Microsoft Word - NEF089BF

Dr. K. Farrington, Renal Unit, Lister Hospital Stevenage, Coreys Mill Lane, Stevenage, Herts SG1 4AB (UK) Dear Sir, Calcium carbonate is the most commonly used phosphate binder in chronic renal failure (CRF). Recently it has been shown that its phosphate-binding capacity is limited at low pH [1]. This study was performed to assess the effect of the proton pump inhibitor omeprazole on the phosphate-binding capacity of calcium carbonate. Six normal subjects aged 25-44 years were studied. Subjects fasted for 10 h prior to and during each of the 3 phases of the study. Each phase commenced at 09.00 h on 3 separate days within a 2-week period. Phase 1. After a baseline blood sample (5 ml) an oral phosphate load consisting of 17.4 g of disodium hydrogen phosphate B.R (1.5 g of elemental phosphate) dissolved in 200 ml of water was administered over a 2-min period [2]. Further 5-ml samples were taken at 30,60, 90, 120 and 180 min. Samples were centrifuged immediately and the serum stored for later analysis of total calcium and phosphate concentrations. Phase 2. The protocol was identical to phase 1 except that the administration of the phosphate load was immediately preceded by the oral administration of calcium carbonate (Calcichew, Shire pharmaceuticals Ltd.) in a dose of 1.5 g of elemental calcium. Phase 3. The protocol was identical to phase 2 except that omeprazole (Losec, Astra pharmaceuticals Ltd.) (20 mg) was administered at 22.00 h on the day preceding the study and again at 08.00 h on the day of the study. The increments in serum phosphate levels in response to oral phosphate loading were calculated by subtracting the baseline serum phosphate level from values obtained at 30, 60, 90, 120 and 180 min after the oral phosphate load. The results in each phase of the study are shown in the figure. The mean area under the phosphate increment curve obtained after oral phosphate loading alone (phase 1) was 40.6 ± 16.8 (SD) mmol 1> min. This was significantly reduced by prior in-gestion of calcium carbonate (phase 2) to 20.5 + 10.5 mmol 1-’ min (p = 0.008 by paired t test, 95% confidence interval for the mean difference = 8.01-32). The prior ingestion of both calcium carbonate and omeprazole (phase 3) produced a further significant reduction to 14.0 ± 9.7 mmol l-1 min (p = 0.035, 95% confidence interval = 0.69-12.4). The changes in serum calcium level in each phase of the study were calculated in a similar fashion. The mean area under the calcium increment curve (fig. 1) obtained after oral phosphate loading alone (phase 1) was –7.53 ± 5.63 mmol L1 min. Prior ingestion of calcium carbonate (phase 2) caused a