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The Hypercalcemia of Adrenal Insufficiency

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The Hypercalcemia of Adrenal Insufficiency THE HYPERCALCEMIA OF ADRENAL INSUFFICIENCY Mackenzie Walser, … , Brian H. B. Robinson, John W. Duckett Jr. J Clin Invest. 1963;42(4):456-465. https://doi.org/10.1172/JCI104734. Research Article Find the latest version: https://jci.me/104734/pdf Journal of Clinical Investigation Vol. 42, No. 4, 1963 THE HYPERCALCEMIA OF ADRENAL INSUFFICIENCY * By MACKENZIE WALSER, BRIAN H. B. ROBINSON,t AND JOHN W. DUCKETT, JR.t (From the Department of Pharinacology and Experimental Therapeutics and the Departmnent of Medicine, The Johns Hopkins University School of Medicine and The Johns Hopkins Hospital, Baltimore, Md.) (Submitted for publication October 3, 1962; accepted December 6, 1962) An interrelationship between the adrenal glands cium in this condition appear to have been re- and calcium metabolism was demonstrated in 1911 ported. Increased parathyroid gland activity dur- by Guleke (1), who showed that adrenalectomy ing adrenal insufficiency was suggested by the re- ameliorates tetany in parathyroidectomized ani- ported finding of parathyroid hyperplasia in mals. This observation has been repeatedly con- adrenalectomized animals (23). Against this firmed (2). view is the occurrence of hypercalcemia in adre- Hypercalcemia after adrenalectomy was first nalectomized parathyroidectomized dogs (22), as demonstrated in 1924 by Kisch (3) in rabbits, and well as the antagonistic effects of cortisone and soon thereafter by other workers in dogs (4-8), parathyroid extract mentioned above. cats (5, 9), and in patients with Addison's disease Adrenal steroids block the excessive intestinal (10-12). An early report (13) of hypercalcemia absorption of calcium in sarcoidosis (24) and tend in adrenalectomized rats was based upon dubious to inhibit the active transport of calcium by the methods of analysis; later reports indicate that isolated gut (25). Calcium absorption might plasma calcium remains constant or falls in this therefore be excessive in adrenal insufficiency. species after adrenalectomy (14-16). Balance studies in an Addisonian subject (26) and Administration of adrenocortical steroids often in adrenalectomized rats (27) do not support this ameliorates spontaneous hypercalcemia (17), ex- possibility. The same objections apply to the hy- cept when it is caused by hyperparathyroidism ( 18). pothesis that cortisone acts by antagonizing the in- Nevertheless, in rats cortisone modifies or prevents testinal action of vitamin D. The possibility that the hypercalcemic response to parathyroid extract the skeletal actions of vitamin D are antagonized (16, 2). This discrepancy may be a matter of by adrenal steroids has not been excluded, al- dosage, since large amounts of steroids may some- though the morphologic effects of vitamin D de- times reduce plasma calcium even in hyperpara- ficiency and steroid excess on bone are quite dif- thyroidism (19, 20). In normal subjects, adminis- ferent (28). tration of adrenocortical steroids has little effect Steroid administration and hypercorticism are on plasma calcium concentration, and Cushing's usually associated with increased urinary calcium disease is not associated with hypocalcemia. A excretion (29, 30). After withdrawal of hormone report of hypercalcemia after cortisone adm-ninistra- therapy in Addison's disease (26), urinary excre- tion to nephrectomized dogs (21) has not been tion of calcium may fall. Contrary results have confirmed (22). also been reported (31). In hypercalcemic states Several hypotheses have been advanced to ex- treated with steroids, urinary calcium excretion plain these observations. The possibility that falls concomitantly with the reduction in plasma hemoconcentration might explain the hypercal- calcium (22) ; clearly this effect on plasma calcium cemia of adrenal insufficiency was suggested by the cannot be ascribed to a renal effect of the hormone. earliest workers; however, no mneasurenments of Nevertheless, a renal role in the hypercalcemia of plasma protein concentration or ultrafiltrable cal- adrenal insufficiency remains a possibility. Finally, evidence for a direct action of adrenal * Supported by U. S. Public Health Service grant A-2306. steroids on the equilibrium between bone and ex- t Present address: Guy's Hospital, London, England. tracellular fluid has been presented (32). Ap- t Present address: Peter Bent Brigham Hospital, parently it has not been determined whether Boston, Mass. changes in ionic calcium concentration or some 456 THE HYPERCALCEMIA OF ADRENAL INSUFFICIENCY 457 relevant ion product occur in hyper- and hypo- and litter-mate controls weighing 150 to 200 g were ob- adrenal states as plasma calcium concentration tained the day after operation 1 and placed on diets of either milk or sodium-free milk (Lonalac) containing changes. 