The difference in efficacy between the two treatment regimens was not significant. However, the cure rates in this study are comparable to combination treatments with omeprazole. Treatment failures were due to acquired clarithromycin resistance.
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The use of antiretroviral agents and drugs for the treatment and prophylaxis of opportunistic infections has lengthened the survival of persons with AIDS. In the era of multidrug therapy, drug interactions are important considerations in designing effective and tolerable regimens. Clarithromycin has had a significant impact on the treatment of disseminated Mycobacterium avium complex infection, and zidovudine is the best-studied and one of the most widely used antiretroviral agents in this population. We conducted a study to determine the maximally tolerated dose of clarithromycin and the pharmacokinetics of clarithromycin and zidovudine individually and in combination. Mixing studies were conducted to simulate potential interaction in the gastric environment. The simultaneous administration of zidovudine and clarithromycin had little impact on the pharmacokinetics of clarithromycin or of its major metabolite. However, coadministration of zidovudine and clarithromycin at three doses (500 mg orally [p.o.] twice daily [b.i.d.], 1,000 mg p.o. b.i.d., and 2,000 mg p.o. b.i.d.) reduced the maximum concentration of zidovudine by 41% (P < 0.005) and the area under the concentration-time curve from 0 to 4 h for zidovudine by 25% (P < 0.05) and increased the time to maximum concentration of zidovudine by 84% (P < 0.05), compared with zidovudine administered alone. Mixing studies did not detect the formation of insoluble complexes due to chelation, suggesting that the decrease in zidovudine concentrations results from some other mechanism. Simultaneous administration of zidovudine and clarithromycin appears to decrease the levels of zidovudine in serum, and it may be advisable that these drugs not be given at the same time. Drug interactions should be carefully evaluated in persons with advanced human immunodeficiency virus infection who are receiving multiple pharmacologic agents.
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It is possible that UBT values also tend to be higher in cases of CAM resistance.
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To investigate antimicrobial resistance among pathogens responsible for adult community-acquired respiratory tract infections from 11 hospitals of China.
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Helicobacter pylori-positive patients complaining of dyspeptic symptoms referred for gastroscopy.
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Earlier semi-synthetic studies of erythromycin A culminated in the discovery of two successful second generation macrolide antibiotics, azithromycin and clarithromycin, for the treatment of community-acquired bacterial infections. More recent structural modifications of erythromycin A have resulted in the discovery of novel ketolide antibiotics and new motilide prokinetic agents. This review is an account of the semi-synthetic developments from erythromycin A by chemical transformations.
The eradication rate of H. pylori was 92% (CI, 83-100%) in the gastric ulcer group and 94% (CI, 86-100%) in the duodenal ulcer group at 5 months, as determined by per-protocol analysis. Resistance to clarithromycin was present in 1 of 71 (1%) patients before treatment and in 2 of 5 (40%) patients after treatment. No resistance to amoxicillin and lansoprazole was found in patients before or after treatment. The resistance to clarithromycin changed during the observation period.
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In the eradicated group (n = 138), blood leukocytes, neutrophils and monocytes decreased significantly after eradication, but there was no significant change in eosinophils, basophils, lymphocytes or platelets. In the non-eradicated group (n = 26), there was no significant change in any studied parameter. With regard to smoking status, although leukocytes and neutrophils did not decrease after eradication in the smoking group, they significantly decreased after eradication in the nonsmoking group.
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The objective of this study was to assess the outcome of antimicrobial susceptibility-guided therapies in Helicobacter pylori-infected individuals who had undergone unsuccessful prior eradication treatments.
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To develop a new method for the determination of clarithromycin.
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The aim of the study was to evaluate the prevalence of resistance to amoxicillin, metronidazole, and clarithromycin before treatment of Helicobacter pylori infection in children and to assess the evolution of resistance with time. The study was carried out between 1994 and 1999 with 150 H. pylori-positive children through gastric culture (antimicrobial susceptibility) and histology. All cultured H. pylori strains were sensitive to amoxicillin, 64 (43%) were resistant to metronidazole, 32 (21%) were resistant to clarithromycin, and 14 (9%) were resistant to both metronidazole and clarithromycin. The overall prevalence of resistance to metronidazole and clarithromycin did not change significantly with time. The study highlights the generalized high-level and stable metronidazole and clarithromycin resistance of H. pylori strains from children.
We performed invasive tests for H. pylori in naive patients who underwent gastroduodenoscopy in the Endoscopy Unit, Ankara University, Faculty of Medicine, and patients who were diagnosed as H. pylori-positive by these tests were rechecked by the same invasive tests one month after the completion of eradication treatment. The group receiving sequential therapy was given pantoprazole + amoxicillin during the first seven days and pantoprazole + metronidazole + tetracycline during the second seven days. These patients were compared with the H. pylori-positive naive control group patients, who were given ranitidine bismuth citrate + clarithromycin + amoxicillin. The patients in whom eradication was achieved in the 4th week with sequential therapy were reevaluated one year later regarding the success of eradication with the H. pylori stool antigen test.
