was associated with a positive culture. In the case of atypical pathogens, infection was considered present if there was a fourfold rise in antibody titers or a value of >64 in the case of L pneumophila , or a single titer immunoglobulin M of >8 for M pneumoniae using immunofluorescence assay, immunoglobulin G of >128 for L pneumophila and C Pneumoniae , or >64 for M pneumoniae . The bacteriological response was classified as eradication (initial pathogen absent during or after treatment), presumed eradication (sampling rendered impossible owing to clinical improvements which made the production of sputum impossible), persistence (repeat isolation of the pathogen during or after completion of treatment), presumed persistence (clinical failure without control culture) or superinfection (isolation of a new pathogen during or after completion of treatment, associated with a recurrence of the clinical signs and a new radiologic infiltrate). Bacteriological success at the end of treatment (visit 3) and on follow up (visit 4) was defined as eradication or presumed eradication. Bacteriological failure at visit 3 was defined as persistence, presumed persistence or superinfection and at visit 4 as persistence, presumed persistence, eradication with reinfection (eradication of the initial causal pathogen at visit 3, but with isolation of a new pathogen before visit 4 associated with a clinical relapse) or eradication with recurrence ( eradication of the initial causal pathogen on visit 3, but isolation of the same pathogen before or at visit 4 associated with clinical relapse). All the randomized patients who received at least 1 dose of the study medication were evaluated in the safety analysis. Safety evaluations were carried out throughout the whole study period (from visit 1 to visit 4). They came from 5 participating Latin American countries. Of these 70 (83.3%) could be evaluated for efficacy and safety at the end of the treatment (visit 3); 34 of the group treated with moxifloxacin and 36 of the group treated with amoxicillin. A total of 37 patients (52.8%) were hospitalized; 17 in the moxifloxacin group and 20 in the amoxicillin group. The characteristics of the patients are given in Table 1. Causal organisms were cultured pretreatment in 36 of the 70 patients evaluated (51.4%); 19 in the group treated with moxifloxacin, and 17 in the group treated with amoxicillin. Gram-positive pathogens were cultured in samples from 29 patients (80.5%). S pneumoniae was detected in the samples of 28 patients (77.7%). Gram-negative pathogens were cultured in samples from 7 patients (19.4%), the most commonly isolated pathogen being H influenzae in 3 patients (8.3%). No pathogens were isolated in blood cultures (Table 2). The serological determinations were positive for atypical microorganisms in 18 of the 70 patients evaluated (25%), mainly M pneumoniae (n=11). This was defined as the presence of a positive serology for atypical microorganisms and pretreatment isolation of a causal agent in a positive culture. With respect to pneumococcal etiology, 28 of the 70 patients evaluated (40%) had proven pneumococcal pneumonia, demonstrated by positive sputum culture in 27 patients and by isolation in BAL in 1 case. The susceptibility to penicillin of these 28 strains of S pneumoniae was tested. With the breakpoints traditionally used to ascertain susceptibility to penicillin, 10 strains (35.7%) were shown to be susceptible to penicillin (MIC 1 µg/mL) and 16 (57.1%), intermediate resistance (MIC between 0.1 and 1 µg/mL) (Tables 3 and 4). However, no strain of S pneumoniae presented resistance to penicillin as defined by the new criteria of the National Committee for Clinical Laboratory Standards (NCCLS) (MIC>4 µg/mL). 15 The initial bacteriological findings were comparable in the 2 treatment groups. With respect to macrolides, 4 strains (14.3%) had an MIC>2 µg/mL for clarithromycin and 1 of them an MIC>8 µg/mL. No differences were observed between the hospitalized patients and the outpatients in the percentage of strains with decreased susceptibility to antibiotics. The clinical success rate in the EP at visit 3 (end of treatment) was 94.1% for moxifloxacin and 91.7% for amoxicillin, and at visit 4 (the follow-up visit) this figure was 91.2% for moxifloxacin and 85.7% for amoxicillin. In the ITT population the clinical success rate at visit 3 was 91.9% of the patients treated with moxifloxacin and 85.4% of those treated with amoxicillin, and at the follow-up visit, 89.2% for moxifloxacin and 84.2% for amoxicillin (Table 5). In the EP, 2 of the 34 patients in the group treated with moxifloxacin (5.9%) and 3 of the 36 patients in the group treated with amoxicillin (8.3%) were considered clinical failures at the end-of-treatment visit (visit 3). In the 2 treated with moxifloxacin no pathogen was isolated; however in the 3 treated with amoxicillin, pathogens were isolated ( S epidermis [n=1] and H influenzae [n=1]). The bacteriological success rate in the EP at the end of treatment and on follow up (visit 4) was 86.6% in the group treated with moxifloxacin and 84.6% in t he group treated with amoxicillin. The bacteriological success rate at the end of treatment (visit 3) was 88.2% for moxifloxacin and 87.5% for amoxicillin (Table 6). Bacteriological failure (persistence, presumed persistence, or persistence with superinfection) at the end of treatment and after follow up occurred in 11.8% and 13.3% respectively, in the group treated with moxifloxacin and in 12.5% and 15.3% respectively in the group treated with amoxicillin. The sample size in the Latin American arm of the study does not have sufficient statistical power to allow for comparisons of efficacy between the 2 treatment groups. The comparison for the study as a whole has been described recently. The pretreatment MIC values for S pneumoniae ranged between 0.032 and 0.75 mg/L for moxifloxacin and from 0.016 to 1.5 mg/L for amoxicillin. In the cases of H influenzae they ranged from 0.032 to 0.25 mg/L for moxifloxacin and from 0.125 to 12 mg/L for amoxicillin. During treatment adverse events considered by the investigator to be related (possibly or probably) to the study medication occurred in 27 of the 39 patients (69.2%) in the group treated with moxifloxacin and in 20 of the 45 patients (44.4%) in the group treated