6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Aluminum toxicity to bone: A multisystem effect?

      review-article
      Osteoporosis and Sarcopenia
      Korean Society of Osteoporosis
      Aluminum toxicity, Bone, Parathyroid glands, Liver, Osteomalacia

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Aluminum (Al) is the third most abundant element in the earth's crust and is omnipresent in our environment, including our food. However, with normal renal function, oral and enteral ingestion of substances contaminated with Al, such as antacids and infant formulae, do not cause problems. The intestine, skin, and respiratory tract are barriers to Al entry into the blood. However, contamination of fluids given parenterally, such as parenteral nutrition solutions, or hemodialysis, peritoneal dialysis or even oral Al-containing substances to patients with impaired renal function could result in accumulation in bone, parathyroids, liver, spleen, and kidney. The toxic effects of Al to the skeleton include fractures accompanying a painful osteomalacia, hypoparathyroidism, microcytic anemia, cholestatic hepatotoxicity, and suppression of the renal enzyme 25-hydroxyvitamin D-1 alpha hydroxylase. The sources of Al include contamination of calcium and phosphate salts, albumin and heparin. Contamination occurs either from inability to remove the naturally accumulating Al or from leeching from glass columns used in compound purification processes. Awareness of this long-standing problem should allow physicians to choose pharmaceutical products with lower quantities of Al listed on the label as long as this practice is mandated by specific national drug regulatory agencies.

          Related collections

          Most cited references32

          • Record: found
          • Abstract: found
          • Article: not found

          Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease.

          Calcium, phosphorus, and magnesium homeostasis is altered in chronic kidney disease (CKD). Hypocalcemia, hyperphosphatemia, and hypermagnesemia are not seen until advanced CKD because adaptations develop. Increased parathyroid hormone (PTH) secretion maintains serum calcium normal by increasing calcium efflux from bone, renal calcium reabsorption, and phosphate excretion. Similarly, renal phosphate excretion in CKD is maintained by increased secretion of fibroblast growth factor 23 (FGF23) and PTH. However, the phosphaturic effect of FGF23 is reduced by downregulation of its cofactor Klotho necessary for binding FGF23 to FGF receptors. Intestinal phosphate absorption is diminished in CKD due in part to reduced levels of 1,25 dihydroxyvitamin D. Unlike calcium and phosphorus, magnesium is not regulated by a hormone, but fractional excretion of magnesium increases as CKD progresses. As 60-70% of magnesium is reabsorbed in the thick ascending limb of Henle, activation of the calcium-sensing receptor by magnesium may facilitate magnesium excretion in CKD. Modification of the TRPM6 channel in the distal tubule may also have a role. Besides abnormal bone morphology and vascular calcification, abnormalities in mineral homeostasis are associated with increased cardiovascular risk, increased mortality and progression of CKD.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Evidence of aluminum loading in infants receiving intravenous therapy.

            To investigate the possibility that premature infants may be vulnerable to aluminum toxicity acquired through intravenous feeding, we prospectively studied plasma and urinary aluminum concentrations in 18 premature infants receiving intravenous therapy and in 8 term infants receiving no intravenous therapy. We also measured bone aluminum concentrations in autopsy specimens from 23 infants, including 6 who had received at least three weeks of intravenous therapy. Premature infants who received intravenous therapy had high plasma and urinary aluminum concentrations, as compared with normal controls: plasma aluminum, 36.78 +/- 45.30 vs. 5.17 +/- 3.1 micrograms per liter (mean +/- S.D., P less than 0.0001); urinary aluminum:creatinine ratio, 5.4 +/- 4.6 vs. 0.64 +/- 0.75 (P less than 0.01). The bone aluminum concentration was 10 times higher in infants who had received at least three weeks of intravenous therapy than in those who had received limited intravenous therapy: 20.16 +/- 13.4 vs. 1.98 +/- 1.44 mg per kilogram of dry weight (P less than 0.0001). Creatinine clearances corrected for weight did not reach expected adult values until 34 weeks of gestation. Many commonly used intravenous solutions are found to be highly contaminated with aluminum. We conclude that infants receiving intravenous therapy have aluminum loading, which is reflected in increased urinary excretion and elevated concentrations in plasma and bone. Such infants may be at high risk for aluminum intoxication secondary to increased parenteral exposure and poor renal clearance.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Aluminum is associated with low bone formation in patients receiving chronic parenteral nutrition.

              Patients treated with chronic total parenteral nutrition may develop metabolic bone disease. We evaluated 22 bone biopsy specimens from 16 patients. Compared with those of age- and sex-matched normal controls, these specimens had significantly higher osteoid area and lower total bone area and bone formation rate, as measured by double tetracycline labels. Aluminum was found in specimens from the 14 patients receiving casein hydrolysate but not in the two receiving amino acids as their nitrogen source. The reduced bone formation correlated inversely with the logarithm of the aluminum level. Aluminum was localized to the surface of mineralized bone; tetracycline uptake was absent at those sites. These bone findings are similar to those from aluminum intoxicated patients on hemodialysis. Both groups also have low parathyroid hormone levels. Thus, aluminum appears to be an important pathogenic factor in the osteodystrophy of patients receiving dialysis or total parenteral nutrition.
                Bookmark

                Author and article information

                Contributors
                Journal
                Osteoporos Sarcopenia
                Osteoporos Sarcopenia
                Osteoporosis and Sarcopenia
                Korean Society of Osteoporosis
                2405-5255
                2405-5263
                15 February 2019
                March 2019
                15 February 2019
                : 5
                : 1
                : 2-5
                Affiliations
                [1]Department of Orthopaedic Surgery and Rehabilitation, University of Texas Medical Branch, Galveston, TX, USA
                Author notes
                []Department of Orthopaedic Surgery and Rehabilitation, University of Texas Medical Branch, 301 University Boulevard, Galveston, TX 77555-0165, USA. gordonklein@ 123456ymail.com
                Article
                S2405-5255(18)30176-6
                10.1016/j.afos.2019.01.001
                6453153
                31008371
                435e8a5d-0766-4356-9219-1a914200e190
                © 2019 The Korean Society of Osteoporosis. Publishing services by Elsevier B.V.

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 19 November 2018
                : 12 December 2018
                : 7 January 2019
                Categories
                Review Article

                aluminum toxicity,bone,parathyroid glands,liver,osteomalacia

                Comments

                Comment on this article