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Research Article| Volume 7, ISSUE 1, P201-214, January 1991

Hypophosphatemia and Hyperphosphatemia

  • Michael P. Peppers
    Correspondence
    Address reprint requests to: Michael P. Peppers, BS, PharmD RPh Coodinator of Clinical Services Department of Pharmacy Mineral Area Regional Medical Center Farmington, MO 63640
    Affiliations
    Currently, Coordinator of Clinical Services, Department of Pharmacy, Mineral Area Regional Medical Center, Farmington Missouri; Formerly, Clinical Specialist, Critical Care Department of Pharmacy Services, Detroit Receiving Hospital, Detroit, Michigan
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  • Michael Geheb
    Affiliations
    Associate Professor and Vice Chairman, Department of Internal Medicine, Wayne State University, Detroit, Michigan
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  • Tusar Desai
    Affiliations
    Assistant Professor of Medicine, Division of Gastroenterology, Wayne State University, Detroit, Michigan
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      Pathophysiology, clinical sequelae, and treatment for hypophosphatemia and hyperphosphatemia are discussed. Hypophosphatemia results from a variety of conditions including malnutrition, carbohydrate refeeding, acid-base disorders, and hormonal and drug effects. Patients suffering from severe hypophosphatemia may present with a variety of syndromes that can become detrimental and even life-threatening if this electrolyte depletion goes untreated. Hyperphosphatemia occurs because of increased extracellular phosphate load from either endogenous or exogenous sources or from a decrease in renal phosphate excretion. Left untreated, hyperphosphatemia can result in dangerous calcium-phosphate precipitation into vital organs and tissues.
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