Phosphorus Depletion in Limb and Respiratory Muscles of Patients with Chronic Obstructive Pulmonary Disease (COPD): A Preliminary Report

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