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Endocrine Abstracts (2020) 69 P48 | DOI: 10.1530/endoabs.69.P48

Pinderfields General Hospital, Wakefield, UK


Case history: A 74-year old gentleman was referred from Urology clinic for hypercalcemia after being treated for left vesico-ureteric calculus causing mild hydronephrosis. Past medical history included asthma, eczema and hypertension. He had been taking calcium supplements for 5 years, but stopped 2 months prior to clinic. He was asymptomatic and quite well with no recent fracture.

Investigations: Adjusted Ca ranged from 2.62 to 2.78 mmol/l, PTH from 2.6 to 9.5 pmol/l, ALP from 250 to 394 u/l. LFTs including GGT were normal. Vitamin D was depleted at 40 nmol/l. 24 h urinary Ca was high at 15.7 mmol/d. Serum electrophoresis & urine Bence Jones protein were negative. PSA was normal at 3.9 mcg/l. ALP isoenzymes were raised for bone isoenzymes. Radionuclide bone whole body scan showed superscan result. ALP was consistently getting higher and these results with the bone scan were concerning for malignancy.

Results and treatment: He was proceeded to bone marrow biopsy, which showed increased osteoclastic activity & suggestive of hyperparathyroidism or ectopic hormone production. Next step was CT(TAP) to exclude malignancy and it only showed inflammatory changes in lingular nodes, but nil other significant findings. Serum ACE level was normal. PTHrP level was undetectable. Sestamibi scan did not localise parathyroid adenoma. USG (neck) showed no abnormalities. DEXA showed osteoporosis. Bone histopathology report was suggestive of hyperparathyroidism. ALP was elevated to 1747 u/l at this point. Bone turnover markers were significantly raised (P1NP 3489 ug/l & CTX 2.17 H ug/l). He was treated with zoledronic infusion and improved markedly after 3 lots of treatment. All investigations point towards metabolic bone disease with increased bone turn over and high urinary calcium probably primary hyperparathyroidism. MDT decision was to proceed with neck exploration. Biopsy confirmed parathyroid adenoma. Bone turnover markers improved significantly and have normalised after surgery (P1NP 53 ug/l, CTX 0.49 H ug/l). Post-surgery ALP 80 u/l, adjusted Ca 2.46 mmol/l and PTH 3.7 pmol/l. He is waiting for a repeat radionuclide scan.

Conclusions and discussion points: This case demonstrates that primary hyperparathyroidism can present with the form of metabolic bone disease despite fairly normal calcium and PTH levels with negative localisation scans. Differentials to be considered for ‘superscan’ include metabolic bone disease, disseminated malignancy & haematological disorder. MDT approach is vital in managing such cases. This patient has a remission after surgery even with negative senstamibi scan.

Volume 69

National Clinical Cases 2020

London, United Kingdom
12 Mar 2020 - 12 Mar 2020

Society for Endocrinology 

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