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Journal Article
Multicenter Study
Randomized Controlled Trial
Research Support, Non-U.S. Gov't
Penetration and accumulation of moxifloxacin in uterine tissue.
OBJECTIVE: To determine whether moxifloxacin penetrates the uterine tissue and accumulates at levels sufficient to eradicate the major pathogens causing pelvic inflammatory disease (PID).
METHOD: In a prospective, multicenter, open-label, parallel-group study we determined the concentration of moxifloxacin in plasma and uterine tissue after a single, 400-mg intravenous dose of moxifloxacin. Study participants were randomized for time of tissue sampling, which was performed 1, 2, 4, 7, or 24 hours following the moxifloxacin infusion.
RESULTS: Of 43 participants, 40 were randomized to tissue sampling. Moxifloxacin accumulated in uterine tissue and concentrations were highest 1 hour after infusion in both plasma and tissue. Tissue to plasma ratios remained between 1.7 and 2.1 for 24 hours. Moxifloxacin was found to be safe and well tolerated.
CONCLUSION: Based on known minimum inhibitory concentration data, the uterine tissue concentrations of moxifloxacin achieved over 24 hours would be sufficient to eradicate the range of bacterial pathogens responsible for PID.
METHOD: In a prospective, multicenter, open-label, parallel-group study we determined the concentration of moxifloxacin in plasma and uterine tissue after a single, 400-mg intravenous dose of moxifloxacin. Study participants were randomized for time of tissue sampling, which was performed 1, 2, 4, 7, or 24 hours following the moxifloxacin infusion.
RESULTS: Of 43 participants, 40 were randomized to tissue sampling. Moxifloxacin accumulated in uterine tissue and concentrations were highest 1 hour after infusion in both plasma and tissue. Tissue to plasma ratios remained between 1.7 and 2.1 for 24 hours. Moxifloxacin was found to be safe and well tolerated.
CONCLUSION: Based on known minimum inhibitory concentration data, the uterine tissue concentrations of moxifloxacin achieved over 24 hours would be sufficient to eradicate the range of bacterial pathogens responsible for PID.
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