Magnesium supplements

[mom2lillian]

dramamama woudl be a good one to ask about this she has done alot of research. I think I have one of her other articles about mg and aminoglycoside antibiotics robbing you of your mg and a correlation to hearing loss. I will see if I still have it.

I started taking a mg supplement when on IV's and will at least finish out htis bottle.

 

[mom2lillian]

dramamama woudl be a good one to ask about this she has done alot of research. I think I have one of her other articles about mg and aminoglycoside antibiotics robbing you of your mg and a correlation to hearing loss. I will see if I still have it.

I started taking a mg supplement when on IV's and will at least finish out htis bottle.

 

[mom2lillian]

dramamama woudl be a good one to ask about this she has done alot of research. I think I have one of her other articles about mg and aminoglycoside antibiotics robbing you of your mg and a correlation to hearing loss. I will see if I still have it.

I started taking a mg supplement when on IV's and will at least finish out htis bottle.

 

[mom2lillian]

dramamama woudl be a good one to ask about this she has done alot of research. I think I have one of her other articles about mg and aminoglycoside antibiotics robbing you of your mg and a correlation to hearing loss. I will see if I still have it.

I started taking a mg supplement when on IV's and will at least finish out htis bottle.

 

[mom2lillian]

Proteomic analysis of Pseudomonas aeruginosa grown under magnesium limitation.

Guina T,
Wu M,
Miller SI,
Purvine SO,
Yi EC,
Eng J,
Goodlett DR,
Aebersold R,
Ernst RK,
Lee KA.
Department of Pediatrics, Division of Infectious Diseases, University of Washington, Seattle, Washington 98195, USA. tguina@u.washington.edu
In this study, large-scale qualitative and quantitative proteomic technology was applied to the analysis of the opportunistic bacterial pathogen Pseudomonas aeruginosa grown under magnesium limitation, an environmental condition previously shown to induce expression of various virulence factors. For quantitative analysis, whole cell and membrane proteins were differentially labeled with isotope-coded affinity tag (ICAT) reagents and ICAT reagent-labeled peptides were separated by two-dimensional chromatography prior to analysis by electrospray ionization-tandem mass spectrometry (ESI-MS/MS) in an ion trap mass spectrometer (ITMS). To increase the number of protein identifications, gas-phase fractionation (GPF) in the m/z dimension was employed for analysis of ICAT peptides derived from whole cell extracts. The experiments confirmed expression of 1331 P. aeruginosa proteins of which 145 were differentially expressed upon limitation of magnesium. A number of conserved Gram-negative magnesium stress-response proteins involved in bacterial virulence were among the most abundant proteins induced in low magnesium. Comparative ICAT analysis of membrane versus whole cell protein indicated that growth of P. aeruginosa in low magnesium resulted in altered subcellular compartmentalization of large enzyme complexes such as ribosomes. This result was confirmed by 2-D PAGE analysis of P. aeruginosa outer membrane proteins. This study shows that large-scale quantitative proteomic technology can be successfully applied to the analysis of whole bacteria and to the discovery of functionally relevant biologic phenotypes.
PMID: 12837596 [PubMed - indexed for MEDLINE]

My read on it, its possible that PA becomes more virulent in a low magnesium environment. This did not address whether higher magnesium environments were better nor did it address what level of magnesium resulted in increased virulence.

 

[mom2lillian]

Proteomic analysis of Pseudomonas aeruginosa grown under magnesium limitation.

Guina T,
Wu M,
Miller SI,
Purvine SO,
Yi EC,
Eng J,
Goodlett DR,
Aebersold R,
Ernst RK,
Lee KA.
Department of Pediatrics, Division of Infectious Diseases, University of Washington, Seattle, Washington 98195, USA. tguina@u.washington.edu
In this study, large-scale qualitative and quantitative proteomic technology was applied to the analysis of the opportunistic bacterial pathogen Pseudomonas aeruginosa grown under magnesium limitation, an environmental condition previously shown to induce expression of various virulence factors. For quantitative analysis, whole cell and membrane proteins were differentially labeled with isotope-coded affinity tag (ICAT) reagents and ICAT reagent-labeled peptides were separated by two-dimensional chromatography prior to analysis by electrospray ionization-tandem mass spectrometry (ESI-MS/MS) in an ion trap mass spectrometer (ITMS). To increase the number of protein identifications, gas-phase fractionation (GPF) in the m/z dimension was employed for analysis of ICAT peptides derived from whole cell extracts. The experiments confirmed expression of 1331 P. aeruginosa proteins of which 145 were differentially expressed upon limitation of magnesium. A number of conserved Gram-negative magnesium stress-response proteins involved in bacterial virulence were among the most abundant proteins induced in low magnesium. Comparative ICAT analysis of membrane versus whole cell protein indicated that growth of P. aeruginosa in low magnesium resulted in altered subcellular compartmentalization of large enzyme complexes such as ribosomes. This result was confirmed by 2-D PAGE analysis of P. aeruginosa outer membrane proteins. This study shows that large-scale quantitative proteomic technology can be successfully applied to the analysis of whole bacteria and to the discovery of functionally relevant biologic phenotypes.
PMID: 12837596 [PubMed - indexed for MEDLINE]

My read on it, its possible that PA becomes more virulent in a low magnesium environment. This did not address whether higher magnesium environments were better nor did it address what level of magnesium resulted in increased virulence.

