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Journal of the American College of Nutrition Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/uacn20
Response to a special report from the ASCN/ ASPEN Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions. W W Koo & R W Chesney Published online: 02 Sep 2013.
To cite this article: W W Koo & R W Chesney (1992) Response to a special report from the ASCN/ASPEN Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions., Journal of the American College of Nutrition, 11:1, 3-4, DOI: 10.1080/07315724.1992.10718187 To link to this article: http://dx.doi.org/10.1080/07315724.1992.10718187
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
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Guest Editorial: Response to a Special Report From the ASCN/ASPEN Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions
Efforts of the ASCN/ASPEN Working Group on the role of aluminum (Al) contamination of parenteral nutri tion (PN) solutions are laudable [1,2]. The potential toxicity in patients with chronic renal failure from Al contam ination of dialysate fluids and Al-containing antacids is eloquently reported by certain members of this group and other investigators, although not all investigators support the central role of Al in tissue pathology [3]. It is also important to discuss the issue of Al intake from nutrient contamination in patients with apparently normal renal function. This is essential to minimize any misinformation regarding cause-and-effect relationship be tween Al contamination of parenteral nutrients and the serious complications of long-term PN therapy such as bone and liver disease. The role of Al in causing tissue toxicity from PN in patients with normal renal function remains ill defined. In adults receiving PN with casein hydrolysate, the Al intake is estimated to be about 60 μg/kg/day [4]. However, casein hydrolysate is no longer used in PN, and the concentration of Al in current PN solutions containing crystalline amino acid is as low as 16 /itg/L with daily Al intake as low as 12 Mg/kg/day [5]. The initial report [6] of an increase in osteoid area, an abnormal feature associated with alumi num toxicity, occurred in only six of the 16 patients, and there was no significant difference in the osteoid and resorbing surfaces between patients and controls. There were three patients [6] who had serial data on bone for mation rate (BFR). Two patients showed significantly im proved BFR on subsequent biopsy in spite of continuing casein hydrolysate infusion in one patient while the third patient continued to have low BFR on subsequent biopsy. In the same report, continued use of the same PN solution did not significantly alter histomorphometric measure ments in patients who had serial bone biopsies over a 654-month interval. Furthermore, bone biopsies in one of these patients showed an absence of Al 5 years after the use of low Al-containing amino acid formulation. Unfor tunately, subsequent reports contributed little additional information on longitudinal data in patients who received both the high and low Al PN solutions.
A criticism of early reports on bone histomorphometric changes is the inconsistent diagnostic criteria used to define the toxic effects of Al or other causative factors [7]. How ever, more recent data indicated that decreased bone for mation persisted despite PN solutions with minimal Al contamination and the presence of minimal or no eleva tion in plasma, urine, or bone Al (by histochemical staining or by quantitative measurement) [5]. In another report, PN-related bone disease and increased bone Al were suc cessfully treated with additional calcium supplement which was heavily contaminated with Al [8]. A preliminary report on longitudinal follow-up in patients receiving long-term PN with low Al-containing amino acid formulation over a mean interval of 2 years showed continued bone histomor phometric deterioration [9]. In patients receiving high Al PN solution, the depressed serum concentrations of 1,25 dihydroxyvitamin D, a po tent calciotropic hormone, are reported to increase after lowering of Al intake. However, these patients also simul taneously had a 60% decrease in phosphorus intake [10], an important regulator of serum 1,25 (OH)2D concentra tions. Based on the above studies, it is difficult to implicate Al as critical to the development of PN-related bone dis ease. In infants receiving PN solutions, elevated serum, urine, and tissue (bone) Al are documented from an Al intake of 20-40 μg/kg/day, depending on the amount of minerals in the PN solution. The tissue (bone) accumula tion of Al warrants further study to determine its clinical and pathological significance. However, bone accumula tion of toxins such as lead and strontium is well known and does not always result in tissue toxicity. In addition, osteopenia in small preterm infants improved with addi tional intake of minerals contaminated with Al [11]. The role of Al in PN-related liver disease remains speculative. Our intent is not to contradict the laudable effort of the Working Group to eliminate Al, a potential toxin, from parenteral nutrients, but rather, to plea for more studies to obtain scientifically valid recommendation for legislation that will limit Al content in PN solutions.
