Endocrine Abstracts

Section 1: Case history: A 58 year old lady presented to the Emergency Department with a two week history of general lethargy, weight loss, increased thirst and polyuria as well as muscle cramps in her legs. Aside from sinus tachycardia, her observations and physical examination were unremarkable on admission. She had a background of hypertension on Indapamide as well as idiopathic hypoparathyroidism on Alfacalcidol. The latter had been diagnosed nine years prior following admission with difficulty in speaking due to jaw stiffness as well as facial weakness and hand numbness in the context of marked hypocalcaemia. Three years later, she developed hypercalcaemia related to a diagnosis of Graves’ thyrotoxicosis for which she completed 18 months of Carbimazole therapy to good biochemical and clinical effect.

Section 2: Investigations: Her biochemical profile on this admission revealed a marked hypercalcaemia and hyperthyroidism; adjusted Calcium 3.35 (2.20–2.60), Phosphate 1.65 (0.80–1.50), free T4 level 51.5 (9.0–23.0), free T3 level >30.7 (2.5–5.7) and Thyroid Stimulating Hormone (TSH) <0.01 (0.30–4.20). Her Parathyroid Hormone level was supressed at <0.3 (1.6–7.2), she had a very low Vitamin D level of 14.3 (70–150) and a raised TSH receptor antibody level of 1.1 (<0.4). There was an increased uptake function of 5.58% (normal <3.5%) of the thyroid gland on imaging with Technitium in keeping with mildly active Graves’ thyrotoxicosis. A DEXA scan revealed normal bone density of the hips and lumbar spine.

Section 3: Results and treatment: The patient was recommenced on Carbimazole which was uptitrated to 40 mg and Propanolol was introduced for palpitations. She received intravenous fluid rehydration as an inpatient whilst her Indapamide was held. She improved clinically and her bloods were closely monitored as an outpatient; the Calcium level normalised as her thyroid function improved on Carbimazole treatment and her Alfacalcidol was eventually reinstated. She proceeded to have definitive treatment of her thyroid with radioiodine therapy.

Section 4: Conclusion and points for discussion: A mildly raised Calcium level can be found in the hyperthyroid state due to increased bone metabolism. However, this lady interestingly presented with recurrent and severe Graves’ thyrotoxicosis that manifested with hypercalcaemic crisis on both occasions. The hypercalcaemia persisted even when off Alfacalcidol for her concurrent idiopathic hypoparathyroidism which had initially presented with a marked hypocalcaemia. This case shows a remarkable biochemical pattern over the course of nine years where the patient’s calcium status significantly shifts with her thyroid state, despite an underlying hypoparathyroidism.