 

[mom2lillian]

Proteomic analysis of Pseudomonas aeruginosa grown under magnesium limitation.

Guina T,
Wu M,
Miller SI,
Purvine SO,
Yi EC,
Eng J,
Goodlett DR,
Aebersold R,
Ernst RK,
Lee KA.
Department of Pediatrics, Division of Infectious Diseases, University of Washington, Seattle, Washington 98195, USA. tguina@u.washington.edu
In this study, large-scale qualitative and quantitative proteomic technology was applied to the analysis of the opportunistic bacterial pathogen Pseudomonas aeruginosa grown under magnesium limitation, an environmental condition previously shown to induce expression of various virulence factors. For quantitative analysis, whole cell and membrane proteins were differentially labeled with isotope-coded affinity tag (ICAT) reagents and ICAT reagent-labeled peptides were separated by two-dimensional chromatography prior to analysis by electrospray ionization-tandem mass spectrometry (ESI-MS/MS) in an ion trap mass spectrometer (ITMS). To increase the number of protein identifications, gas-phase fractionation (GPF) in the m/z dimension was employed for analysis of ICAT peptides derived from whole cell extracts. The experiments confirmed expression of 1331 P. aeruginosa proteins of which 145 were differentially expressed upon limitation of magnesium. A number of conserved Gram-negative magnesium stress-response proteins involved in bacterial virulence were among the most abundant proteins induced in low magnesium. Comparative ICAT analysis of membrane versus whole cell protein indicated that growth of P. aeruginosa in low magnesium resulted in altered subcellular compartmentalization of large enzyme complexes such as ribosomes. This result was confirmed by 2-D PAGE analysis of P. aeruginosa outer membrane proteins. This study shows that large-scale quantitative proteomic technology can be successfully applied to the analysis of whole bacteria and to the discovery of functionally relevant biologic phenotypes.
PMID: 12837596 [PubMed - indexed for MEDLINE]

My read on it, its possible that PA becomes more virulent in a low magnesium environment. This did not address whether higher magnesium environments were better nor did it address what level of magnesium resulted in increased virulence.

 

[mom2lillian]

Proteomic analysis of Pseudomonas aeruginosa grown under magnesium limitation.

Guina T,
Wu M,
Miller SI,
Purvine SO,
Yi EC,
Eng J,
Goodlett DR,
Aebersold R,
Ernst RK,
Lee KA.
Department of Pediatrics, Division of Infectious Diseases, University of Washington, Seattle, Washington 98195, USA. tguina@u.washington.edu
In this study, large-scale qualitative and quantitative proteomic technology was applied to the analysis of the opportunistic bacterial pathogen Pseudomonas aeruginosa grown under magnesium limitation, an environmental condition previously shown to induce expression of various virulence factors. For quantitative analysis, whole cell and membrane proteins were differentially labeled with isotope-coded affinity tag (ICAT) reagents and ICAT reagent-labeled peptides were separated by two-dimensional chromatography prior to analysis by electrospray ionization-tandem mass spectrometry (ESI-MS/MS) in an ion trap mass spectrometer (ITMS). To increase the number of protein identifications, gas-phase fractionation (GPF) in the m/z dimension was employed for analysis of ICAT peptides derived from whole cell extracts. The experiments confirmed expression of 1331 P. aeruginosa proteins of which 145 were differentially expressed upon limitation of magnesium. A number of conserved Gram-negative magnesium stress-response proteins involved in bacterial virulence were among the most abundant proteins induced in low magnesium. Comparative ICAT analysis of membrane versus whole cell protein indicated that growth of P. aeruginosa in low magnesium resulted in altered subcellular compartmentalization of large enzyme complexes such as ribosomes. This result was confirmed by 2-D PAGE analysis of P. aeruginosa outer membrane proteins. This study shows that large-scale quantitative proteomic technology can be successfully applied to the analysis of whole bacteria and to the discovery of functionally relevant biologic phenotypes.
PMID: 12837596 [PubMed - indexed for MEDLINE]

My read on it, its possible that PA becomes more virulent in a low magnesium environment. This did not address whether higher magnesium environments were better nor did it address what level of magnesium resulted in increased virulence.

