Endocrine Abstracts

A 54 year old woman was admitted by her GP to our Medical Admissions Unit earlier this year with a suspected diagnosis of malignancy due to her history of weight loss, lethargy and breathlessness. She was found to be hypercalcaemic with calcium of 3.35 mmol/l. Unfortunately, our acute physicians treated her with pamidronate before her hypercalcaemia was fully investigated which resulted in transient but symptomatic hypocalcaemia (with a nadir calcium of 1.72 mmol/l). A resting tachycardia and goitre suggested the possibility of thyrotoxicosis and subsequent TFTs confirmed this (TSH <0.05, FT4 >100 pmol/l). In view of her breathlessness and signs of right heart failure an echocardiogram was performed which showed dilated right heart chambers, moderate TR and an elevated estimated PA pressure. The possibility of pulmonary embolic disease was excluded with a CTPA and subsequent V/Q scan. She was started on treatment with 40 mg carbimazole daily and in two weeks her FT4 levels had fallen to 13.5 pmol/l. A repeat echocardiogram 2 months after starting carbimazole revealed normal right heart chambers, no evidence of TR and no evidence of pulmonary hypertension. Mild hypercalcaemia occurs in up to 20 percent of thyrotoxic patients, due to a thyroid hormone mediated increase in bone resorption. It resolves following correction of hyperthyroidism. Severe hypercalcaemia is less common although previously reported. Pulmonary hypertension has been reported with increasing frequency in patients with overt hyperthyroidism. Antithyroid antibodies could play a role in the pathogenesis of pulmonary hypertension. An autoimmune mechanism associated with vascular endothelial damage may play a key pathogenic role in the development of pulmonary hypertension. To the best of our knowledge, this is the first case report describing a patient with severe hypercalcaemia and clinically significant pulmonary hypertension both of which completely resolved with treatment of her thyrotoxicosis.

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.