Disease relevance of AIDS-008709

• The early bactericidal activity of a low-clearance liposomal amikacin in pulmonary tuberculosis [1].
• Liposomal amikacin: improved treatment of Mycobacterium avium complex infection in the beige mouse model [2].
• The pharmacokinetics and toxicity of liposomal amikacin in a patient treated for advanced pulmonary multidrug-resistant tuberculosis are described [3].
• The influence of liposomal amikacin on Pseudomonas aeruginosa was studied [4].

High impact information on AIDS-008709

• The free amikacin concentration in plasma never exceeded 17.4 +/- 1 micrograms/ml and fell rapidly (half-life, 1.47 to 1.85 h) after the administration of each dose of liposomal amikacin [5].
• In view of the considerable activity of liposomal amikacin in experimental murine tuberculosis, this finding indicates that liberation of amikacin from the long-life liposomes occurs only in macrophages that are not usually present in the vicinity of the large extracellular clumps of bacilli in the cavity caseum [1].
• We compared the systemic bioavailability (F) of low-clearance liposomal amikacin in rats following intravenous (i.v.), intraperitoneal (i.p.), intramuscular (i.m.) and subcutaneous (s.c.) injection (20 mg/kg) and intratracheal (i.t.) instillation (10 mg/kg) [6].
• The plasma AUCs of liposomal amikacin exceeded the AUC of conventional i.v. amikacin by at least 25-fold for all routes [6].
• Amikacin AUCs in regional lymph nodes exceeded plasma AUCs by 4-fold after s.c. and i.m. injection of liposomal amikacin [6].

Chemical compound and disease context of AIDS-008709

• Most of the amikacin in low-clearance liposomal amikacin is excreted very slowly, offering the possibility of maintaining effective treatment of pulmonary tuberculosis with widely separated supervised doses [7].

Anatomical context of AIDS-008709

• The patient's sputum remained smear- and culture-positive during the treatment period with liposomal amikacin and for 9 months afterward [3].
• Although complete eradication of M. avium was never achieved following intravenous infection, mycobacterial CFUs decreased by 3 to 4 logs in the spleens and livers of mice treated for three weeks with twice-weekly intravenous injections of liposomal amikacin and continued to stay low in the liver, even in the absence of specific immunity [8].

References