 

[mom2lillian]

Proteomic analysis of Pseudomonas aeruginosa grown under magnesium limitation.

Guina T,
Wu M,
Miller SI,
Purvine SO,
Yi EC,
Eng J,
Goodlett DR,
Aebersold R,
Ernst RK,
Lee KA.
Department of Pediatrics, Division of Infectious Diseases, University of Washington, Seattle, Washington 98195, USA. tguina@u.washington.edu
In this study, large-scale qualitative and quantitative proteomic technology was applied to the analysis of the opportunistic bacterial pathogen Pseudomonas aeruginosa grown under magnesium limitation, an environmental condition previously shown to induce expression of various virulence factors. For quantitative analysis, whole cell and membrane proteins were differentially labeled with isotope-coded affinity tag (ICAT) reagents and ICAT reagent-labeled peptides were separated by two-dimensional chromatography prior to analysis by electrospray ionization-tandem mass spectrometry (ESI-MS/MS) in an ion trap mass spectrometer (ITMS). To increase the number of protein identifications, gas-phase fractionation (GPF) in the m/z dimension was employed for analysis of ICAT peptides derived from whole cell extracts. The experiments confirmed expression of 1331 P. aeruginosa proteins of which 145 were differentially expressed upon limitation of magnesium. A number of conserved Gram-negative magnesium stress-response proteins involved in bacterial virulence were among the most abundant proteins induced in low magnesium. Comparative ICAT analysis of membrane versus whole cell protein indicated that growth of P. aeruginosa in low magnesium resulted in altered subcellular compartmentalization of large enzyme complexes such as ribosomes. This result was confirmed by 2-D PAGE analysis of P. aeruginosa outer membrane proteins. This study shows that large-scale quantitative proteomic technology can be successfully applied to the analysis of whole bacteria and to the discovery of functionally relevant biologic phenotypes.
PMID: 12837596 [PubMed - indexed for MEDLINE]

My read on it, its possible that PA becomes more virulent in a low magnesium environment. This did not address whether higher magnesium environments were better nor did it address what level of magnesium resulted in increased virulence.

 

[mom2lillian]

Proteomic analysis of Pseudomonas aeruginosa grown under magnesium limitation.

Guina T,
Wu M,
Miller SI,
Purvine SO,
Yi EC,
Eng J,
Goodlett DR,
Aebersold R,
Ernst RK,
Lee KA.
Department of Pediatrics, Division of Infectious Diseases, University of Washington, Seattle, Washington 98195, USA. tguina@u.washington.edu
In this study, large-scale qualitative and quantitative proteomic technology was applied to the analysis of the opportunistic bacterial pathogen Pseudomonas aeruginosa grown under magnesium limitation, an environmental condition previously shown to induce expression of various virulence factors. For quantitative analysis, whole cell and membrane proteins were differentially labeled with isotope-coded affinity tag (ICAT) reagents and ICAT reagent-labeled peptides were separated by two-dimensional chromatography prior to analysis by electrospray ionization-tandem mass spectrometry (ESI-MS/MS) in an ion trap mass spectrometer (ITMS). To increase the number of protein identifications, gas-phase fractionation (GPF) in the m/z dimension was employed for analysis of ICAT peptides derived from whole cell extracts. The experiments confirmed expression of 1331 P. aeruginosa proteins of which 145 were differentially expressed upon limitation of magnesium. A number of conserved Gram-negative magnesium stress-response proteins involved in bacterial virulence were among the most abundant proteins induced in low magnesium. Comparative ICAT analysis of membrane versus whole cell protein indicated that growth of P. aeruginosa in low magnesium resulted in altered subcellular compartmentalization of large enzyme complexes such as ribosomes. This result was confirmed by 2-D PAGE analysis of P. aeruginosa outer membrane proteins. This study shows that large-scale quantitative proteomic technology can be successfully applied to the analysis of whole bacteria and to the discovery of functionally relevant biologic phenotypes.
PMID: 12837596 [PubMed - indexed for MEDLINE]

My read on it, its possible that PA becomes more virulent in a low magnesium environment. This did not address whether higher magnesium environments were better nor did it address what level of magnesium resulted in increased virulence.

 

[mom2lillian]

I had posted these articles that Mandy posted originally on my P67L board and someone asked for interpretation so I have some words thrown in there with my own loose interpretation, my words are in brown but I dont think it is going to keep the formating--you will be able to tell though.


: J Cyst Fibros. 2005 Dec;4(4):221-5. Epub 2005 Oct 18. Links
The effects of intravenous tobramycin on renal tubular function in children with cystic fibrosis.