Journal of the American College of Nutrition, Vol. 11, No. 1,3-4(1992) Published by the American College of Nutrition 3
Al Content of PN Solutions
Downloaded by [New York University] at 06:11 13 May 2015
REFERENCES 1. ASCN/ASPEN Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions: Parenteral drug products containing aluminum as an ingredient or a contam inant: response to FDA notice of intent. Am J Clin Nutr 53:399-402, 1991. 2. ASCN/ASPEN Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions: Parenteral drug products containing aluminum as an ingredient or a contam inant: response to Food and Drug Administration notice of intent and request for information. J Parenter Enterai Nutr 15: 194-198, 1991. 3. Quarles LD, Gitelman HJ, Drezner MK: Aluminum-associ ated bone disease: What's in a name. J Bone Miner Res 2:389-390, 1986. 4. Klein GL: Metabolic bone disease of total parenteral nutri tion. In Favus MJ (ed): "Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism." Kelseyville, CA: American Society for Bone and Mineral Research, pp 197-200, 1990. 5. Heyman MB, Klein GL, Wong A, Recker RR, Tyrrell JB, Alfrey AC, Sherrard DJ, Hohn DC: Aluminum does not accumulate in teenagers and adults on prolonged parenteral nutrition containing free amino acids. J Parenter Enterai Nutr 10:86-87, 1986. 6. Ott SM, Maloney NA, Klein GL, Alfrey AC, Ament ME, Coburn JW, Sherrard DJ: Aluminum is associated with low bone formation in patients receiving chronic parenteral nu trition. Ann Intern Med 98:910-914, 1983.
4
7. Frame B, Marel G: Reflections on bone disease in total parenteral nutrition. In Coburn JW, Klein GL (eds): "Meta bolic Bone Disease in Total Parenteral Nutrition." Baltimore: Urban & Schwarzenberg, pp 3-15, 1985. 8. Lidor C, Schwartz I, Freund U, Gazit D: Successful high-dose calcium treatment of aluminum-induced metabolic bone dis ease in long-term home parenteral nutrition. J Parenter En terai Nutr 15:202-206, 1991. 9. Saitta JC, Lipkin EW, Ott SM, Sherrard DJ: Longitudinal measurements of bone histomorphology and bone density in parenteral nutrition with solutions low in aluminum and vitamin D2. J Parenter Enterai Nutr 15(Suppl):20S, 1991. 10. Klein GL, Horst RL, Alfrey AC, Slatopolsky E: Serum levels of 1,25 dihydroxyvitamin D in children receiving parenteral nutrition with reduced aluminum content. J Pediatr Gastroenterol Nutr 4:93-96, 1985. 11. Koo WWK, Tsang RC: Mineral requirements of low birth weight infants. J Am Coll Nutr 10:474-486, 1991.
Winston W. K. Koo, MBBS, FACN Russell W. Chesney, MD College of Medicine Department of Pediatrics 853 Jefferson Ave., 2nd Floor Memphis, TN 38163
Received Received May 1991.
VOL. 11, NO. 1
Journal of the American College of Nutrition Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/uacn20
Response to a special report from the ASCN/ ASPEN Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions. W W Koo & R W Chesney Published online: 02 Sep 2013.
To cite this article: W W Koo & R W Chesney (1992) Response to a special report from the ASCN/ASPEN Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions., Journal of the American College of Nutrition, 11:1, 3-4, DOI: 10.1080/07315724.1992.10718187 To link to this article: http://dx.doi.org/10.1080/07315724.1992.10718187
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms & Conditions of access and use can be found at http:// www.tandfonline.com/page/terms-and-conditions
Downloaded by [New York University] at 06:11 13 May 2015
Guest Editorial: Response to a Special Report From the ASCN/ASPEN Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions
Efforts of the ASCN/ASPEN Working Group on the role of aluminum (Al) contamination of parenteral nutri tion (PN) solutions are laudable [1,2]. The potential toxicity in patients with chronic renal failure from Al contam ination of dialysate fluids and Al-containing antacids is eloquently reported by certain members of this group and other investigators, although not all investigators support the central role of Al in tissue pathology [3]. It is also important to discuss the issue of Al intake from nutrient contamination in patients with apparently normal renal function. This is essential to minimize any misinformation regarding cause-and-effect relationship be tween Al contamination of parenteral nutrients and the serious complications of long-term PN therapy such as bone and liver disease. The role of Al in causing tissue toxicity from PN in patients with normal renal function remains ill defined. In adults receiving PN with casein hydrolysate, the Al intake is estimated to be about 60 μg/kg/day [4]. However, casein hydrolysate is no longer used in PN, and the concentration of Al in current PN solutions containing crystalline amino acid is as low as 16 /itg/L with daily Al intake as low as 12 Mg/kg/day [5]. The initial report [6] of an increase in osteoid area, an abnormal feature associated with alumi num toxicity, occurred in only six of the 16 patients, and there was no significant difference in the osteoid and resorbing surfaces between patients and controls. There were three patients [6] who had serial data on bone for mation rate (BFR). Two patients showed significantly im proved BFR on subsequent biopsy in spite of continuing casein hydrolysate infusion in one patient while the third patient continued to have low BFR on subsequent biopsy. In the same report, continued use of the same PN solution did not significantly alter histomorphometric measure ments in patients who had serial bone biopsies over a 654-month interval. Furthermore, bone biopsies in one of these patients showed an absence of Al 5 years after the use of low Al-containing amino acid formulation. Unfor tunately, subsequent reports contributed little additional information on longitudinal data in patients who received both the high and low Al PN solutions.
