Some Problems of Hyperparathyroidism

Dent, C. E.

doi:10.1136/bmj.2.5317.1419

Cited by 248 publications

(73 citation statements)

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“…Ideally the patient should be fasting but in our experience this is not essential as increments in plasma calcium concentration have been found to be, at the most, 0.5--0.8 mgfl00 ml after normal meals or even large oral calcium loads (Wills, unpublished data). The use of a protein correction factor as proposed by Dent (1962) is of value in the interpretation ofplasma calcium values if 'artificially' high values due to venous stasis are to be excluded. The use of such a factor is also of value in comparing Urinary calcium themselves little help in the differentiation of the hypercalcaemia of primary hyperparathyroidism from that due to other causes.…”

Section: Plasma Calciummentioning

confidence: 99%

Laboratory Tests in the Differentiation of Hyperparathyroidism from other Causes of Hypercalcaemia

Wills

1970

Ann Clin Biochem

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Section: Plasma Calciummentioning

confidence: 99%

Laboratory Tests in the Differentiation of Hyperparathyroidism from other Causes of Hypercalcaemia

Wills

1970

Ann Clin Biochem

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“…Parathyroid extract3 (PTE) was given subcutaneously in rotated sites. Blood samples in these special 5 studies were always obtained in the fasting state in the 5 45 morning to minimize the effect of diurnal and dietary F variation; all serum calcium values were corrected to @ a standard specific gravity of 1.027 [14]. Figure 2A indicates the relation of the initial calcium value to the urinary amino acid excretion; figure 2 B shows the relation of initial phosphorus value to urinary amino acid excretion in the same patients.…”

Section: Methodsmentioning

confidence: 99%

Hyperparathyroidism as the Cause of Hyperaminoaciduia and Phosphaturia in Human Vitamin D Deficiency

1967

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ExtractThirty-nine infants with simple vitamin D deficiency were studied; three stages of deficiency were recognized. Stage I comprised hypocalcemia, usually as the sole important biochemical finding, while convulsions were a common clinical sign. Stage I1 revealed normocalcemia with hyperaminoaciduria, hypophosphatemia, and hyperphosphaturia; rickets was also in evidence. Stage I11 was comparable to stage 11, but with recurrence of hypocalcemia and convulsions, the rickets was more severe. Patients progressed spontaneously from the early to the later stages of the deficiency syndrome; administration of parathyroid extract appeared to accelerate the rate of progression. Calcium infusion and vitamin D therapy each initially raised the serum calcium level in hypocalcemic patients; thereafter, aminoaciduria and hyperphosphaturia were suppressed.These diverse observations were interpreted in accordance with current knowledge of vitamin D and parathyroid hormone interrelations. The acquired excretory abnormality involving amino acid and phosphorus is the result of impaired tubular absorption; this defect is considered to be dependent on the development of endogenous reactive hyperparathyroidism, and not dependent on cellular deficiency of vitamin Dper se. The stimulus for the hyperparathyroidism is hypocalcemia induced by deficiency of vitamin D. Normocalcemia is restored if sufficient vitamin D is present in cellular membranes to amplify the stimulative action of parathyroid hormone on intestinal transport of calcium and its release from bone. Severe deficiency of vitamin D blocks this regulatory effect upon calcium, but does not block the inhibitory effect of parathyroid hormone on renal tubular transport of amino acids and phosphorus. SpeculationAn excess of parathyroid hormone rather than a simple deficiency of vitamin D at the renal tubular epithelial cell appears to cause the disturbance of transport affecting the absorption phosphorus, amino acids and other solutes. This impairment of function is the price paid in renal cellular economy for the conservation of calcium. The cellular mechanisms underlying this coexistent inhibitory effect of parathyroid hormone constitutes an important and fascinating subject for further investigation.

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“…The preceding meal will also reveal any peptic ulceration or stenosis. (Bowden & Patston, 1963) and all values were corrected for total serum protein, as suggested by Dent (1962). The normal range of plasma calcium in this laboratory is 8-4-10-5 mg/ 100 ml.…”

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confidence: 99%

“…Rarely, the raised serum calcium does not respond to steroids, and may only fall when the hyperthyroidism is controlled (David, Verner & Engel, 1962). Very occasionally, the hypercalcaemia of hyperparathyroidism may be suppressed by steroids (Gwinup & Sayle, 1961;Dent, 1962;Hodges & Waterhouse, 1967;Garcia & Yendt, 1968).…”

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confidence: 99%