Endocrine Abstracts

Introduction: Severe hypercalcaemia is a medical emergency which can result in severe cardiovascular and neurological dysfunction. Pathophysiological mechanisms of hypercalcaemia include increased osteoclastic activity, osteolytic bone metastasis, extra-renal activation/production of 1,25 hydroxyvitamin D and decreased urinary calcium excretion. Understanding these mechanisms is important to guide the diagnostic process and the long-term management of hypercalcaemia.

Case report: We present a 26 years old Afro-Caribbean man who presented with 8 months history of diarrhoea, 10 kg weight loss, abdominal pain and arthralgia; associated with a recent history of dry cough and breathlessness. He was not on any long term medicines. Apart from bilateral episcleritis, clinical examination was not of note. Blood tests showed a corrected serum calcium of 4.18 mmol/l, serum phosphate of 1.73 mmol/l and acute kidney injury. Parathyroid hormone was fully suppressed with normal serum angiotensin converting enzyme level and normal vitamin D. Parathyroid hormone related peptide and 1,25 hydroxyvitamin D were undetectable. Serum immunoglobulins were normal and antinuclear antibodies were negative. Computed tomography scan of chest and abdomen demonstrated features of organizing pneumonia (not typical of sarcoidosis) and oedematous proximal small bowel. Upper gastrointestinal endoscopy and colonoscopy showed diffuse patchy inflammation of the colon and duodenum. Capsule endoscopy showed ulceration and blunted villi with inflammation in the distal small bowel and terminal ileum. Colonic and duodenal biopsies demonstrated diffuse chronic inflammation. No granulomata were seen. Cultures for bacteriology and tuberculosis were negative. Renal biopsy showed tubular calcification in keeping with hypercalcaemia, no significant inflammation or granulomata. He was treated with prednisolone 20 mg tds and intravenous normal saline hydration. His corrected calcium improved to 3.08 mmol/l within 10 days with normalization of his kidney function. Hydroxychloroquine 200 mg od was added with subsequent normalization of corrected calcium to 2.38 mmol/l within 7 days. He was discharged on hydroxychloroquine 200 mg once daily and prednisolone 15 mg once daily, which was then reduced to 10 mg once daily. Video assisted thoracoscopic lung biopsy and push enteroscopy for small bowel biopsy were planned as outpatient. Unfortunately, the patient declined any further investigations as he remained completely asymptomatic. Although the final diagnosis has not been reached yet, the impressive response to glucocorticoids and hydroxychloroquine is suggestive of a macrophage dependant inflammatory process responsible for the severe hypercalcaemia, with low grade gastrointestinal lymphoma remaining a possible cause.