Glass S,
Plant ND,
Spencer DA.
Department of Respiratory Paediatrics, Freeman Hospital, Freeman Road, Heaton, Newcastle upon Tyne, England, NE7 7DN, UK. sueglass10@hotmail.com
BACKGROUND: Tobramycin, used to treat respiratory exacerbations in cystic fibrosis (CF), is also a renal tubular toxin. Tubular dysfunction leads to increased urinary levels of the proximal tubular lysosomal enzyme, N-acetyl-beta-D-glucosaminidase (NAG) and the proximal tubular protein, retinol-binding protein (RBP). Hypermagnesuria abnormally high levels magnesium in urine and resulting hypomagnesaemia low levels magnesium in body are indicative of more severe tubular damage low magnesium = greater damage to hearing on TOBI IV's, occasionally seen following repeated courses of intravenous tobramycin. Using these biochemical markers we studied the effect of a 2-week course of this agent on tubular function. METHODS: Twenty-two children (11 boys) with CF were studied. Median age = 10.9 years, range 3.1-16.4 years. All had a normal predicted glomerular filtration rate (pGFR). They received tobramycin 3 mg/kg/dose tds. Urinary NAG, RBP, creatinine and plasma magnesium and creatinine were assayed: a) immediately before commencing tobramycin, b) immediately following the course, c) 4 weeks after the end of the course. RESULTS: Mean log UrNAG and UrRBP rose significantly between time points a) and b) before falling to almost pre-treatment levels by time c). Using two way ANOVA analysis the results for UrNAG and UrRBP were both highly statistically significant (p<0.0001). Paired t-tests on the logged values revealed highly significant differences between all time points for UrNAG and in the case of UrRBP for all other than a) compared to c). In all patients plasma magnesium and pGFR remained within normal limits. CONCLUSIONS: Intravenous tobramycin produces acute tubular injury, which showed evidence of almost complete recovery after 4 weeks. The insult to the tubules was not sufficient to produce hypomagnesaemia in our study group. To assess cumulative tubular damage in more detail it would be necessary to repeat this study after further courses of tobramycin. We recommend monitoring plasma magnesium during courses of intravenous tobramycin. Basically, I think they are sayign while on IV TOBI the magnesium goes down and can cause insult to the ears (correlation inferred) but magnesium returns to almost the same level as pre-iv'snormal 4 weeks following IV's.This is only after 1 treatment, after repeated treatments who knows if levels will continue return to pre-treatmen levels-that is now needing to be studied next. However it also states that even at its lwoest levels during treatment the magnesium levels were still considered in the 'nromal' range. However, there is not alot good data to determine difference of ANY vitamin levels the currentl levels set by USDA etc are the levels required to stave off disease no one knows what 'optimum' vitamin levels are.

 

[mom2lillian]

I had posted these articles that Mandy posted originally on my P67L board and someone asked for interpretation so I have some words thrown in there with my own loose interpretation, my words are in brown but I dont think it is going to keep the formating--you will be able to tell though.


: J Cyst Fibros. 2005 Dec;4(4):221-5. Epub 2005 Oct 18. Links
The effects of intravenous tobramycin on renal tubular function in children with cystic fibrosis.

Glass S,
Plant ND,
Spencer DA.
Department of Respiratory Paediatrics, Freeman Hospital, Freeman Road, Heaton, Newcastle upon Tyne, England, NE7 7DN, UK. sueglass10@hotmail.com
BACKGROUND: Tobramycin, used to treat respiratory exacerbations in cystic fibrosis (CF), is also a renal tubular toxin. Tubular dysfunction leads to increased urinary levels of the proximal tubular lysosomal enzyme, N-acetyl-beta-D-glucosaminidase (NAG) and the proximal tubular protein, retinol-binding protein (RBP). Hypermagnesuria abnormally high levels magnesium in urine and resulting hypomagnesaemia low levels magnesium in body are indicative of more severe tubular damage low magnesium = greater damage to hearing on TOBI IV's, occasionally seen following repeated courses of intravenous tobramycin. Using these biochemical markers we studied the effect of a 2-week course of this agent on tubular function. METHODS: Twenty-two children (11 boys) with CF were studied. Median age = 10.9 years, range 3.1-16.4 years. All had a normal predicted glomerular filtration rate (pGFR). They received tobramycin 3 mg/kg/dose tds. Urinary NAG, RBP, creatinine and plasma magnesium and creatinine were assayed: a) immediately before commencing tobramycin, b) immediately following the course, c) 4 weeks after the end of the course. RESULTS: Mean log UrNAG and UrRBP rose significantly between time points a) and b) before falling to almost pre-treatment levels by time c). Using two way ANOVA analysis the results for UrNAG and UrRBP were both highly statistically significant (p<0.0001). Paired t-tests on the logged values revealed highly significant differences between all time points for UrNAG and in the case of UrRBP for all other than a) compared to c). In all patients plasma magnesium and pGFR remained within normal limits. CONCLUSIONS: Intravenous tobramycin produces acute tubular injury, which showed evidence of almost complete recovery after 4 weeks. The insult to the tubules was not sufficient to produce hypomagnesaemia in our study group. To assess cumulative tubular damage in more detail it would be necessary to repeat this study after further courses of tobramycin. We recommend monitoring plasma magnesium during courses of intravenous tobramycin. Basically, I think they are sayign while on IV TOBI the magnesium goes down and can cause insult to the ears (correlation inferred) but magnesium returns to almost the same level as pre-iv'snormal 4 weeks following IV's.This is only after 1 treatment, after repeated treatments who knows if levels will continue return to pre-treatmen levels-that is now needing to be studied next. However it also states that even at its lwoest levels during treatment the magnesium levels were still considered in the 'nromal' range. However, there is not alot good data to determine difference of ANY vitamin levels the currentl levels set by USDA etc are the levels required to stave off disease no one knows what 'optimum' vitamin levels are.

