Abstract
Phosphorus plays a key role in cellular biochemical reactions responsible for energy production, storage, and utilization and represents a major component of membranes and other cell structures: thus, the maintenance of normal phosphorus balance and both normal serum and cellular phosphorus levels is critical for the normal function of the organism.1,2 In both experimental and clinical conditions hypophosphatemia and phosphorus depletion are associated with a wide spectrum of clinical syndromes such as myocardial failure, hepatocellular damage, hemolysis, platelet and leucocyte disfunction, osteomalacia and spontaneous fractures, hypoparathyroidism, impaired glucose tolerance, etc.3 Moreover, neurologic and neuromuscular signs and symptoms such as ataxia, confusion, delirium, tremor, hyporeflexia, skeletal muscle weakness, and rhabdomyolysis have been observed.1,3 Hypophosphatemia and/or phosphorus depletion have been equally indicated as possible determinants of respiratory muscle weakness in the course of respiratory failure.4,5 In fact, an impairment of respiratory muscle contractile properties has been demonstrated in the course of hypophosphatemia, which improves with phosphorus repletion.6,7 Hypophosphatemia is a common finding in the course of respiratory illnesses, with a prevalence of about 25%; in 5% of the same patients serum phosphate (Ps) levels may be extremely low (less than 1 mg% or 0.33 mmol/1).8,9
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© 1991 Springer-Verlag Italia
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Fiaccadori, E. et al. (1991). Phosphorus Depletion in Limb and Respiratory Muscles of Patients with Chronic Obstructive Pulmonary Disease (COPD): A Preliminary Report. In: Grassino, A., Rampulla, C., Ambrosino, N., Fracchia, C. (eds) Chronic Pulmonary Hyperinflation. Current Topics in Rehabilitation. Springer, London. https://doi.org/10.1007/978-1-4471-3782-5_14
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DOI: https://doi.org/10.1007/978-1-4471-3782-5_14
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