Salma Sidahmed, Ali Hassan, and Emily Mudenha
A 37-year old female who was known to have a diagnosis of sarcoidosis which was conservatively managed, presented to the emergency department with a few days history of lethargy, exertional dyspnoea and palpitations. She was noted to be slightly confused and clinically dehydrated on arrival. Her initial investigations showed an adjusted calcium level of 5.5 mmol/L, acute kidney injury, normal phosphate and vitamin D levels with suppressed parathyroid hormone level of 7 ng/L. She also had a raised Angiotensin Converting Enzyme (ACE) level of 169 u/L. She had no abnormalities on her electrocardiogram. Recent radiological investigations had excluded any malignancy. Her calcium and ACE levels had previously been stable, and she denied any vitamin D supplementation prior to this admission. The mechanism of hypercalcaemia in sarcoidosis occurs due to enhanced intestinal calcium absorption and increased endogenous calcitriol production therefore treatment modalities are usually a low calcium diet and corticosteroids which have a peak action within 2-5 days by reducing calcitriol production. This case highlights an atypical presentation of very high calcium levels secondary to sarcoidosis that was resistant to aggressive intravenous fluids, necessitating the use of calcitonin in addition to high dose steroids for a rapid calcium reduction to prevent complications such as renal failure and arrhythmias.
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