Aluminium bone disease

Maharaj D, Fell GS, Boyce BF, Ng IP, Smith GD, Boulton-Jones JM, Gumming RL, Davidson IF. Aluminium bone disease in patients receiving plasma exchange with contaminated albumin. BMJ (Clin Res Ed) 1987 295(6600) 693-6. 

Care should be taken when administering aluminium salts such as aluminium hydroxide in patients with renal dysfunction and bone diseases. Patients with renal... 

Aluminium is the third most abundant element on earth but it is known to have toxic effects that cause brain disease, bone disease, and anaemia. There is concern especially in relation to its possible role in Alzheimer s disease. The changes observed in animals exposed to aluminium are similar to those observed in patients with Alzheimer s disease. Aluminium has been found in some areas of the brain of victims of Alzheimer s at levels not too dissimilar from that in the brains of the animals exposed. Some of the findings and their interpretation are controversial. Unfortunately, the amounts of aluminium absorbed by the residents of Camelford are... 

Unexpected persistent aluminium-related bone disease occurred after renal transplantation following earlier use of aluminium hydroxide (62). 

A 59-year-old man presented with end-stage renal insufficiency. While on hemodialysis he had used aluminium hydroxide as a phosphate binder but then used calcium lactate instead after total parathyroidectomy. Oral vitamin D was discontinued after the parathyroidectomy. However, after he had received a renal transplant he developed aluminium-related bone disease and was treated with infusions of deferoxamine. 

This is the first report of worsening aluminium-related bone disease after renal transplantation. 

Hyperparathyroidism and aluminium hydroxide lead to aluminium-related bone disease however, total parathyroidectomy does not lead to failure of aluminium mobilization after renal transplantation. This man had satisfactory graft function, and the aluminium excretion that was achieved by deferoxamine suggests that the renal transplant was not the limiting factor for the mobihzation of aluminium. The most likely explanation was that he developed adynamic bone through a combination of vitamin D deficiency, hypoparathyroidism, and aluminium deposition. Vitamin D supplementation failed to prevent the osteodystrophy on its own. When aluminium chelation therapy was used, bone healing occurred and his symptoms improved. 

Nicholas JC, Dawes PT, Davies SJ, Freemont AJ. Persisting aluminium-related bone disease after cadaveric renal transplantation. Nephrol Dial Transplant 1999 14(l) 202-4. 

Yaqoob M, Ahmad R, Roberts N, Helliwell T. Low-dose desferrioxamine test for the diagnosis of aluminium-related bone disease in patients on regular haemodialysis. Nephrol Dial Transplant 1991 6(7) 484-6. 

Over the years, problems have arisen as a result of the presence of significant amounts of aluminium in parenteral nutrition solutions in particular they have been held responsible for hypercalciuria and its consequences (54). Parenterally administered aluminium bypasses the gastrointestinal tract, which normally serves as a protective barrier to aluminium entry into the blood. In the past, aluminium contamination of casein hydrolysate, which was used as a source of protein in parenteral nutrition solutions, was associated with low-turnover osteomalacia and with encephalopathy in uremic patients. Premature infants are still at risk of aluminium accumulation as a result of prolonged parenteral nutrition (as are patients receiving plasmapheresis with albumin contaminated in its preparation with aluminium). Metabolic bone disease can result (54). 

Metabolic bone disease in children receiving parenteral nutrition manifests primarily as osteopenia and, on occasion, fractures (5). The etiology is multifactorial calcium and phosphate deficiency play a major role in the preterm infant but the part played by aluminium toxicity in this population is unknown. Lack of reference values of bone histomorphometry in the premature infant, as well as lack of reference data for biochemical markers of bone turnover in these patients, contributes to the uncertainty. Other factors that may play a role in the pathogenesis of bone disease associated with parenteral nutrition include lack of periodic enteral feeding underljdng intestinal disease, including malabsorption and inflammation the presence of neoplasms and drug-induced alterations in calcium and bone metabohsm. However, the true incidence and prevalence of parenteral nutrition-associated bone abnormalities in pediatric patients are unknown. 

Vargas JH, Klein GL, Ament ME, Ott SM, Sherrard DJ, Horst RL, Berquist WE, Alfrey AC, Slatopolsky E, Coburn JW. Metabolic bone disease of total parenteral nutrition course after changing from casein to amino acids in parenteral solutions with reduced aluminium content. Am J Clin Nutr 1988 48(4) 1070-8. 

Treatments of diseases such as osteoporosis, rickets and osteomalacia, in which there is a disturbance of phosphate levels, is complicated by the interdependence of calcium metabolism. This topic has recently been discussed in relation to clinical medicine21. There is the further difficulty that absorption of phosphate from the bowel can be decreased in the presence of calcium or aluminium salts because of the formation of their insoluble phosphates. Uptake of phosphate by bone is exploited in the treatment of polycythaemia vera by intravenous injection of 32P as sodium phosphate. The resulting irradiation of the neighbouring red bone marrow diminishes the production of red cells. 

A 39-year-old woman who took high doses of aluminium and magnesium hydroxide for peptic ulcer disease (over 18 kg of elemental aluminium and 15 kg of elemental magnesium over 8 years) developed severe osteomalacia due to profound phosphate depletion (60). Bone biopsy showed stainable aluminium deposits along 28% of the total bone surface, a unique observation in a patient with normal renal function. Treatment included withdrawal of the antacid and supplementation with phosphate, calcium, and vitamin D. Her bone mineral density increased over the next 2 years. 

The recommended daily dose of sflicon has not yet been established. The total daily intake of sflicon in the diet is estimated to be 20 50 mg. Sflicon intake (e.g. in beer) can reportedly reduce the bioavaflabflity of aluminium, which has been imphcated as one of the possible causal factors contributing to Alzheimer s disease. Sflicone intake might also help to prevent bone thinning and osteoporosis. High doses of sflicon may contribute to the formation of kidney and urinary stones. 

Aluminium is the most widely used element in our daily lives. Some of the sources of aluminium include drinking water, food additives and cooking utensils made of aluminium. High amoxmts of aluminium have been reported to be mixed with mashed tomatoes and yogurt during processing from normal and noncoated aluminium pans as a result of acidity. Aluminium is not essential for life processes, but increased amounts have been linked to various disorders such as microcytic anaemia, bone disturbances, neurodegenerative disorders such as Alzheimer s disease (AD) and Parkinson s disease, amyotrophic lateral sclerosis and encephalopathy. Smaller studies have demonstrated that aluminium exposure is associated with the impairment of mitochondrial function in vitro. 

---