Endocrine Abstracts

A 50-year-old man presented with a week history of feeling unwell and urinary symptoms. He was confused. His wife gave H/O 2 stone weight loss. Recent investigation for haematuria showed 3.6 cm bladder tumour. He underwent TURBT and the histology was awaited. No other significant PMH or family H/O. Not on any medication and was an ex-smoker.

Initial investigations showed leucocytosis and evidence of UTI. CXR showed chronic fibrotic changes. As a part of confusion screen his calcium level came very high at 3.94 with normal PO₄. His creatinine was 135 and LFT was normal.

Further investigations including TFT, Vitamin D and PSA were normal. SST showed peak Cortisol of 523. PTH was appropriately suppressed. His ACE level and serum electrophoresis were normal. Histology from bladder resection showed poorly differentiated TCC with squamous differentiation as well (T3N1M0). Bone scan showed no evidence of bone metastasis. Unfortunately, he deteriorated very rapidly. Whole body CT at this stage showed ascites and extensive mediastinal, para-aortic and pelvic lymphadenopathy and peritoneal seedling.

Calcium started creeping up. In view of his tumour load, he was considered not suitable for any intervention from the Urologist as well as Oncologist and died shortly thereafter.

The cause of hypercalcaemia was assumed to be humoral and was confirmed by a 10-fold raise in PTHrP level.

Hypercalcaemia in malignancy is usually due to osteolytic secondaries which are mediated via cytokines. Humoral hypercalcaemia mediated by PTHrP is the cause of hypercalcaemia in 80% of malignancies, usually solid tumours that has not caused lytic secondaries. Association of PTHrP and hypercalcaemia in bladder tumour is very rare.

We present a rare association of PTHrP secretion from a bladder tumour.

A literature search reveals very few similar cases.