The clinical biochemistry of aluminum.

The methods for aluminum analysis vary from the simple and often nonspecific chemical and physical procedures to the highly sophisticated types such as neutron activation and atomic absorption spectrometry. Atomic absorption procedures are the techniques of choice for most routine hospital laboratories. The wide distribution of aluminum in nature can create severe contamination problems in aluminum analysis. Procedures to avoid contamination are discussed. In recent years aluminum has been implicated as a possible etiological agent in DES and in Alzheimer's Disease. A common finding in these two conditions is an elevated brain aluminum content. The patients with Alzheimer's Disease develop characteristic neurofibrillary tangles which lead to the degeneration of the affected neurons. Similar tangles can be induced in laboratory animals injected intracerebrally with aluminum salts. Even though the laboratory animals develop tangles resembling those seen in patients with Alzheimer's Disease, no evidence has been published to show that the tangles seen in Alzheimer's Disease are induced by the elevated brain aluminum content. Although there are some similar clinical symptoms in both Alzheimer's Disease and DES, the hemodialysis patients with DES do not develop neurofibrillary tangles despite an elevated brain aluminum content. The significance of this difference is not understood. The sources of the increase in tissue aluminum levels found in hemodialysis patients are from the gastrointestinal absorption of aluminum in aluminum containing phosphate-binding gels and by transfer from the dialyzate to the blood during the hemodialysis procedure. Plasma aluminum values may be reduced by the administration of a minimum dosage of phosphate-binding gels and by the use of purified water to make up the dialysate. The incidence of DES is reduced by the use of these procedures to maintain the hemodialysis patients' plasma aluminum at a low concentration. The increased brain aluminum content of patients with Alzheimer's Disease is derived from the environment. Because of the ubiquitous occurrence of aluminum, we are exposed to it daily in our food, water, and in the air. The low levels of aluminum absorbed from the environment may explain why susceptible patients do not develop Alzheimer's Disease until after many years of exposure, if indeed aluminum is the etiological agent in Alzheimer's Disease. The many papers that have been published concerning aluminum, DES, and Alzheimer's Disease make a strong case for linking elevated tissue aluminum content with these conditions. However, conclusive evidence to support this theory has not been published. Until the effect of aluminum on cellular chemistry is more fully understood, the possibility that DES and Alzheimer's Disease may result from other causes or from aluminum and another agent acting concomitantly must be considered.