 

[mom2lillian]

I had posted these articles that Mandy posted originally on my P67L board and someone asked for interpretation so I have some words thrown in there with my own loose interpretation, my words are in brown but I dont think it is going to keep the formating--you will be able to tell though.


: J Cyst Fibros. 2005 Dec;4(4):221-5. Epub 2005 Oct 18. Links
The effects of intravenous tobramycin on renal tubular function in children with cystic fibrosis.

Glass S,
Plant ND,
Spencer DA.
Department of Respiratory Paediatrics, Freeman Hospital, Freeman Road, Heaton, Newcastle upon Tyne, England, NE7 7DN, UK. sueglass10@hotmail.com
BACKGROUND: Tobramycin, used to treat respiratory exacerbations in cystic fibrosis (CF), is also a renal tubular toxin. Tubular dysfunction leads to increased urinary levels of the proximal tubular lysosomal enzyme, N-acetyl-beta-D-glucosaminidase (NAG) and the proximal tubular protein, retinol-binding protein (RBP). Hypermagnesuria abnormally high levels magnesium in urine and resulting hypomagnesaemia low levels magnesium in body are indicative of more severe tubular damage low magnesium = greater damage to hearing on TOBI IV's, occasionally seen following repeated courses of intravenous tobramycin. Using these biochemical markers we studied the effect of a 2-week course of this agent on tubular function. METHODS: Twenty-two children (11 boys) with CF were studied. Median age = 10.9 years, range 3.1-16.4 years. All had a normal predicted glomerular filtration rate (pGFR). They received tobramycin 3 mg/kg/dose tds. Urinary NAG, RBP, creatinine and plasma magnesium and creatinine were assayed: a) immediately before commencing tobramycin, b) immediately following the course, c) 4 weeks after the end of the course. RESULTS: Mean log UrNAG and UrRBP rose significantly between time points a) and b) before falling to almost pre-treatment levels by time c). Using two way ANOVA analysis the results for UrNAG and UrRBP were both highly statistically significant (p<0.0001). Paired t-tests on the logged values revealed highly significant differences between all time points for UrNAG and in the case of UrRBP for all other than a) compared to c). In all patients plasma magnesium and pGFR remained within normal limits. CONCLUSIONS: Intravenous tobramycin produces acute tubular injury, which showed evidence of almost complete recovery after 4 weeks. The insult to the tubules was not sufficient to produce hypomagnesaemia in our study group. To assess cumulative tubular damage in more detail it would be necessary to repeat this study after further courses of tobramycin. We recommend monitoring plasma magnesium during courses of intravenous tobramycin. Basically, I think they are sayign while on IV TOBI the magnesium goes down and can cause insult to the ears (correlation inferred) but magnesium returns to almost the same level as pre-iv'snormal 4 weeks following IV's.This is only after 1 treatment, after repeated treatments who knows if levels will continue return to pre-treatmen levels-that is now needing to be studied next. However it also states that even at its lwoest levels during treatment the magnesium levels were still considered in the 'nromal' range. However, there is not alot good data to determine difference of ANY vitamin levels the currentl levels set by USDA etc are the levels required to stave off disease no one knows what 'optimum' vitamin levels are.

 

[mom2lillian]

I had posted these articles that Mandy posted originally on my P67L board and someone asked for interpretation so I have some words thrown in there with my own loose interpretation, my words are in brown but I dont think it is going to keep the formating--you will be able to tell though.


