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Endocrine Abstracts (2023) 91 P23 | DOI: 10.1530/endoabs.91.P23

SFEEU2023 Society for Endocrinology National Clinical Cases 2023 Poster Presentations (48 abstracts)

A case of persistent hypercalcaemia in the treatment of granulomatous disease

Nadia Osman , Henna Patel & Kirun Gunganah


Barts Health NHS Trust, London, United Kingdom


Section 1: Case history : A 49 year old South Asian gentleman was admitted to the emergency department after monitoring blood tests showed hypercalcaemia (corrected calcium of 3.67mmol/l) and acute kidney injury. He had a recent admission with a new diagnosis of miliary tuberculosis and superadded bacterial infection, complicated by a long and complex ITU admission after initiation of treatment. He was discharged home on colecalciferol 4000 units daily in addition to his anti-tuberculosis agents. On admission, he reported some osmotic symptoms but was otherwise well. He appeared clinically dehydrated but haemodynamically stable. Colecalciferol was stopped and he was managed with IV fluid rehydration whilst further investigations were carried out.

Section 2: Investigations : Blood tests showed a corrected calcium of 3.64mmol/l, PTH 1.0pmol/l, 25 OH vitamin D 95nmol/l, ALP 77units/L, phosphate 1.28mmol/l and serum ACE 73. Myeloma screen was negative. CT imaging showed some improvement of the original pulmonary changes and no evidence of malignancy. A serum 1,25 dihydroxyvitamin D3 was requested in the context of slow to recover hypercalcaemia and was found to be raised at 149pmol/l.

Section 3: Results and treatment : The patient was managed with a combination of IV fluid rehydration, bisphosphonate infusion, a course of steroids to cover for concomitant granulomatous disease with eventual normalisation of corrected calcium (2.41mmol/l) and PTH (2.2pmol/l).

Section 4: Conclusions and points for discussion: Hypercalcaemia has been described in granulomatous diseases1 and occurs via endogenous Vitamin D activation through extra-renal production of 1-alpha-hydroxylase. This is mediated through activated macrophages producing 1-alpha-hydroxylase, independently of negative feedback loops5; often with a normal 25OH Vitamin D. Vitamin D may have a role in the treatment of tuberculosis. In vitro studies have shown that the up-regulation of 1,25OH2 Vitamin D can induce an anti-mycobacterial response alongside modifying immune response6. Several randomised controlled trials show varying evidence with Vitamin D supplementation and the rates of sputum smear conversion. However given the potential anti-inflammatory benefits and low cost this remains a part of the treatment regime in many centres.9 When considering the treatment of hypercalcaemia secondary to granulomatous disease, steroid supplementation will down regulate the immune related activation of 25OH vitamin D.8 Although to avoid the need for these management plans the decision to use Vitamin D in the treatment of TB should be carefully considered given the potential systemic complication of hypercalcaemia in a high risk patient.

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