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Effect of gastric acid suppression with pantoprazole on the efficacy of calcium carbonate as a phosphate binder in haemodialysis patients
Author(s) -
CERVELLI MATTHEW J,
SHAMAN AHMED,
MEADE ANTHONY,
CARROLL ROBERT,
MCDONALD STEPHEN P
Publication year - 2012
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1111/j.1440-1797.2012.01604.x
Subject(s) - pantoprazole , medicine , crossover study , calcium , phosphate , placebo , gastroenterology , calcium carbonate , parathyroid hormone , endocrinology , chemistry , biochemistry , omeprazole , alternative medicine , organic chemistry , pathology
Aim: Metallic phosphate binders require acidity to dissociate to the free metallic ion and bind phosphorus. Altered gastric acidity may, therefore, influence phosphate‐binding efficacy. We evaluated the clinical effect of pantoprazole on the efficacy of calcium carbonate phosphate binders in haemodialysis patients. Methods: The study had two parts: a cross‐sectional study ( n = 67), and an interventional, crossover, double‐blind, randomized, placebo‐controlled trial in 26 patients given pantoprazole 40 mg daily or placebo for two consecutive 6‐week periods. Results: The cross‐sectional study showed no difference between those on and off acid suppressants in phosphate (1.43 ± 0.45 vs 1.46 ± 0.31 mmol/L, P = 0.782) or other parameters except age (72.2 ± 9.8 vs 63.8 ± 14.8 years, P = 0.01). In the interventional study, phosphate was higher during pantoprazole than placebo (1.59 ± 0.3 vs 1.42 ± 0.3 mmol/L, P = 0.005). Serum calcium (2.37 ± 0.2 vs 2.46 ± 0.2 mmol/L, P = 0.012) and ionized calcium (1.17 ± 0.1 vs 1.22 ± 0.1 mmol/L, P = 0.013) were lower during pantoprazole treatment. CaxPO 4 (3.76 ± 0.7 vs 3.48 ± 0.7 mmol 2 /L 2 , P = 0.032) and intact parathyroid hormone (31.9 ± 21.4 vs 23.6 ± 17.7 pmol/L, P = 0.004) were higher on pantoprazole. Conclusion: These results demonstrate clinical evidence for an adverse effect of gastric acid suppression on the effectiveness of calcium carbonate phosphate binders. Given their frequent co‐prescription, this interaction may be a minor but common reason why some patients fail to control hyperphosphataemia. Clinicians should regularly assess the need for acid suppressants. Further studies are needed to investigate interactions with other phosphate binders.