A 45-year old lady admitted to hospital in October 2018 with generally unwell and nausea. She has a background of disseminated T.B. confirmed by EBUS with bronchoalveolar lavage in September 2018. She had previous CT thorax, abdomen and pelvis in September 2018 which was reported as extensive lymphadenopathy with omental and peritoneal thickening. She also has a history of vitamin D deficiency in August 2018 at 7.1 nmol/l and was treated with oral colecalciferol. The biochemical results on admission showed adjusted calcium 4.22 (2:202:60 mmol/l), PTH 1.5 (1.66.9 pmol/l), Vitamin D 100.3 nmol/l, sodium 141 (133146 mmol/l), potassium 4.7 (3.55.3 mmol/l), urea 4.2 (2.57.8 mmol/l), creatinine 61 (4584 mmo/l), eGFR >90, ALT 19 (135 IU/l), ALP 150 (30130 u/l), total protein 80 (6080 g/l), albumin 37(3448 g/l), bilirubin 6.0 (021 umol/l), phosphate 1.05 (0.81.5 mmol/l),
Historically, the biochemistry trends as per table below:
The patient was treated initially with intravenous saline 0.9% and received subsequently zoledronic acid infusion for hypercalcaemia. She was previously started in community with oral colecalcifreol due to to severe vitamin D deficiency in August 2018 at 7.1 nmol/l which seems quite appropriately, treated her Vitamin D deficiency at that time. Unfortunately this extra colecalciferol has been subject to unregulated hydroxylation in her granulomatous tissue leading to the hypercalcaemia. The hypercalcemia thought to be secondary to high extra-renal production of 1,25 hydroxy vitamin D was seen in tuberculosis, including in individuals with 25 hydroxy vitamin D in the deficient range. These abnormalities of calcium metabolism are due to dysregulated production of 1,25 hydroxy vitamin D by activated macrophages trapped in pulmonary alveoli and granulomatous inflammation. Macrophage-derived 1α-hydroxylase as the source of the elevated 1,25 hydroxy vitamin D.