A criticism of early reports on bone histomorphometric changes is the inconsistent diagnostic criteria used to define the toxic effects of Al or other causative factors [7]. How ever, more recent data indicated that decreased bone for mation persisted despite PN solutions with minimal Al contamination and the presence of minimal or no eleva tion in plasma, urine, or bone Al (by histochemical staining or by quantitative measurement) [5]. In another report, PN-related bone disease and increased bone Al were suc cessfully treated with additional calcium supplement which was heavily contaminated with Al [8]. A preliminary report on longitudinal follow-up in patients receiving long-term PN with low Al-containing amino acid formulation over a mean interval of 2 years showed continued bone histomor phometric deterioration [9]. In patients receiving high Al PN solution, the depressed serum concentrations of 1,25 dihydroxyvitamin D, a po tent calciotropic hormone, are reported to increase after lowering of Al intake. However, these patients also simul taneously had a 60% decrease in phosphorus intake [10], an important regulator of serum 1,25 (OH)2D concentra tions. Based on the above studies, it is difficult to implicate Al as critical to the development of PN-related bone dis ease. In infants receiving PN solutions, elevated serum, urine, and tissue (bone) Al are documented from an Al intake of 20-40 μg/kg/day, depending on the amount of minerals in the PN solution. The tissue (bone) accumula tion of Al warrants further study to determine its clinical and pathological significance. However, bone accumula tion of toxins such as lead and strontium is well known and does not always result in tissue toxicity. In addition, osteopenia in small preterm infants improved with addi tional intake of minerals contaminated with Al [11]. The role of Al in PN-related liver disease remains speculative. Our intent is not to contradict the laudable effort of the Working Group to eliminate Al, a potential toxin, from parenteral nutrients, but rather, to plea for more studies to obtain scientifically valid recommendation for legislation that will limit Al content in PN solutions.
Journal of the American College of Nutrition, Vol. 11, No. 1,3-4(1992) Published by the American College of Nutrition 3
Al Content of PN Solutions
Downloaded by [New York University] at 06:11 13 May 2015
REFERENCES 1. ASCN/ASPEN Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions: Parenteral drug products containing aluminum as an ingredient or a contam inant: response to FDA notice of intent. Am J Clin Nutr 53:399-402, 1991. 2. ASCN/ASPEN Working Group on Standards for Aluminum Content of Parenteral Nutrition Solutions: Parenteral drug products containing aluminum as an ingredient or a contam inant: response to Food and Drug Administration notice of intent and request for information. J Parenter Enterai Nutr 15: 194-198, 1991. 3. Quarles LD, Gitelman HJ, Drezner MK: Aluminum-associ ated bone disease: What's in a name. J Bone Miner Res 2:389-390, 1986. 4. Klein GL: Metabolic bone disease of total parenteral nutri tion. In Favus MJ (ed): "Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism." Kelseyville, CA: American Society for Bone and Mineral Research, pp 197-200, 1990. 5. Heyman MB, Klein GL, Wong A, Recker RR, Tyrrell JB, Alfrey AC, Sherrard DJ, Hohn DC: Aluminum does not accumulate in teenagers and adults on prolonged parenteral nutrition containing free amino acids. J Parenter Enterai Nutr 10:86-87, 1986. 6. Ott SM, Maloney NA, Klein GL, Alfrey AC, Ament ME, Coburn JW, Sherrard DJ: Aluminum is associated with low bone formation in patients receiving chronic parenteral nu trition. Ann Intern Med 98:910-914, 1983.
4
7. Frame B, Marel G: Reflections on bone disease in total parenteral nutrition. In Coburn JW, Klein GL (eds): "Meta bolic Bone Disease in Total Parenteral Nutrition." Baltimore: Urban & Schwarzenberg, pp 3-15, 1985. 8. Lidor C, Schwartz I, Freund U, Gazit D: Successful high-dose calcium treatment of aluminum-induced metabolic bone dis ease in long-term home parenteral nutrition. J Parenter En terai Nutr 15:202-206, 1991. 9. Saitta JC, Lipkin EW, Ott SM, Sherrard DJ: Longitudinal measurements of bone histomorphology and bone density in parenteral nutrition with solutions low in aluminum and vitamin D2. J Parenter Enterai Nutr 15(Suppl):20S, 1991. 10. Klein GL, Horst RL, Alfrey AC, Slatopolsky E: Serum levels of 1,25 dihydroxyvitamin D in children receiving parenteral nutrition with reduced aluminum content. J Pediatr Gastroenterol Nutr 4:93-96, 1985. 11. Koo WWK, Tsang RC: Mineral requirements of low birth weight infants. J Am Coll Nutr 10:474-486, 1991.
Winston W. K. Koo, MBBS, FACN Russell W. Chesney, MD College of Medicine Department of Pediatrics 853 Jefferson Ave., 2nd Floor Memphis, TN 38163
Received Received May 1991.
VOL. 11, NO. 1
