Postgraduate Medicine

ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20

Differential diagnosis of hypercalcemia David Juan To cite this article: David Juan (1979) Differential diagnosis of hypercalcemia, Postgraduate Medicine, 66:4, 72-81, DOI: 10.1080/00325481.1979.11715271 To link to this article: http://dx.doi.org/10.1080/00325481.1979.11715271

Published online: 07 Jul 2016.

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First of a group of four related articles in this issue

Differentiai diagnosis of hypercalcemia A mechanistic approach Consider Which form of calcium, ionized or bound, is more important physiologically? Of the pathogenic mechanisms of hypercalcemia, which is most common? What laboratory investigations are useful in determining the cause of hypercalcemia?

David Juan, MD

Hypercalcemia is often encountered in clinical practice, frequently in asymptomatic patients. The basis is usually an imbalance between boue resorption and boue formation. The history, pbysical examination, and appropriate laboratory and radiologie studies sbould allow definitive diagnosis.

Hypercalcemia presents clinically in a variety of ways. The practicing physician most commonly encounters the problem in asymptomatic patients routinely screened by multichannel biochemical analysis (SMA 6 or 12). In a large series from Sweden, 1 the incidence of hypercalcemia detected in this way was 3.9%. The second most common encounter is in patients with known malignant disease, primary hyperparathyroidism, or both. Third, the physician may suspect the presence of hypercalcemia on the basis of certain symptoms and signs, eg, vomiting, polyuria, polydipsia, fatigue, constipation, nephrolithiasis, soft-tissue calcification, and coma. This article reviews pathophysiology and differentiai diagnosis of hypercalcemia. Patbopbysiology Half of the calcium in blood is in ionized form and half is bound to albumin. Most laboratories have been measuring total calcium concentration. However, since the realization that the ionized form is more important physiologically than the bound form and is invariably elevated in clinically significant hypercalcemic states, many major medical centers have also begun to measure the ionized fraction. Three factors may alter the distribution of calcium in plasma: albumin concentration, acid-base disturbances, and protein abnormalities. In clinica} practice, hypoalbuminemia is found most often in patients with cirrhosis, nephrosis, or protein-losing enteropathy. Acidosis decreases continued

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Three factors may alter the dis· tribution of calcium in plasma: albumin concentration, acid-base balance, and protein abnormalities.

Downloaded by [Australian Catholic University] at 07:35 22 August 2017

Table1. Leu common causes of hypercalcemia and auociated mechaniama

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Cause

Mechaniam(a)

Commenta

Vitamin D intoxication

lncreased intestinal absorption of calcium

Usually diagnosed from history Soft-tissue calcification Measure 25-hydroxy-vitamin D, level Very responsive to steroid therapy Persists for months because of storage in fat

Vitamin A intoxication

lncreased bone resorption

Usually diagnosed from history Periosteal calcification Steroid-responsive

Sarcoidosis

Vitamin D hypersensitivity lncreased intestinal absorption of calcium

Rule out coïncident hyperparathyroidism Hypercalciuria more common than hypercalcemia (

Differential diagnosis of hypercalcemia: a mechanistic approach.

Postgraduate Medicine ISSN: 0032-5481 (Print) 1941-9260 (Online) Journal homepage: http://www.tandfonline.com/loi/ipgm20 Differential diagnosis of h...
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