20% dextrose. Each day for 5 days, groups of animals In the present study, the incidence of hypercal- were anesthetized with ether and exsanguinated via the cemia in adrenocortical insufficiency has been ex- abdominal aorta. The adrenal regions were inspected amined in three species, man, dog. and rat, and to confirm completeness of adrenalectomy. the mechanism of this change has been investigated Dogs. Male and female mongrel dogs weighing from in the dog. 7 to 16 kg were used. Twenty-five successful bilateral adrenalectomies were performed in one or two stages In studying the incidence of hypercalcemia, it through flank incisions under pentobarbital anesthesia. is necessary to establish some criterion for adrenal Cortisone,' desoxycorticosterone,3 and antibiotics were insufficiency. The absence of adrenal function is provided postoperatively and when required. From time clearly an inadequate criterion for this purpose. to time, hormone therapy was withdrawn and daily blood since the syndrome of adrenal insufficiency samples were obtained until frank adrenal insufficiency may developed. This required from 2 to 10 days (usually 4 fail to occur in adrenalectomized animals main- to 6) and was heralded by loss of appetite and decline in tained on salt alone, whereas adrenal crisis may weight. develop despite hormone therapy under conditions Three feeding regimens were employed: canned dog of stress. One of the most characteristic features meat supplemented with sodium chloride and sodium bi- of the syndrome of adrenal insufficiency is hypo- carbonate, sweetened milk freed of calcium and magnes- ium, and ordinary dog chow. The milk diet was pre- natremia. Therefore the incidence of hypercalce- pared by passing homogenized pasteurized cow's milk mia has been compared with the incidence of hy- through a well-washed 10 X 50 cm column of Dowex Al ponatremia in patients with Addison's disease and resin in the sodium form, acidifying to pH 6 to 7 with in adrenalectomized dogs. In rats, hypercalcemia HCl, adding 200 g dextrose per L, and freezing 400-ml failed to occur after adrenalectomy. so no further samples in plastic containers. Neither calcium nor mag- nesium could be detected in this material. Sodium con- study of this species was made. centrations varied from 100 to 120 mEq per L. Activated In examining the mechanism of this form of charcoal was mixed with the resin in order to remove a hypercalcemia. observations in human subjects bitter-tasting material which this resin releases. The are not readily available because patients with the rate of onset of symptoms of adrenal insufficiency was of adrenal insufficiency are uncommon not appreciably different with any of these three regi- syndrome mens. and are treated as soon as the diagnosis is made. Venous blood samples, usually from the jugular vein, Therefore the mechanism of this disturbance has were obtained in syringes containing heparin. been studied in dogs. AtnalWtical methods The methods for determination of plasma pH, protein MATERIALS AND METHODS concentration, calcium, magnesium, sodium, potassium, Subjetcts phosphate, and citrate were the same as those cited in Patients. Records of 31 patients with Addison's disease previous reports from this laboratory (33, 34). Ultra- have been collected in which hyponatremia, or hypercal- filtrates were prepared from a number of samples, and cemia, or both have been observed in a single blood the concentration of free calcium ions and free magnesium sample or in a single day. These include both treated ions was determined spectrophotometrically (33). It was and untreated subjects. WN:e have arbitrarily selected 135 not possible to perform all of the determinations on every mEq per L as the lowter limit of normal sodium concen- sample. Consequently, in the calculation of individual tration and 11 mg per 100 ml (2.75 mmoles per L) as calcium complexes in plasma ultrafiltrate (34), values the upper limit of normal calcium concentration. Sixty for magnesium ion concentration have been assumed cases of proven Addison's disease in the records of the when not available Johns Hopkins Hospital have been examined, and 22 re- ports have been found of analyses of blood samples from RESULTS sixteen cases that meet these criteria. Apart from scat- Incidence of in adrenal insufficiency tered reports of one or two cases, the only published ac- hypercalcemtia counts that include appreciable numbers of calcium de- In miani. In Figure 1, plasma calcium concentra- terminations in Addisonian patients appear to be those tions have been plotted against plasma sodium of Loeb (10), Helve (11) and Leeksma, De Graeff, and De Cock (12). The results of these authors are in- 1 Charles River Breeding Laboratories, Boston, Mass. cluded in Figure 1. 2 17a,21-dihydroxy-4-pregnene-3,11,20-trione.
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