Efficacy, tolerability, and safety of lanthanum carbonate in hyperphosphatemia: a 6-month, randomized, comparative trial versus calcium carbonate.

BACKGROUND/AIMS: Hyperphosphatemia is an important clinical consequence of renal failure, and its multiple adverse systemic effects are associated with significantly increased risks of morbidity and mortality in dialysis patients. Existing oral phosphate binders have not permitted control of serum phosphate within currently accepted guidelines. This study compares lanthanum carbonate with calcium carbonate for control of serum phosphate in hemodialysis patients. METHODS: In this European multicentre study, 800 patients were randomised to receive either lanthanum or calcium carbonate and the dose titrated over 5 weeks to achieve control of serum phosphate. Serum levels of phosphate, calcium and parathryoid hormone were followed over the following 20 weeks. RESULTS: Around 65% of patients in each group achieved phosphate control, but in the calcium carbonate group this was at the expense of significant hypercalcemia (20.2% of patients vs. 0.4%). Consequently, calcium x phosphate product tended to be better controlled in the lanthanum group. CONCLUSION: This 6-month study demonstrates that serum phosphate control with lanthanum carbonate (750-3,000 mg/day) is similar to that seen with calcium carbonate (1,500-9,000 mg/day), but with a significantly reduced incidence of hypercalcemia. Lanthanum carbonate is well tolerated and may be more effective in reducing calcium x phosphate product than calcium carbonate.

Thyroid function after bronchography with propyliodone.

Thyroid function was studied in 27 subjects who underwent bronchography with propyliodone (18-70 ml, containing 30% of organic iodine). Sustained elevations of serum non-hormonal iodine were observed, indicating that significant amounts of propyliodone were absorbed from the bronchial tree and also that elimination may take several weeks. During the period of anaesthesia, there was an increase in thyroxine-binding globulin and all thyroid hormones which was transient and probably reflected vascular response to the anaesthetic. T4-T3 conversion was inhibited with a nadir of T3 and a peak of rT3 occurring on the 2nd day after propyliodone exposure. FT4 increased gradually during the 2 weeks after bronchography, but remained within the normal range. 6 out of the 27 patients developed pathologic T4 levels, 3 elevated T3 levels, and 2 an abnormal response to thyrotropin-releasing hormone; these changes might have been confused with hyperthyroidism. None of the patients developed clinical thyrotoxicosis; however, in patients with autonomous thyroid tissue, the same precautions should be taken with propyliodone as with other iodine-containing agents which are known to induce hyperthyroidism in this situation.