Evidence for a Phosphorus-Depletion Syndrome in Man

Lotz, Myron; Zisman, Elias; Bartter, Frederic C.

doi:10.1056/nejm196802222780802

Cited by 467 publications

(123 citation statements)

References 27 publications

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“…Paraesthesia and tremors have been reported with severe hypophosphataemia and have been shown to resolve with phosphate administration [54]. A severe neuropathy which resembles Guillain-Barré syndrome has been reported in patients with a serum phosphate of less that 0.2 mmol.l À1 .…”

Section: Neurological Effectsmentioning

confidence: 99%

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

1998

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SummaryRoutine detection and treatment of hypophosphataemia on the intensive care unit is commonplace. Hypophosphataemia has been associated with a multitude of clinical effects and there are many associations between correction of hypophosphataemia and improvement in symptoms. However, there is no evidence at present to support the routine correction of hypophosphataemia in the absence of clinical symptoms or signs.

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Section: Neurological Effectsmentioning

confidence: 99%

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

1998

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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.…”

mentioning

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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“…who showed no alleviation in acidosis. In these 2 refractory cases, plasma calcium increased during the combined administration of DHT and Long-term administration of aluminum hydroxide gel has been reported to augment intestinal absorption of calcium (Lotz et al 1968;Ansari 1970). This suggests that the effects of calcium carbonate as an alkalinizing salt would be strengthened by the simultaneous administration of aluminum hydroxide gel.…”

Section: Resultsmentioning

confidence: 99%

“…Aluminum hydroxide gel, administered orally, does not affect the acid-base equilibrium (Hurst et al 1963), but long-term administration of aluminum hydroxide gel has been reported to augment intestinal absorption of calcium (Lotz et al 1968;Ansari 1970). Dihydrotachysterol (DHT) increases intestinal absorption of calcium not only in normal persons but also in patients with chronic renal failure (Liu and Chu 1943).…”

mentioning

confidence: 99%

Effect of oral administration of calcium carbonate, aluminum hydroxide gel and dihydrotachysterol on renal acidosis.

Ueda

Ikeda

Sasaki

et al. 1978

Tohoku J. Exp. Med.

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Evidence for a Phosphorus-Depletion Syndrome in Man

Cited by 467 publications

References 27 publications

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

HypophosphataemiaPathophysiology, effects and management on the intensive care unit

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

Effect of oral administration of calcium carbonate, aluminum hydroxide gel and dihydrotachysterol on renal acidosis.

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