Severe Tophaceous Gout Causing PTH-Independent Hypercalcemia: An Uncommon Association
https://doi.org/10.15605/jafes.041.S1
- Author:
Hu Chong Siang
1
;
Kuan Yueh Chien
1
;
Lee Ho Mi
1
;
Cheong Yaw Kiet
2
Author Information
1. Miri Hospital
2. Sarawak General Hospital
- Publication Type:Journal Article
- From:
Journal of the ASEAN Federation of Endocrine Societies
2026;41(S1):79-
- CountryPhilippines
- Language:English
-
Abstract:
Introduction:Chronic tophaceous gout is a rare cause of parathyroid
hormone (PTH)-independent hypercalcemia. This is
due to increased 1-alpha hydroxylase activity within
granulomatous inflammation surrounding gouty tophi,
resulting in excess calcitriol production. In advanced
disease, immobilization from pain and joint deformity may
further exacerbate hypercalcemia due to immobilizationrelated bone resorption, leading to clinically significant
symptoms and complications.
Case:A 59-year-old male with chronic tophaceous gout complicated with CKD and nephrocalcinosis was referred for
inpatient evaluation of hypercalcemia. He had an episode
of acute pancreatitis attributed to hypercalcemia 1 month
prior. Serum calcium levels have risen progressively over
the preceding year, from 2.48 mmol/L (reference 2.0–2.65)
to 3.17 mmol/L.
His gout was poorly controlled with uric acid levels ranging
641–709 umol/L, with extensive tophi over the upper and
lower limbs and gluteal regions. He had been maintained on
low-dose allopurinol 150 mg/day for 2 years. Functionally,
he was largely bedbound and wheelchair-dependent.
On admission, corrected calcium was 3.48 mmol/L with
suppressed intact parathyroid hormone (<0.6 pmol/L)
consistent with PTH-independent hypercalcemia. Malignancy and myeloma workup, including tumor markers, was unremarkable. Serum phosphate (0.9 mmol/L) and
alkaline phosphatase (152 IU/L) were normal.
Hypercalcemia persisted despite intravenous hydration
and calcitonin. Low-dose prednisolone was then initiated,
followed by pamidronate, resulting in normalization
of corrected calcium to 2.17 mmol/L. He remained
normocalcemic while on tapering prednisolone for a month.
However, calcium rebounded months after cessation.
Gradual escalation of allopurinol to 900 mg/day improves
uric acid levels to 389–429 umol/L with better functional
status (standing unsupported briefly and mobilizing
with assistance). However, calcium remains moderately
elevated 2.65–2.85 mmol/L.
Conclusion:This case highlights severe tophaceous gout as a rare but
significant cause of PTH-independent hypercalcemia, in
which glucocorticoids can be effective in treating refractory
hypercalcemia. It also underscores the importance of
addressing the underlying disease through optimization
of urate-lowering therapy and functional rehabilitation.
- Full text:2026080413320307299EP_A108.pdf
