Audiologic monitoring of multi-drug resistant tuberculosis patients on aminoglycoside treatment with long term follow-up

<p>Abstract</p> <p>Background</p> <p>Multi-drug resistant tuberculosis has emerged as a significant problem with the resurfacing of tuberculosis and thus the need to use the second line drugs with the resultant increased incidence of adverse effects. We discuss the effect of second line aminoglycoside anti-tubercular drugs on the hearing status of MDR-TB patients.</p> <p>Methods</p> <p>Sixty four patients were put on second line aminoglycoside anti-TB drugs. These were divided into three groups: group I, 34 patients using amikacin, group II, 26 patients using kanamycin and group III, 4 patients using capreomycin.</p> <p>Results</p> <p>Of these, 18.75% of the patients developed sensorineural hearing loss involving higher frequencies while 6.25% had involvement of speech frequencies also. All patients were seen again approximately one year after aminoglycoside discontinuation and all hearing losses were permanent with no threshold improvement.</p> <p>Conclusion</p> <p>Aminoglycosides used in MDR-TB patients may result in irreversible hearing loss involving higher frequencies and can become a hearing handicap as speech frequencies are also involved in some of the patients thus underlining the need for regular audiologic evaluation in patients of MDR-TB during the treatment.</p

Aluminum toxicity in childhood

Aluminum intoxication is an iatrogenic disease caused by the use of aluminum compounds for phosphate binding and by the contamination of parenteral fluids. Although organ aluminum deposition was noted as early as 1880 and toxicity was documented in the 1960s, the inability to accurately measure serum and tissue aluminum prevented delineation of its toxic effects until the 1970s. Aluminum toxicity has now been conclusively shown to cause encephalopathy, metabolic bone disease, and microcytic anemia.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/47831/1/467_2004_Article_BF00869743.pd

The influence of heparin on the bactericidal activity rate of gentamicin

Several authors have demonstrated the interaction between gentamicin and heparin and their formation of a high molecular weight complex. The dosages of this antibiotic are not exact, the diffusion in agar of the heparin gentamicin complex being slower than that of gentamicin alone. Therapeutically, heparin and gentamicin are sometimes simultaneously used (hemodialysis, intravascular coagulation syndrome) and a loss of antibacterial activity of gentamicin, is, in this case, possible. The object of this study is the influence of heparin on the bactericidal activity of gentamicin. These procedures, undertaken in a liquid medium, set aside the influence of the molecular weight of the complex, a determining factor of 'antagonism' shown by the methods of agar diffusion. In order to approach the in vivo situation, the bactericidal study was performed in serum of a patient treated with high gentamicin dosage. It was found that in the presence of heparin, the bactericidal action rate of the serum of the patients treated with gentamicin was slowed down.SCOPUS: ar.jinfo:eu-repo/semantics/publishe

Oxidative Injury To Erythrocytes, Cell Rigidity and Splenic Hemolysis in Hemodialyzed Patients Before and During Erythropoietin Treatment

The oxidative injury to erythrocytes, red blood cell (RBC) rigidity and splenic hemolysis was assayed in 17 chronically hemodialyzed patients before and during recombinant erythropoietin (EPO) treatment. When a stable hematocrit between 30 and 35% had been established for at least 4 months, a statistically significant increase in RBC volume, hemoglobin concentration, hematocrit, reticulocyte count, and several RBC enzymes (2,3-diphosphoglycerate, glucose 6-phosphate dehydrogenase, pyruvate kinase, hexokinase) was noted. This indicated significant RBC rejuvenation under the influence of EPO. However, no significant improvement in the RBC oxidative sensitivity, RBC deformability, splenic RBC volume, slow mixing splenic RBC volume, and the intrasplenic RBC transit time could be disclosed. These data confirm the existence of an extraerythrocytic factor in uremic plasma, which is partly responsible for a reduced RBC life span in hemodialysis patients despite EPO treatment

Early Effects of Gentamicin, Tobramycin, and Amikacin On the Human-kidney

AbstractEarly effects of gentamicin, tobramycin, and amikacin on the human kidney. The early alterations at the level of the proximal tubule of the human kidney caused by the three most currently used aminoglycosides, gentamicin, tobramycin, and amikacin, were studied. A prospective, randomized, and comparative approach using multidisciplinary methods was used. The patients received either no treatment or one of the three aminoglycosides at a therapeutic dose for 4 days preceeding nephrectomy for neoplasia partly involving one kidney. The three aminoglycosides studied induce an early lysosomal phospholipidosis. Gentamicin and tobramycin cannot be distinguished on the basis of drug tissue accumulation, lysosomal overloading, or effect on lysosomal phospholipase A1. Amikacin induces significantly lower lysosomal overloading and no loss of phospholipase A1 activity.Effets précoces de la gentamicine, de la tobramycine, et de l'amikacine sur le rein humain. Les altérations précoces au niveau du tubule proximal dans le rein humain, entraînées par les trois aminoglycosides les plus utilisés, la gentamicine, la tobramycine, et l'amikacine ont été étudiées. Une approche prospective, randomisée, et comparative, utilisant des méthodes multidisciplinaires a été employée. Les malades ont reçu soit aucun traitement, soit un des trois aminoglycosides à une dose thérapeutique pendant 4 jours avant une néphrectomie pour néoplasie touchant partiellement un rein. Les trois aminoglycosides étudiés induisent une phospholipidose lysosomiale précoce. La gentamicine et la tobramycine ne peuvent pas être distinguées sur la base de leur accumulation tissulaire, de la surcharge lysosomiale, ou de leur effet sur la phospholipase A1 lysosomiale. L'amikacine induit une surcharge lysosomiale significativement plus faible et n'entraîne pas de perte d'activité de la phospholipase A1