Abstract
An ICP-OES method has been developed to estimate Calcium and Phosphorous in In vitro phosphate binding study of Eliphos Tablets. The method is selective and is capable of detecting calcium and phosphorous in the presence of other trace elements. The method has been validated using RF power of 1500 watts, plasma flow of 15L/min, Nebuliser flow of 0.8 L/min and plasma view at radial mode for calcium and axial mode for phosphorus. The wavelength was monitored for calcium and phosphorous at 317.933 nm and 213.677 nm respectively. The method has been validated in terms of specificity, precision, linearity, accuracy, limit of quantification and ruggedness. The In vitro binding studies were performed for Eliphos Tablets at eight dif- ferent phosphate concentrations by incubating at 37.0?C and analysis was performed using the validated method to estimate free calcium and phosphorus. The objective of the study is to provide an alternate In vitro method to estimate the binding capacity of calcium acetate tablets to avoid the expensive in-vivo bio clinical studies.
Highlights
Calcium Acetate is the Active ingredient in Eliphos TabletsTM and is indicated for haemodialysis and peritoneal dialysis
The method has been validated in terms of specificity, precision, linearity, accuracy, limit of quantification and ruggedness
This paper describes the methodology and validation it includes the study of In vitro phosphate binding of Eliphos Tablets 667 mg by Inductively Coupled Plasma
Summary
Calcium Acetate is the Active ingredient in Eliphos TabletsTM and is indicated for haemodialysis and peritoneal dialysis. Blood levels of phosphate may raise leading to bone problems. Calcium Acetate binds phosphate in the diet to lower blood phosphate levels. This medication is used in kidney disease to control blood phosphate. Phosphorus is an essential element necessary for the normal function of human body, required for skeletal construction and synthesis of DNA, proteins and adenosine Triphosphate. Serum phosphorus concentrations are maintained between 2.5 and 4.5 mg/dL through diet and renal excretion. The body’s compensation mechanisms cause secondary hyperparathyroidism and renal osteodystrophy
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