Proximal myopathy caused by latrogenic phosphate depletion

Ravid, M.

doi:10.1001/jama.236.12.1380

Cited by 8 publications

(3 citation statements)

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“…Rickets or osteomalacia, defined as a defect in bone mineralization, often occurs in individuals with long‐standing phosphorus deficiency. Chronic phosphorus deficiency in humans causes proximal myopathy 5 . Proximal muscle atrophy and weakness may be striking.…”

Section: Introductionmentioning

confidence: 99%

Dietary phosphorus in bone health and quality of life

et al. 2012

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Awareness of phosphorus intake is important because both phosphorus deficiency and overloading impair bone health and quality of life. Phosphorus consumption is increasing in many countries. Most dietary phosphorus is contained in protein-rich foods such as meat, milk, cheese, poultry, fish, and processed foods that contain phosphate-based additives to improve their consistency and appearance. Elevation of extracellular phosphorus levels causes endothelial dysfunction and medial calcification, which are closely associated with the development of cardiovascular disease (CVD). Long-term excessive phosphorus loading, even if it does not cause hyperphosphatemia, can be a risk factor for CVD. In epidemiological studies, higher levels of phosphorus intake have been associated with reduced blood pressure. Interestingly, when examined further, phosphorus from dairy products, but not from other sources, was usually associated with lower blood pressure. A dietary approach to phosphorus reduction is particularly important to prevent bone impairment and CVD in patients with chronic kidney disease. In order to improve bone health and quality of life in the general population, the impact of phosphorous, including in processed foods, should be considered, and measures to indicate the amount of phosphorous in food products should be implemented.

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Section: Introductionmentioning

confidence: 99%

Dietary phosphorus in bone health and quality of life

et al. 2012

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“…These studies suggest that INTRODUCTION Hypophosphatemia and intracellular deficiency of inorganic phosphate result in dysfunction of a wide range of organ systems in man and experimental animals. Erythrocyte hemolysis (1-3), derangements in the mechanical and phagocytic properties of leukocytes (1, 4), decreased survival and abnormal function of platelets (1,5), central nervous system abnormalities compatible with metabolic encephalopathy (1,6,7), abnormalities in renal function (1,8), and cardiac (1,(9)(10)(11)13), and skeletal myopathy (1,(12)(13)(14)(15)(16)(17) have been described in patients or animals with phosphate deficiency.…”

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confidence: 99%

Defective adenosine triphosphate synthesis. An explanation for skeletal muscle dysfunction in phosphate-deficient mice.

Hettleman¹,

Sabina²,

Drezner³

et al. 1983

J. Clin. Invest.

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A B S T R A C T The basis for skeletal muscle dysfunction in phosphate-deficient patients and animals is not known, but it is hypothesized that intracellular phosphate deficiency leads to a defect in ATP synthesis. To test this hypothesis, changes in muscle function and nucleotide metabolism were studied in an animal model of hypophosphatemia. Mice were made hypophosphatemic through restriction of dietary phosphate intake. Gastrocnemius function was assessed in situ by recording isometric tension developed after stimulation of the nerve innervating this muscle. Changes in purine nucleotide, nucleoside, and base content of the muscle were quantitated at several time points during stimulation and recovery.Serum concentration and skeletal muscle content of phosphorous are reduced by 55 and 45%, respectively, in the dietary restricted animals. The gastrocnemius muscle of the phosphate-deficient mice fatigues more rapidly compared with control mice. ATP and creatine phosphate content fall to a comparable extent during fatigue in the muscle from both groups of animals; AMP, inosine, and hypoxanthine (indices of ATP catabolism) appear in higher concentration in the muscle of phosphate-deficient animals. Since total ATP use in contracting muscle is closely linked to total developed tension, we conclude that the comparable drop in ATP content in association with a more rapid loss of tension is best explained by a slower rate of ATP synthesis in the muscle of phosphate-deficient animals. During the period of recovery after muscle stimulation, ATP use for contraction is minimal, since the muscle is at rest. In the recovery period, ATP content returns to resting levels more slowly in the phosphate-deficient than in the control animals. In association with the slower rate of ATP repletion, the precursors inosine monophosphate and AMP remain elevated for a longer period of time in the muscle of phosphate-deficient animals. The slower rate of ATP repletion correlates with delayed return of normal muscle contractility in the phosphate-deficient mice. These studies suggest that the slower rate of repletion of the ATP pool may be the consequence of a slower rate of ATP synthesis and this is in part responsible for the delayed recovery of normal muscle contractility.

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“…Consequently, a phosphate-deprived state may be associated with decreased ATP synthesis and increased formation ofATP degradation products. Indeed, hypophosphatemia increases ATP degradation products in skeletal muscle (5,6) and is correlated with a myriad of clinical manifestations in-cluding hemolytic anemia, respiratory failure, myopathy, and neurologic abnormalities in humans (7)(8)(9)(10)(11)(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%