: J Cyst Fibros. 2005 Dec;4(4):221-5. Epub 2005 Oct 18. Links
The effects of intravenous tobramycin on renal tubular function in children with cystic fibrosis.

Glass S,
Plant ND,
Spencer DA.
Department of Respiratory Paediatrics, Freeman Hospital, Freeman Road, Heaton, Newcastle upon Tyne, England, NE7 7DN, UK. sueglass10@hotmail.com
BACKGROUND: Tobramycin, used to treat respiratory exacerbations in cystic fibrosis (CF), is also a renal tubular toxin. Tubular dysfunction leads to increased urinary levels of the proximal tubular lysosomal enzyme, N-acetyl-beta-D-glucosaminidase (NAG) and the proximal tubular protein, retinol-binding protein (RBP). Hypermagnesuria abnormally high levels magnesium in urine and resulting hypomagnesaemia low levels magnesium in body are indicative of more severe tubular damage low magnesium = greater damage to hearing on TOBI IV's, occasionally seen following repeated courses of intravenous tobramycin. Using these biochemical markers we studied the effect of a 2-week course of this agent on tubular function. METHODS: Twenty-two children (11 boys) with CF were studied. Median age = 10.9 years, range 3.1-16.4 years. All had a normal predicted glomerular filtration rate (pGFR). They received tobramycin 3 mg/kg/dose tds. Urinary NAG, RBP, creatinine and plasma magnesium and creatinine were assayed: a) immediately before commencing tobramycin, b) immediately following the course, c) 4 weeks after the end of the course. RESULTS: Mean log UrNAG and UrRBP rose significantly between time points a) and b) before falling to almost pre-treatment levels by time c). Using two way ANOVA analysis the results for UrNAG and UrRBP were both highly statistically significant (p<0.0001). Paired t-tests on the logged values revealed highly significant differences between all time points for UrNAG and in the case of UrRBP for all other than a) compared to c). In all patients plasma magnesium and pGFR remained within normal limits. CONCLUSIONS: Intravenous tobramycin produces acute tubular injury, which showed evidence of almost complete recovery after 4 weeks. The insult to the tubules was not sufficient to produce hypomagnesaemia in our study group. To assess cumulative tubular damage in more detail it would be necessary to repeat this study after further courses of tobramycin. We recommend monitoring plasma magnesium during courses of intravenous tobramycin. Basically, I think they are sayign while on IV TOBI the magnesium goes down and can cause insult to the ears (correlation inferred) but magnesium returns to almost the same level as pre-iv'snormal 4 weeks following IV's.This is only after 1 treatment, after repeated treatments who knows if levels will continue return to pre-treatmen levels-that is now needing to be studied next. However it also states that even at its lwoest levels during treatment the magnesium levels were still considered in the 'nromal' range. However, there is not alot good data to determine difference of ANY vitamin levels the currentl levels set by USDA etc are the levels required to stave off disease no one knows what 'optimum' vitamin levels are.

 

[mom2lillian]

I had posted these articles that Mandy posted originally on my P67L board and someone asked for interpretation so I have some words thrown in there with my own loose interpretation, my words are in brown but I dont think it is going to keep the formating--you will be able to tell though.


: J Cyst Fibros. 2005 Dec;4(4):221-5. Epub 2005 Oct 18. Links
The effects of intravenous tobramycin on renal tubular function in children with cystic fibrosis.

