title: Effect of gastric acid suppression with pantoprazole on the efficacy of sevelamer hydrochloride as a phosphate binder in haemodialysis patients: a pilot study.
abstract: Sevelamer hydrochloride (HCL) is thought to require an appropriately acidic environment in order to bind gastrointestinal phosphate. Changes in gastric acidity with acid suppressants may therefore alter the efficacy of sevelamer HCL. Given the widespread use of acid suppression therapy in chronic kidney disease patients, there is potential for a common significant drug interaction to occur. This pilot study evaluated the in vivo effect of gastric acid suppression with pantoprazole on the efficacy of sevelamer HCL as a phosphate binder in maintenance haemodialysis patients. The study protocol was a cross-over, double-blinded, randomized, placebo-controlled trial in 10 haemodialysis patients randomly assigned to pantoprazole 40 mg daily or placebo for two consecutive 6-week periods. Serum phosphate was not significantly altered during pantoprazole compared with placebo treatment (1.61 ± 0.45 mmol/L vs 1.76 ± 0.42 mmol/L, P = 0.204). There were no differences in serum calcium, parathyroid hormone and bicarbonate. This pilot study demonstrates preliminary in vivo evidence for no effect of gastric acid suppression on the effectiveness of sevelamer HCL. Our results are limited by small sample size and therefore, larger experimental studies should be conducted. Although our study did not find a significant drug interaction, given the high prevalence of acid suppressant use in dialysis patients, physicians should be aware of the potential influence of acid suppression on the efficacy of phosphate binders and regularly assess the clinical need for acid suppression therapy.
authors.affiliation: Department of Pharmacy, The Queen Elizabeth Hospital School of Pharmacy, University of South Australia, Australia.
authors.forename: Beryl
authors.initials: B
authors.lastname: Lai
authors.forename: Matthew J
authors.initials: MJ
authors.lastname: Cervelli
mesh_terms: D053799:2-Pyridinylmethylsulfinylbenzimidazoles / Q000627:therapeutic use*; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002614:Chelating Agents / Q000627:therapeutic use*; D018592:Cross-Over Studies; D004311:Double-Blind Method; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D006863:Hydrogen-Ion Concentration; D054559:Hyperphosphatemia / Q000097:blood / Q000188:drug therapy* / Q000209:etiology; D007674:Kidney Diseases / Q000097:blood / Q000150:complications / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D000077402:Pantoprazole; D010710:Phosphates / Q000097:blood; D010865:Pilot Projects; D010919:Placebos; D011073:Polyamines / Q000627:therapeutic use*; D054328:Proton Pump Inhibitors / Q000627:therapeutic use*; D006435:Renal Dialysis / Q000009:adverse effects; D000069603:Sevelamer; D013021:South Australia; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D015415:Biomarkers; D002614:Chelating Agents; D010710:Phosphates; D010919:Placebos; D011073:Polyamines; D054328:Proton Pump Inhibitors; D000069603:Sevelamer; D000077402:Pantoprazole