The survival rate in patients with AIDS who have CD4+ cell counts < 75 cells/microliter is increasing because of improved preventive and treatment strategies for opportunistic infections and also because of the efficacy of antiretroviral drug treatment. These patients are at high risk of developing disseminated Mycobacterium avium-intracellulare (MAC) disease, which decreases both quality of life and life expectancy. Measures aimed at preventing MAC contamination are largely ineffective in decreasing the incidence of disseminated MAC disease in patients with AIDS, because of the large natural reservoir of MAC. Chemoprophylaxis is superior to early bacteriological diagnosis as a preventive strategy, and it is preferable to wait for the appearance of symptoms of disseminated MAC disease before a curative treatment is initiated. Well-conducted studies of clarithromycin or rifabutin monotherapy as chemoprophylaxis have demonstrated a decrease in the incidence of disseminated MAC disease, as well as an increase in quality of life and survival. Clarithromycin, azithromycin and rifabutin have all been shown to be effective as prophylaxis against disseminated MAC disease. Although some combinations of drugs have been shown to be more effective than monotherapy in preventing disseminated MAC disease, these regimens are more costly and have less favourable tolerability profiles than single-agent treatment. In conclusion, chemoprophylaxis is the most effective preventive strategy against disseminated MAC disease and has been shown to improve quality of life and to decrease the risk of death associated with this disease in AIDS patients.
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These results seem to confirm the in vitro anti-H. pylori effect of L. acidophilus, suggesting that the inactivated L. acidophilus could be effective in increasing eradication rates of a standard anti-H. pylori therapy.
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Prescription data on all incident users of several antibacterial and antiarrhythmic drugs over the period July 1997 through December 1999 were retrieved from the Drug Prescription Database (DPD) of the Italian Province of Varese. The association between the use of antibacterial and antiarrhythmic drugs was investigated by applying prescription sequence symmetry, cohort and nested case-control designs.
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Following their use for a few years, the place of new macrolides can be assessed.
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Recently, the case history of a 44-year-old woman who experienced acute hepatitis subsequent to therapy for chronic sinusitis was reviewed. The patient sequentially was administered clarithromycin, levofloxacin, amoxicillin-clavulanate, and gatifloxacin. Her adverse events were attributed definitively to gatifloxacin, a surprising conclusion because many other possible causes of hepatitis existed in this case. Not ruled out as potential causes of the clinical and laboratory adverse events were hepatitis other than hepatitis A or B. Other antimicrobials administered were dismissed. In particular, extended treatment with amoxicillin-clavulanate has been clearly linked to hepatotoxic effects that may occur long after therapy begins. Thus, while we agree that physicians must be aware of the potential for antimicrobial hepatotoxicity, we believe that this case study is not a solidly documented case of hepatitis attributable to gatifloxacin and overlooks other possible causes of acute hepatitis of which prescribers should be aware.
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A total of 348 naïve H. pylori-infected patients from six hospitals in Korea were randomly assigned to concomitant therapy and standard triple therapy groups. The concomitant regimen consisted of 30 mg of lansoprazole, 1g of amoxicillin, 500 mg of clarithromycin, and 500 mg of metronidazole, twice daily for 10 days. The standard triple regimen consisted of 30 mg of lansoprazole, 1g of amoxicillin, and 500 mg of clarithromycin, twice daily for 10 days.
We studied the clinical characteristics of nine patients with pulmonary Mycobacterium avium complex disease occurring in association with corticosteroid drugs collected from our associated hospitals during the past 6 years. The average age of the nine patients was 62.2 years and the male/female ratio was 3 : 6. Regarding underlying disease, respiratory diseases existed in four of the patients and nonrespiratory diseases in the other five patients. The duration of corticosteroid treatment ranged from 5 months to 5 years, and the total dose of corticosteroid drugs ranged from 1.78 to 43.20 g. Pulmonary Mycobacterium avium complex disease was detected by clinical symptoms during corticosteroid treatment in six patients, and purified protein derivative was positive in three of eight patients tested. Radiological findings showed an infiltration shadow without cavity and bronchiectasis in the lower lung field. Microbiological examination was smear-positive in three patients, and the isolated mycobacterium was Mycobacterium intracellulare in five patients and Mycobacterium avium in four. Tolerance was shown to all antituberculous drugs, except for clarithromycin, in all patients. Although treatment including clarithromycin was performed for seven patients, the sputum conversion rate was 33% and an improved clinical effect was noted in only one patient. No change occurred in four and worsening occurred in four. Attention should be paid to the clinical symptoms and radiological findings of patients who have received corticosteroid drugs over a long period of time, because pulmonary Mycobacterium avium complex is characterized by atypical radiographic findings with no relationship to the total dose or duration of the administered corticosteroid drugs.