Glass S,
Plant ND,
Spencer DA.
Department of Respiratory Paediatrics, Freeman Hospital, Freeman Road, Heaton, Newcastle upon Tyne, England, NE7 7DN, UK. sueglass10@hotmail.com
BACKGROUND: Tobramycin, used to treat respiratory exacerbations in cystic fibrosis (CF), is also a renal tubular toxin. Tubular dysfunction leads to increased urinary levels of the proximal tubular lysosomal enzyme, N-acetyl-beta-D-glucosaminidase (NAG) and the proximal tubular protein, retinol-binding protein (RBP). Hypermagnesuria abnormally high levels magnesium in urine and resulting hypomagnesaemia low levels magnesium in body are indicative of more severe tubular damage low magnesium = greater damage to hearing on TOBI IV's, occasionally seen following repeated courses of intravenous tobramycin. Using these biochemical markers we studied the effect of a 2-week course of this agent on tubular function. METHODS: Twenty-two children (11 boys) with CF were studied. Median age = 10.9 years, range 3.1-16.4 years. All had a normal predicted glomerular filtration rate (pGFR). They received tobramycin 3 mg/kg/dose tds. Urinary NAG, RBP, creatinine and plasma magnesium and creatinine were assayed: a) immediately before commencing tobramycin, b) immediately following the course, c) 4 weeks after the end of the course. RESULTS: Mean log UrNAG and UrRBP rose significantly between time points a) and b) before falling to almost pre-treatment levels by time c). Using two way ANOVA analysis the results for UrNAG and UrRBP were both highly statistically significant (p<0.0001). Paired t-tests on the logged values revealed highly significant differences between all time points for UrNAG and in the case of UrRBP for all other than a) compared to c). In all patients plasma magnesium and pGFR remained within normal limits. CONCLUSIONS: Intravenous tobramycin produces acute tubular injury, which showed evidence of almost complete recovery after 4 weeks. The insult to the tubules was not sufficient to produce hypomagnesaemia in our study group. To assess cumulative tubular damage in more detail it would be necessary to repeat this study after further courses of tobramycin. We recommend monitoring plasma magnesium during courses of intravenous tobramycin. Basically, I think they are sayign while on IV TOBI the magnesium goes down and can cause insult to the ears (correlation inferred) but magnesium returns to almost the same level as pre-iv'snormal 4 weeks following IV's.This is only after 1 treatment, after repeated treatments who knows if levels will continue return to pre-treatmen levels-that is now needing to be studied next. However it also states that even at its lwoest levels during treatment the magnesium levels were still considered in the 'nromal' range. However, there is not alot good data to determine difference of ANY vitamin levels the currentl levels set by USDA etc are the levels required to stave off disease no one knows what 'optimum' vitamin levels are.

 

[mom2lillian]

I had posted these articles that Mandy posted originally on my P67L board and someone asked for interpretation so I have some words thrown in there with my own loose interpretation, my words are in brown but I dont think it is going to keep the formating--you will be able to tell though.


: J Cyst Fibros. 2005 Dec;4(4):221-5. Epub 2005 Oct 18. Links
The effects of intravenous tobramycin on renal tubular function in children with cystic fibrosis.

Glass S,
Plant ND,
Spencer DA.
Department of Respiratory Paediatrics, Freeman Hospital, Freeman Road, Heaton, Newcastle upon Tyne, England, NE7 7DN, UK. sueglass10@hotmail.com
BACKGROUND: Tobramycin, used to treat respiratory exacerbations in cystic fibrosis (CF), is also a renal tubular toxin. Tubular dysfunction leads to increased urinary levels of the proximal tubular lysosomal enzyme, N-acetyl-beta-D-glucosaminidase (NAG) and the proximal tubular protein, retinol-binding protein (RBP). Hypermagnesuria abnormally high levels magnesium in urine and resulting hypomagnesaemia low levels magnesium in body are indicative of more severe tubular damage low magnesium = greater damage to hearing on TOBI IV's, occasionally seen following repeated courses of intravenous tobramycin. Using these biochemical markers we studied the effect of a 2-week course of this agent on tubular function. METHODS: Twenty-two children (11 boys) with CF were studied. Median age = 10.9 years, range 3.1-16.4 years. All had a normal predicted glomerular filtration rate (pGFR). They received tobramycin 3 mg/kg/dose tds. Urinary NAG, RBP, creatinine and plasma magnesium and creatinine were assayed: a) immediately before commencing tobramycin, b) immediately following the course, c) 4 weeks after the end of the course. RESULTS: Mean log UrNAG and UrRBP rose significantly between time points a) and b) before falling to almost pre-treatment levels by time c). Using two way ANOVA analysis the results for UrNAG and UrRBP were both highly statistically significant (p<0.0001). Paired t-tests on the logged values revealed highly significant differences between all time points for UrNAG and in the case of UrRBP for all other than a) compared to c). In all patients plasma magnesium and pGFR remained within normal limits. CONCLUSIONS: Intravenous tobramycin produces acute tubular injury, which showed evidence of almost complete recovery after 4 weeks. The insult to the tubules was not sufficient to produce hypomagnesaemia in our study group. To assess cumulative tubular damage in more detail it would be necessary to repeat this study after further courses of tobramycin. We recommend monitoring plasma magnesium during courses of intravenous tobramycin. Basically, I think they are sayign while on IV TOBI the magnesium goes down and can cause insult to the ears (correlation inferred) but magnesium returns to almost the same level as pre-iv'snormal 4 weeks following IV's.This is only after 1 treatment, after repeated treatments who knows if levels will continue return to pre-treatmen levels-that is now needing to be studied next. However it also states that even at its lwoest levels during treatment the magnesium levels were still considered in the 'nromal' range. However, there is not alot good data to determine difference of ANY vitamin levels the currentl levels set by USDA etc are the levels required to stave off disease no one knows what 'optimum' vitamin levels are.

 

[mom2lillian]

Aminoglycoside-associated hypomagnesaemia in children with cystic fibrosis.

