Issue Section:. Download all slides. View Metrics. Email alerts Article activity alert. Advance article alerts. New issue alert. Receive exclusive offers and updates from Oxford Academic. Related articles in Google Scholar. Citing articles via Google Scholar. 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.
Initiation of thyroxine may cause clinical deterioration in a patient with underlying adrenal insufficiency. Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported. Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.
Browse other volumes. Within 2 days, inflammatory signs and blood pressure were normalized. However, serum calcium and creatinine levels remained elevated, and the patient constantly complained about poor oral intake and general weakness.
On the third hospital day, administration of saline and calcitonin 40 IU per day was begun. Serum calcium level decreased for the next 2 days from To evaluate the cause of hypercalcemia, contrast-enhanced computed tomography of chest and abdomen and whole body bone scintigraphy were performed, but the results showed no evidence of malignancy.
Serum and urine protein electrophoresis, anti-neutrophil cytoplasmic antibody titers, and tumor marker studies were negative. Thyroid function profile revealed normal levels of thyroid stimulating hormone 0. The bone mineral density T -score was —1. Intact parathyroid hormone PTH was 7. These results indicated a suppressed PTH—vitamin D axis.
We found that the patient had multiple steroid injections in both her knee joints in the past, although the amount of steroid could not be quantified. Adrenocortical function was assessed, and showed that her serum cortisol level was 2. As most people with secondary adrenal insufficiency fall within the range limit and usually below 35, the plasma ACTH level and ACTH stimulation test results suggested the diagnosis of secondary adrenal insufficiency.
Her serum calcium level returned to normal within 3 days and her general weakness and anorexia were completely improved Figure 1. With the normalization of calcium level, magnesium level trended toward normal range. After 2 weeks of follow-up, serum calcium level was maintained at 8. As the patient was at a high risk of developing osteoporosis and needed corticosteroid replacement, regular monitoring for bone mineral density was considered, but the patient was lost for follow-up.
Note: Cortisol reference range 6. Abbreviation: ACTH, adrenocorticotropic hormone. Hypercalcemia is a common finding in patients in emergency and in-patients. Although hypercalcemia can be related with adrenal insufficiency, adrenal insufficiency is not easily considered a cause of hypercalcemia.
In this case, thorough evaluation for malignancy and parathyroid disease failed to make the diagnosis, but a test for adrenocortical function demonstrated the cause of hypercalcemia and AKI, and glucocorticoid replacement resolved hypercalcemia.
In this case, the patient had an unclear history of steroid injections. It was certain that the patient had multiple steroid injections in both her knee joints, but the amount of intra-articularly administered glucocorticoids could not be quantified. The prevalence of adrenal insufficiency secondary to locally applied glucocorticoids is not clear.
According to one study, a single injection of intra-articularly administered glucocorticoids can cause adrenal suppression. The development of renal injury in individuals with hypercalcemia is related to the degree and duration of hypercalcemia. The sodium:potassium ratio in this puppy was However, because of the owner's financial limitations and our strong suspicion of hypoadrenocorticism, we did not measure ionized calcium and parathyroid hormone concentrations.
Furthermore, the dog had been receiving a high-quality commercial puppy food and had no known ingestion of toxins such as rodenticides, psoriasis drugs, or excess vitamin D or calcium.
Initial treatment included a ml bolus of 0. Intravenous fluid therapy with 0. The ACTH stimulation test results were available the next day day 8 and confirmed hypoadrenocorticism. The resting cortisol concentration was 0. We treated the dog with a mineralocorticoid, desoxycorticosterone pivalate Percorten—Novartis Animal Health; 2.
Dexamethasone sodium phosphate 0. The patient then began eating, so we switched to treatment with oral prednisone 1. Clinical signs resolved, and serum chemistry profile abnormalities, including the hypercalcemia, improved after three days of treatment for hypoadrenocorticism Table 1 , day 9.
After four days of hospitalization, the patient was eating well and the ocular discharge had resolved, so the patient was released to the owner. Prednisone 0. We emphasized the importance of strict compliance with future desoxycorticosterone pivalate injections and prednisone dosages.
At reevaluation day 14 , the patient was doing well. Its energy level and appetite had improved, and it had gained 1. Most serum chemistry profile results, including the calcium concentration, were normal Table 1 , day Initially, the patient was evaluated every 30 days, and more recently, it has been evaluated every 60 to 90 days. The results of intermittent serum chemistry profiles, including electrolytes, have been normal.
Treatment includes desoxycorticosterone pivalate every four weeks, and the oral prednisone has slowly been tapered to a physiological dose of 0. We instructed the owner to increase the prednisone dose in times of stress, such as boarding or illness. The patient is a clinically normal 2. Hypoadrenocorticism, or Addison's disease, is an endocrine disorder most commonly resulting from atrophy and destruction of the adrenal cortices. This deterioration leads to a deficiency of glucocorticoids alone or both glucocorticoids and mineralocorticoids.
Many causes of this disease have been identified in people, including adrenal gland destruction often autoimmune , tuberculosis, human immunodeficiency virus, adrenoleukodystrophy, and congenital adrenal hypoplasia. Hypoadrenocorticism is most common in young to middle-aged female dogs, but it also occurs in neonatal and pediatric dogs.
Addison's disease may cause electrolyte abnormalities including mild to moderate hypercalcemia. Dehydration leads to hemoconcentration and a relative increase in proteins that bind calcium. Hyponatremia due to mineralocorticoid deficiency increases the affinity of plasma proteins for calcium.
This increased protein binding of calcium leads to an elevated serum calcium concentration. Decreased renal function and decreased glomerular filtration rate due to hypovolemia lead to increased tubular calcium reabsorption and decreased calcium excretion. Increased serum calcium interferes with sodium and water retention in the distal renal tubules.
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