Endocrine Abstracts

Introduction: Dilated cardiomyopathy is the third most common reason for heart failure and transplantation worldwide. The etiology of dilated cardiomyopathy often remains unclear, but in certain cases we can discover the cause, which can then contribute to better and more causal treatment.

Observation: We present a case of a 47-year-old man without any significant comorbidities in his medical history. In 2015 he underwent two hemithyroidectomies with a neck lymph node dissection due to a multifocal papillary thyroid cancer. The second hemithyroidectomy was complicated by a left-sided recurrent nerve paresis and severe postoperative hypocalcaemia caused by the accidental parathyroid removal. The surgery was followed by a radioiodine ablation and levothyroxine suppressive treatment. The radioiodine had to be reapplied twice because of a persistent biochemical incomplete response. From the beginning it was very difficult to achieve adequate calcium substitution mainly because of a previously documented noncompliance of our patient. He was repeatedly intolerant to calcium and vitamin D supplements and therefore adjusted doses himself. In 2020 he was hospitalized due to signs of a heart failure and was diagnosed with dilated cardiomyopathy. Chronic hypocalcaemia and the uncompensated post-operative hypoparathyroidism were considered as the most probable cause. Patient´s heart failure progressed rapidly, which led to LVAD (left ventricular assist device) implantation as a bridge for heart transplantation. Therefore, restoring normocalcaemia became a priority. We started newly available rhPTH (1-84) therapy, that successfully normalized calcium levels. Concerning the thyroid cancer, the thyroglobulin is still rising and newly there is a paratracheal thyroid residuum visible on the PET/CT scan, which will require surgical intervention. Therefore, the heart transplantation is being postponed. However, according to the latest echocardiography there is an improvement of ejection fraction (from less than 20% to 30-35%) with a partial reverse myocardial remodelling and reduction of the end-diastolic diameter of the left ventricle.

Conclusion: Hypocalcaemia induced dilated cardiomyopathy is a rare condition but previous case reports suggest its potential reversibility after a timely hypocalcaemia correction. In our case there is a slight improvement, however not enough to prevent him from the heart transplantation which is now being postponed due to the planned surgery of the thyroid residuum. The non-compliance has contributed significantly to the severity of his condition.