Akbar A,
Rees JH,
Nyamugunduru G,
English MW,
Spencer DA,
Weller PH.
Paediatric Respiratory and Cystic Fibrosis Unit, The Birmingham Children's Hospital NHS Trust, UK.
Hypomagnesaemia in children with cystic fibrosis (CF) is under-recognized. We report a child with CF who developed significant hypomagnesaemia following intravenous (i.v.) treatment with aminoglycosides (a class of antibiotics)exacerbations of Pseudomonas aeruginosa infection. Three additional cases have also been observed. Investigations in two patients have revealed excessive renal loss of magnesium. It is postulated that renal tubular damage secondary to the cumulative effects of repeated courses of aminoglycosides resulted in hypomagnesaemia (damage to the ears as a result of treatment with IV's has resulted in low magnesium -- or perhaps vice versa btu they are showing the link) , and we suggest screening for this problem by monitoring serum magnesium regularly in all patients with CF receiving multiple courses of aminoglycosides. (Recommendation is that now when we get our peaks and troughs measured when on IV's we would aslo have them do a Magnesium check at this time)

 

[mom2lillian]

Aminoglycoside-associated hypomagnesaemia in children with cystic fibrosis.

Akbar A,
Rees JH,
Nyamugunduru G,
English MW,
Spencer DA,
Weller PH.
Paediatric Respiratory and Cystic Fibrosis Unit, The Birmingham Children's Hospital NHS Trust, UK.
Hypomagnesaemia in children with cystic fibrosis (CF) is under-recognized. We report a child with CF who developed significant hypomagnesaemia following intravenous (i.v.) treatment with aminoglycosides (a class of antibiotics)exacerbations of Pseudomonas aeruginosa infection. Three additional cases have also been observed. Investigations in two patients have revealed excessive renal loss of magnesium. It is postulated that renal tubular damage secondary to the cumulative effects of repeated courses of aminoglycosides resulted in hypomagnesaemia (damage to the ears as a result of treatment with IV's has resulted in low magnesium -- or perhaps vice versa btu they are showing the link) , and we suggest screening for this problem by monitoring serum magnesium regularly in all patients with CF receiving multiple courses of aminoglycosides. (Recommendation is that now when we get our peaks and troughs measured when on IV's we would aslo have them do a Magnesium check at this time)

 

[mom2lillian]

Aminoglycoside-associated hypomagnesaemia in children with cystic fibrosis.

Akbar A,
Rees JH,
Nyamugunduru G,
English MW,
Spencer DA,
Weller PH.
Paediatric Respiratory and Cystic Fibrosis Unit, The Birmingham Children's Hospital NHS Trust, UK.
Hypomagnesaemia in children with cystic fibrosis (CF) is under-recognized. We report a child with CF who developed significant hypomagnesaemia following intravenous (i.v.) treatment with aminoglycosides (a class of antibiotics)exacerbations of Pseudomonas aeruginosa infection. Three additional cases have also been observed. Investigations in two patients have revealed excessive renal loss of magnesium. It is postulated that renal tubular damage secondary to the cumulative effects of repeated courses of aminoglycosides resulted in hypomagnesaemia (damage to the ears as a result of treatment with IV's has resulted in low magnesium -- or perhaps vice versa btu they are showing the link) , and we suggest screening for this problem by monitoring serum magnesium regularly in all patients with CF receiving multiple courses of aminoglycosides. (Recommendation is that now when we get our peaks and troughs measured when on IV's we would aslo have them do a Magnesium check at this time)

 

[mom2lillian]

Aminoglycoside-associated hypomagnesaemia in children with cystic fibrosis.

Akbar A,
Rees JH,
Nyamugunduru G,
English MW,
Spencer DA,
Weller PH.
Paediatric Respiratory and Cystic Fibrosis Unit, The Birmingham Children's Hospital NHS Trust, UK.
Hypomagnesaemia in children with cystic fibrosis (CF) is under-recognized. We report a child with CF who developed significant hypomagnesaemia following intravenous (i.v.) treatment with aminoglycosides (a class of antibiotics)exacerbations of Pseudomonas aeruginosa infection. Three additional cases have also been observed. Investigations in two patients have revealed excessive renal loss of magnesium. It is postulated that renal tubular damage secondary to the cumulative effects of repeated courses of aminoglycosides resulted in hypomagnesaemia (damage to the ears as a result of treatment with IV's has resulted in low magnesium -- or perhaps vice versa btu they are showing the link) , and we suggest screening for this problem by monitoring serum magnesium regularly in all patients with CF receiving multiple courses of aminoglycosides. (Recommendation is that now when we get our peaks and troughs measured when on IV's we would aslo have them do a Magnesium check at this time)