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Background: Aluminium overload leads to parathyroid hormone (PTH) suppression. However, it is unclear whether a decrease in synthesis or release of the hormone is mainly involved. The aim of this study was to assess the effect of an acute administration of aluminium on PTH synthesis and release in rats with chronic renal failure and secondary hyperparathyroidism., Methods: The study was performed using 100 adult male Wistar rats (body weight 443+/-54 g). 7/8 nephrectomy was performed and the rats were maintained on a high dietary phosphorous intake. Five weeks after surgery, the rats were randomly divided into two groups, one loaded with aluminium (AlCl3) and the other given placebo. Aluminium or placebo were administered i.p. for two consecutive days. The placebo group received saline at the same pH as the aluminium solution. After 2 weeks, serum calcium, phosphorous, creatinine, PTH, and aluminium were measured. The parathyroid glands were removed and PTH messenger RNA (mRNA) was measured by northern blot. Intact PTH was measured by IRMA (Rat PTH, Nichols Institute)., Results: No differences in serum PTH levels were found between the two groups after 5 weeks of renal failure. At the end of the study the rats given aluminium had higher aluminium levels than the placebo group and lower PTH levels. No significant differences were found for calcium, phosphorous, renal function, or body weight. PTH mRNA expression was lower in the aluminium group than in the placebo group., Conclusion: The administration of aluminium in rats with chronic renal failure resulted in reductions in serum PTH and PTH mRNA. Thus far, previous studies had demonstrated that aluminium suppressed PTH release. The present findings suggest that PTH synthesis is also reduced.

The aim of this study was to compare the sensitivity and specificity of the two histochemical stains most commonly used as indirect markers of the aluminium bone content. The clinical study was made in 28 biopsies from patients undergoing haemodialysis and the experimental study in 17 tibias from Wistar rats aluminium overloaded and with different deposits of iron. All samples were stained with aluminon, solochrome azurine and Perls and aluminium bone content was also measured. When the positive cases with Perls were excluded in the clinical study (without iron interference), the trabecular surface stained with solochrome azurine correlated with the aluminium bone content (r = 0.71, P < 0.001). With aluminon, on the other hand, no correlation was found. Solochrome azurine was always positive with aluminium contents greater than 8 micrograms/g. Aluminon was positive over 17 micrograms/g. In the experimental study, the iron concentration, in addition to other parameters, was also measured. As in the clinical study, the trabecular surface stained with solochrome azurine correlated with the aluminium content. If the positive Perls cases were excluded, the trabecular surface stained with solochrome azurine doubled the trabecular surface stained with aluminon (P < 0.001). No intratrabecular aluminon staining was observed while the intratrabecular solochrome staining correlated with the aluminium content (P < 0.001). Solochrome azurine was more sensitive than the aluminon and its lack of specificity can be easily corrected by employing Perls staining to exclude the iron interference.

Background: The European Vertebral Osteoporosis Study Group (EVOS) developed a questionnaire, back translated into 14 different European languages, for use in a multinational epidemiological study of vertebral osteoporosis. We investigated the reproducibility of this questionnaire in four of the participating study centres., Methods: In all 151 men and women, aged 50-85 years, from Lubeck (Germany), Malmo (Sweden), Warsaw (Poland) and Oviedo (Northern Spain), were retested with the questionnaire on two occasions using a different observer within a 28-day period., Results: Questions relating to personal or medical history were more reproducible than questions concerning subjective symptoms or aspects of lifestyle. The level of agreement for the non-ordinal categorical variables, as estimated by kappa, varied from 0.38 to 1.00 across the four centres. Agreement for the multicategory ordinal, mainly lifestyle, questions was in general poorer though improved when a weighted analysis was performed. For continuous data the 95% limits of agreement were narrow, and there was no evidence of bias between interviewers. There were no important differences in reproducibility across the four centres for either categorical or continuous data., Conclusion: The study indicates that the questionnaire may produce useful and comparable information concerning risk factors for osteoporosis across different countries and in different languages. It also highlights that questionnaire instruments designed for use in multinational population-based studies may provide data of comparable quality across a range of settings.

In this study we have evaluated the haematological consequences of chronic aluminium (Al) overload. We have also investigated 'in vivo' whether aluminium overload may modulate gastrointestinal iron (Fe) absorption and 'in vitro' whether the presence of aluminium may influence the cellular uptake of iron. The in vivo studies were performed in rats with normal renal function and the in vitro experiments were done using the rat intestinal epithelial cell line RIE-1. The results demonstrate that aluminium deposit in tissues even with normal renal function. The intraperitoneal aluminium loading resulted in serum and tissue aluminium increases comparable with concentrations found in aluminium-intoxicated renal patients. The aluminium intoxication was accompanied by a microcytic anaemia with a haematological pattern similar to that observed in iron-deficiency anaemia. Nevertheless, iron absorption was significantly reduced despite an increased total iron binding capacity (TIBC). In addition, aluminium was also able to reduce in vitro cellular uptake of iron in the RIE-1 intestinal cell line. These experimental results demonstrate that aluminium interferes with iron absorption and iron transfer, and suggest that these mechanisms may be responsible for maintaining and even increasing the anaemia observed in aluminium overload.

The investigation of different aluminium-binding agents and metabolic conditions that might act as critical factors in modulating aluminium absorption could yield valuable information in the understanding of aluminium gastrointestinal absorption. We evaluated the effect of iron depletion in aluminium uptake and the role of transferrin and citrate in aluminium incorporation by the intestinal epithelial cell line RIE1. Both complex, aluminium-citrate and aluminium-transferrin were prepared in a molar ratio of 2:1; both facilitated the aluminium uptake although a greater aluminium incorporation was found when aluminium was administered as aluminium-transferrin. This difference became even greater in the iron-depleted cells (normal cells vs iron-depleted cells): 7.7 +/- 1.4 versus 30 +/- 5.6 ng Al/micrograms DNA (P less than 0.05). From these and previous data it is possible to speculate that iron status could modulate the intestinal uptake of aluminium and that both transferrin and citrate would act as effective carriers in the incorporation of aluminium into mucosal cells.