Hypocalcemia following Treatment for Hyperthyroidism

Abstract

CASEA 17-year-old female was referred to the endocrinology clinic after blood test results suggestive of hyperthyroidism. She had mild symptoms of thyrotoxicosis, including menstrual disturbance with intermittent palpitations and tremor. On examination, the patient was normotensive, tachycardic (100 beats/min), and of slim build with poor dentition. She had a small diffuse goiter without retrosternal extension or bruit. There was conjunctival injection but no evidence of lid lag or proptosis. Auscultation of the precordium revealed murmurs in systole and diastole consistent with mixed aortic valve disease.The only child of healthy nonconsanguineous parents, the patient had previously been well. Her medical history included mild learning difficulties, a bicuspid aortic valve, recurrent urinary tract infections, and severe constipation as a child that required a colostomy, which was later reversed. Apart from an osmotic laxative, she received no other regular medication. A recent echocardiogram had demonstrated a bicuspid aortic valve with good flow and minor regurgitation.Biochemically, the patient had an undetectable serum concentration of thyroid-stimulating hormone ( After daily treatment with 30 mg carbimazole and 25 mg atenolol, the fT4 concentration in the patient decreased as expected (fT4, 19.2 pmol/L; TSH, 0.03 mIU/L). Concomitantly, the patient developed asymptomatic hypocalcemia [calcium, 1.72 mmol/L (6.88 mg/dL)]. The total 25-hydroxyvitamin D concentration was 38 nmol/L (reference interval, 15-100 nmol/ L), and her serum magnesium concentration was 0.87 mmol/L (reference interval, 0.74 -1.00 mmol/L). Both were within their respective reference intervals. The serum phosphate concentration was 1.28 mmol/L (reference interval, 0.9 -1.35 mmol/L), and the albumin concentration was 48 g/L (reference interval, 35-50 g/L). The parathyroid hormone (PTH) concentration was also within the reference interval [4.8 pmol/L (4.8 ng/ L); reference interval, 1.6 -9.3 pmol/L] and thus inappropriately normal given the degree of hypocalcemia. A diagnosis of hypoparathyroidism was made, and the patient was treated with 0.5 g alfacalcidol daily. The calcium concentration briefly normalized (Table 1).After this improvement, the patient stopped complying with her carbimazole and alfacalcidol treatment regimen, and the results of thyroid function tests returned to near pretreatment concentrations [fT4, 58.4 pmol/L (4.5 ng/dL); TSH, Ͻ0.03 mIU/L; calcium, 2.34 mmol/L (9.36 ng/dL); Table 1]. With improved patient compliance, the fT4 results improved, approaching euthyroidism. The patient eventually achieved a normocalcemic state [fT4, 13.5 pmol/L (1.0 ng/dL); calcium, 2.35 mmol/L (9.4 mg/dL)]. More recently, compliance has been a concern with recurrent increased fT4 concentrations (Table 1).

A Case of Hypocalcemia with Severe Vitamin D Deficiency following Treatment for Graves’ Disease with Methimazole

“…In addition, in patients with thyroidectomy for Graves' disease, postoperative damages of the parathyroid glands can be also causes of hypocalcemia [1]. However, there have been few reports of symptomatic hypocalcemia after treatment with antithyroid drugs for Graves' disease [2]. …”

“…On the other hand, there have been few reports of hypocalcemia following treatment for Graves' disease with antithyroid drugs such as methimazole (MMI) [2]. Calcium metabolism is under control through the coordinated actions of parathyroid hormone (PTH) and activated vitamin D, and the most common cause of hypocalcemia in primary care is vitamin D deficiency [3].…”

Diagnosed Changes of Bone Mineral Density and Level of Calciotropic Hormones in Juvenile Hyperthyroidism

“…There is no consensus about the change in the level of PTH in the blood during thyrotoxicosis. According to the literature data, thyrotoxicosis is accompanied by an increase in PTH concentration, normalising during successful therapy [21]. Although there are opposite works, indicating hypoparathyroidism in Graves' disease [22].…”

Hashimoto’s Thyroiditis and Graves’ Disease in Genetic Syndromes in Pediatric Age

“…Several studies described an association between 22q11DS and GD [105,106,108,110]. If compared with the general pediatric population, GD in 22q11DS seems to be more frequent and may occur earlier, even under the age of 3 [107].…”

“…Kawame et al reported a case of a 27-month-old 22q11DS female with tachycardia, irritability and seizures due to GD, suggesting that, in addition to the early onset, AITDs in 22q11DS may have an atypical presentation [112]. Additionally, it should be considered that thyrotoxicosis, due to GD, may have a hypercalcemic effect and mask an underling hypoparathyroidism, producing a serum calcium concentration within the normal limits [110].…”