Background. Phosphate-induced hyperparathyroidism still represents an intriguing problem in dialysis patients. Postprandial hyperphosphataemia is considered to be the main stimulus to parathyroid hyperfunction, and therefore many efforts have focused on the use of phosphate binders to prevent phosphate absorption. Methods. We investigated whether the pH-mediated gastric ionization of calcium phosphate dietary salts is necessary for its intestinal absorption. In eight normal subjects we measured 24-h urinary calcium phosphate excretion and the postprandial blood calcium phosphate profile after a meal containing 1 g of calcium and 2 g of phosphate salts in a crossover placeboomeprazole study. On two occasions the subjects received either placebo or omeprazole 60 mg/day 2 days before and during the day test. Results.Serum gastrin levels were measured as an indicator of achlorhydria and were 13.7 ± 1 pg/ml after placebo and 30.4 ± 4.7 after omeprazole (P <0.003). Postprandial plasma phosphate profiles were not significantly different between the two studies (+ 36 ± 8% after placebo and + 24 ± 8% after omeprazole, NS), while plasma calcium increased by + 6.1 ± 1% after placebo and decreased by a 4.2 ± 0.7% after omeprazole (P < 0.01). The 24-h urinary phosphate excretion was 1068 ± 85 mg after placebo and 773 ± 55 after omeprazole (P < 0.002), while the 24-h urinary calcium excretion was 360 ± 21 after placebo and 238 ± 15 after omeprazole (P < 0.0001). A negative relationship was observed between absolute changes in plasma gastrin and those in urinary calcium (P < 0.009) and phosphate (P < 0.05). Conclusions. The inhibition of gastric acid secretion by omeprazole significantly reduces both urinary phosphate and calcium excretion after an oral load. The behaviour of the postprandial calcium-phosphate plasma profile suggests that gastric acid inhibition is more effective in reducing calcium rather than phosphate dietary salts absorption in normal subjects.
Effect of gastric acid secretion on intestinal phosphate and calcium absorption in normal subjects
A. Malesci;
1995-01-01
Abstract
Background. Phosphate-induced hyperparathyroidism still represents an intriguing problem in dialysis patients. Postprandial hyperphosphataemia is considered to be the main stimulus to parathyroid hyperfunction, and therefore many efforts have focused on the use of phosphate binders to prevent phosphate absorption. Methods. We investigated whether the pH-mediated gastric ionization of calcium phosphate dietary salts is necessary for its intestinal absorption. In eight normal subjects we measured 24-h urinary calcium phosphate excretion and the postprandial blood calcium phosphate profile after a meal containing 1 g of calcium and 2 g of phosphate salts in a crossover placeboomeprazole study. On two occasions the subjects received either placebo or omeprazole 60 mg/day 2 days before and during the day test. Results.Serum gastrin levels were measured as an indicator of achlorhydria and were 13.7 ± 1 pg/ml after placebo and 30.4 ± 4.7 after omeprazole (P <0.003). Postprandial plasma phosphate profiles were not significantly different between the two studies (+ 36 ± 8% after placebo and + 24 ± 8% after omeprazole, NS), while plasma calcium increased by + 6.1 ± 1% after placebo and decreased by a 4.2 ± 0.7% after omeprazole (P < 0.01). The 24-h urinary phosphate excretion was 1068 ± 85 mg after placebo and 773 ± 55 after omeprazole (P < 0.002), while the 24-h urinary calcium excretion was 360 ± 21 after placebo and 238 ± 15 after omeprazole (P < 0.0001). A negative relationship was observed between absolute changes in plasma gastrin and those in urinary calcium (P < 0.009) and phosphate (P < 0.05). Conclusions. The inhibition of gastric acid secretion by omeprazole significantly reduces both urinary phosphate and calcium excretion after an oral load. The behaviour of the postprandial calcium-phosphate plasma profile suggests that gastric acid inhibition is more effective in reducing calcium rather than phosphate dietary salts absorption in normal subjects.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