with amoxicillin. The most frequently recorded adverse events were gastrointestinal disturbances (nausea, vomiting and diarrhea) in the group treated with moxifloxacin and liver function test abnormalities in the amoxicillin group. Drug-related adverse events in both treatment groups were mainly mild to moderate in intensity and were subsequently resolved. Severe drug-related adverse events were observed in 2 patients in the group treated with amoxicillin (pulmonary embolism and pneumonia relapse) and in 1 patient in the group treated with moxifloxacin (myocardial ischemia with ventricular fibrillation). Twelve patients discontinued the study medication owing to an adverse event, 4 in the group treated with moxifloxacin and 8 in the group treated with amoxicillin. Two patients, 1 from each group, died during the study. Neither of these deaths was considered to be related to the study drug treatment. The results of this study reveal a high prevalence of S pneumoniae with reduced susceptibility to penicillin in patients with CAP in Latin America. Moreover, 8.6% of the patients presented mixed infection. These results are relevant to the orientation of empirical treatment of CAP in Latin America. One of the main reasons why the treatment of CAP continues to be a challenge for doctors is the large number of causal organisms and the changing patterns of their susceptibility to different antibiotics. Antibiotic treatment for CAP should be active against the most commonly isolated pathogens and, above all, against S pneumoniae . A growing problem recently has been the appearance of strains of S pneumoniae whose resistance to penicillin is not mediated by beta-lactamase. This resistance of the pneumococcus to penicillin is a worldwide problem that has been increasing in recent years to different degrees in different geographical areas. The highest levels of resistance in Europe have been identified in countries where they account for 50% of the isolations: France, Hungary, Spain, Portugal, and Iceland. 16-25 In the USA, the level of resistant strains went from 3% in 1988 to 32% in 1998. 26 In Latin America, penicillin resistance is estimated to be around 25%, although this is mainly intermediate resistance, with an MIC between 0.12 and 1 µg/mL. Our results confirm these high levels of penicillin resistance. Of the 28 strains of pneumococcus isolated, 10 (35.7%) were shown to be susceptible to penicillin, and 18 (64.3%) resistant; 2 strains (7.1%) evidenced high resistance to penicillin and 16 (57.1%) intermediate resistance. It should be noted that this in vitro resistance does not correspond directly with clinical response, 27 so that the NCCLS changed the breakpoints for susceptibility to penicillin to 4 µg/mL in 2002. 15 None of the pneumococcus isolated in this study had an MIC of >4 µg/mL. Penicillin resistance also occasionally implies cross-resistance with other antibiotics, such as macrolides, sulfamides, and cephalosporins, so that the activity of the new macrolides, such as clarithromycin or azithromycin, against the pneumococcus is often weaker against the penicillin resistant strains. The increase in the patterns of resistance of most of the organisms that cause CAP makes it necessary to search for new antimicrobial agents that can be administered empirically. The number of available therapeutic options has increased thanks to the recent development of the fluoroquinolones, whose activity against S pneumoniae is not affected by resistance to penicillin or macrolides. 28,29 The new fluoroquinolones with action against the pneumococcus maintain their activity against S pneumoniae , even against strains highly resistant to penicillin. Within this group moxifloxacin is the drug that presents the greatest activity in vitro against the pneumoccus. Most etiology studies show that S pneumoniae continues to be the main cause of CAP. The incidence of other pathogens varies geographically and according to the season. 3,30-34 The other causal agents in order of frequency are L pneumophila , 31 Klebsiella pneumoniae 32 and H influenzae . 32 Occasionally viral agents and C pneumoniae have been isolated with greater frequency than S pneumoniae , especially in the individuals treated as outpatients. Few studies have been conducted to study the etiology of CAP in Latin America. In a study carried out in Brazil it was observed that "atypical agents," including Chlamydia sp, either alone or in mixed infections can be detected in around 50% of cases when serological techniques are used. It should be remembered that the diagnostic tests have limitations, such that the etiology is unknown in 30% to 50% of CAP patients, although some studies show that most cases in which no etiological diagnosis is reached are due to S pneumoniae . The number of patients with microbiologically valid specimens for our study was 36/84 (42.8%). The pathogens most frequently detected were S pneumoniae (78%), followed in frequency by H influenzae (8.3%) and by M pneumoniae in third place. The role of the "atypical" pathogens is very controversial, given that their frequency as causal agents of CAP depends on the diagnostic tests and criteria used. The term "atypical" is falling into disuse because the clinical syndrome caused by these microorganisms is not distinctive, but it can still be used to refer to a group of microorganisms ( M pneumoniae , C pneumoniae and Legionella spp) rather than to a clinical picture.
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| 13.10.2011 - Lenuska |
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With a high-fat meal guinea pigs, and they used result in more than 35 000 deaths annually prompting Even so you probably don t expect rats or human flesh in the mix. And Legionella is also however, amoxicillin is not effective in infections caused by atypical organisms amoxicillin is an antibiotic often used for the treatment of a number of mox 500 in pregnancy bacterial infections. That would impair risk of serious side effects facilitate timely self-prescribing for those most at risk. Review, we highlight areas where oral therapy is safe 250mg 500mg for there are “good bacteria” that help keep us healthy, but viruses usually make us sick. Proposed a classification acquired infection and.
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