Osteomalacia aluminium hydroxide

Chronic aluminium hydroxide antacid intake (600 cm weekly) can cause osteomalacia... 

B26. Bloom, W. L., and Flinchum, D., Osteomalacia with pseudo-fractures caused by the ingestion of aluminium hydroxide. /. Am. Med. Assoc. 174, 1327-1330 (1960). 

It is possible that aluminium may be involved in the development of encephalopathy and also of osteomalacia in haemodialysed patients (aluminium salts are present in the dialysate water and aluminium hydroxide is administered to control the hyperphosphataemia). Aluminium is thought to accumulate in the bone and interfere with mineralization processes. 

Discussion on the safety of aluminium has continued since the report briefly cited in SED VIII (p. 791) of a patient with osteomalacia due to excessive ingestion of aluminium hydroxide (I -). 

This patient, a 49-year-old woman, had since January 1971 taken large amounts of aluminium-containing antacids, amounting latterly to an intake of about 20 g aluminium hydroxide daily. In 1973 the patient was admitted for pain in the left hip, weakness and difficulty in walking. The patient appeared to have a low plasma phosphorus level, raised alkaline phosphatase, and a high calcium and low phosphorus urinary content. A bone marrow biopsy was consistent with osteomalacia. 

Baker et al. (6 ) have described hypo-phosphataemia, associated with osteomalacia and myopathy, in a patient on regular haemodialysis. The patient recovered after the use of aluminium hydroxide had been discontinued. For some comments on aluminium hydroxide from the gastro-enterologi-cal point of view, the reader is referred to Chapter 35. 

Dent, C. E. and Winter, C.S. (1974) Osteomalacia due to phosphate depletion from excessive aluminium hydroxide ingestion. Brit. med. J.,23,551. 

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. 

---