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Cat-scratch disease is an infection caused by Bartonella henselae, a fastidious gram-negative bacillus acquired from exposure to an infected kitten or cat. The most common manifestation of human disease is lymphadenitis. Atypical forms of infection include Parinaud oculoglandular syndrome, stellate neuroretinitis, persistent fever without localizing signs, hepatosplenic infection, encephalopathy, osteomyelitis, and endocarditis. Immunocompromised individuals with B. hensalae infection may develop bacillary angiomatosis, bacillary peliosis, and relapsing bacteremia with fever syndrome. The bacillus is susceptible to several antibacterial agents in vitro, including penicillins, cephalosporins, aminoglycosides, tetracyclines, macrolides, quinolones, trimethoprim and sulfamethoxazole, and rifampin. Greatest clinical efficacy has been observed following treatment with rifampin, ciprofloxacin, gentamicin, trimethoprim and sulfamethoxazole, clarithromycin, and azithromycin. In one placebo-controlled study, azithromycin therapy was associated with more rapid diminution in size of infected lymph nodes. The majority of cases of cat-scratch disease occurring in normal hosts do not require anti-infective therapy for resolution of infection.
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To report a possible drug interaction between clarithromycin and warfarin in a patient with chronic atrial fibrillation.
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Antimicrobial resistance is a growing problem among upper respiratory tract pathogens. Resistance to beta-lactam drugs among Streptococcus pneumoniae, Haemophilus influenzae, and Streptococcus pyogenes is increasing. As safe and well-tolerated antibiotics, macrolides play a key role in the treatment of community-acquired upper respiratory tract infections (RTIs). Their broad spectrum of activity against gram-positive cocci, such as S. pneumoniae and S. pyogenes, atypical pathogens, H. influenzae (azithromycin and clarithromycin), and Moraxella catarrhalis, has led to the widespread use of macrolides for empiric treatment of upper RTIs and as alternatives for patients allergic to beta-lactams. Macrolide resistance is increasing among pneumococci and recently among S. pyogenes, and is associated with increasing use of the newer macrolides, such as azithromycin. Ribosomal target modification mediated by erm(A) and erm(B) genes and active efflux due to mef(A) and mef(E) are the principal mechanisms of resistance in both S. pneumoniae and S. pyogenes. Recently, ribosomal protein and RNA mutations have been found to be responsible for acquired resistance to macrolides in S. pneumoniae, S. pyogenes, and H. influenzae. Although macrolides are only weakly active against macrolide-resistant streptococci species, producing an efflux pump (mef), and are inactive against pathogens with ribosomal target modification (erm), treatment failures are uncommon. Therefore, macrolide therapy, for now, remains a good alternative for treatment of upper RTIs; however, continuous monitoring of the local resistance patterns is essential.
Burkholderia pseudomallei, the causative agent of melioidosis, is intrinsically resistant to a wide range of antimicrobial agents including beta-lactams, aminoglycosides, macrolides, and polymyxins. We used Tn5-OT182 to mutagenize B. pseudomallei to identify the genes involved in aminoglycoside resistance. We report here on the identification of AmrAB-OprA, a multidrug efflux system in B. pseudomallei which is specific for both aminoglycoside and macrolide antibiotics. We isolated two transposon mutants, RM101 and RM102, which had 8- to 128-fold increases in their susceptibilities to the aminoglycosides streptomycin, gentamicin, neomycin, tobramycin, kanamycin, and spectinomycin. In addition, both mutants, in contrast to the parent, were susceptible to the macrolides erythromycin and clarithromycin but not to the lincosamide clindamycin. Sequencing of the DNA flanking the transposon insertions revealed a putative operon consisting of a resistance, nodulation, division-type transporter, a membrane fusion protein, an outer membrane protein, and a divergently transcribed regulatorprotein. Consistent with the presence of an efflux system, both mutants accumulated [3H] dihydro streptomycin, whereas the parent strain did not. We constructed an amr deletion strain, B. pseudomallei DD503, which was hypersusceptible to aminoglycosides and macrolides and which was used successfully in allelic exchange experiments. These results suggest that an efflux system is a major contributor to the inherent high-level aminoglycoside and macrolide resistance found in B. pseudomallei.
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Triple therapies were safe and effective for H. pylori eradication in Japanese and Swedish peptic ulcer patients. Dual therapy was significantly less effective in the Japanese patients, half of whom had a history of GU and more abnormal histology than in the Swedish patients, all of whom had DU.
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Three clarithromycin-resistant H. pylori isolated from three different patients after treatment with clarithromycin were analyzed for point mutations by cycle sequencing of a 163-bp amplified region surrounding residue 2143 within the conserved loop of the 23S rRNA gene.