She had been recently started on levothyroxine for primary hypothyroidism. She was hypotensive and tachycardic. Adrenal autoantibodies were positive confirming primary autoimmune adrenal insufficiency. Steroid replacement was instituted; observations normalised within a day and calcium corrected spontaneously in 3 days.
Pathophysiology is attributed to increased calcium mobilisation from bone stores, increased gut absorption, decreased eGFR secondary to hypovolaemia - and so increased calcium reabsorption in the proximal tubule concurrent with sodium uptake. Corticosteroid replacement results in calciuresis and improves creatinine clearance so calcium levels rapidly normalise.
Conclusions: 1. The clinical picture may overlap with that of primary hypercalcaemia so the diagnosis is important to consider.
Thyroid replacement therapy mediates increased calcium mobilisation from bone in the setting of corticosteroid deficiency - contributing to hypercalcaemia. Hypercalcemia can lead to a decrease in the glomerular filtration rate mediated by direct renal vasoconstriction and natriuresis-induced volume contraction. However, the patient had hypotension and UTI at the arrival of emergency department and these could have had influence on the renal function.
Patients with hypercalcemia can develop mild hypomagnesemia. This is partially explained by the fact that calcium and magnesium functionally compete for transport in the thick ascending limb of the loop of Henle. Although the PTH level was not checked after the normalization of calcium and magnesium level, considering the change in magnesium level along with calcium level, we speculate that hypercalcemia caused hypomagnesemia and that both hypercalcemia and hypomagnesemia suppressed the PTH level.
Though the mechanism of hypercalcemia in adrenal insufficiency is unknown in detail, a number of mechanisms are thought to be the possible cause. First, adrenal insufficiency causes hypovolemia and a consequent reduction in glomerular infiltration rate. Decreased glomerular infiltration rate results in reduction in the amount of calcium filtered at the glomerulus, and increased calcium renal reabsorption in proximal tubule.
Second, the enzyme activity of 1-alpha-hydroxylase may be increased in adrenal insufficiency. The 1-alpha-hydroxylase is a renal enzyme that participates in conversion of calcidiol to the active form of vitamin D, calcitriol, leading to increased intestinal absorption of calcium.
Third, a decrease in circulating stanniocalcin, a paracrine hormone secreted from the adrenal gland, could result in reduced levels of circulating calcium. Deficient adrenal hormone and decreased level of stanniocalcin may affect skeletal calcium efflux into circulation and result in hypercalcemia.
In conclusion, this case shows that adrenal insufficiency may cause hypercalcemia, and it can present as hypotension and AKI. After excluding more common diseases, such as malignancy and primary hyperparathyroidism, the possibility of adrenal insufficiency should be considered the cause of hypercalcemia, especially in elderly patients with a history of glucocorticoid injection.
Written informed consent and ethical approval from a review board were unnecessary because it was a retrospective case review.
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Abstract Adrenal insufficiency is an uncommon cause of hypercalcemia and not easily considered as an etiology of adrenal insufficiency in clinical practice, as not all cases of adrenal insufficiency manifest as hypercalcemia. Keywords: hypercalcemia, adrenal insufficiency, acute kidney injury. Introduction Hypercalcemia is a common disease found in emergency departments and in-patients.
Case presentation A year-old female presented to the emergency department with 1 week duration of general weakness and poor oral intake. Table 1 Laboratory data on admission and 2 weeks before. Open in a separate window. Figure 1. Clinical course of serum calcium, magnesium, and creatinine level. Discussion Hypercalcemia is a common finding in patients in emergency and in-patients. Footnotes Disclosure The authors report no conflicts of interest in this work.
References 1. Clinical review: Rare causes of hypercalcemia. J Clin Endocrinol Metab. Nerup J. Hypercalcemia is thought to result from a combination of a hypovolemic state seen in adrenal insufficiency which leads to decreased urinary calcium excretion as well as increased bone resorption, which may result from increased serum sclerostin concentrations.
Adrenal insufficiency should be considered in the differential of PTH-independent hypercalcemia. This case highlights the improvement in hypercalcemia that is seen with correction of glucocorticoid deficiency, and supports delaying additional work up for other PTH-independent causes until appropriate treatment has been given.
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