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( Rene Rodriguez Gutierrez ),( Roberto Monreal Robles ),( Maria Azucena Zapata Rivera ),( Karla V Rodriguez Velver ),( Fernando Jj Lavallegonzalez ),( Jose Gerardo Gonzalez Gonzalez ),( Jesus Zacarias 대한내과학회 2014 대한내과학회 추계학술대회 Vol.2014 No.1
Background and Description: The association of chronic tophaceous gout with severe hypercalcemia is extremely rare and has been usually associated with calcitriol secretion. PTHrP has never been described as the responsible cause. A 42-year old man with a long stand history of chronic gout initiated a week before admission with polyuria, polypsia and progressive altered mental status. Neurological examination revealed only lethargy. Characteristic, multiple, non-tender tophi were obvious at inspection (Figures 1-3). Initial laboratory work up revealed a uric acid of 14.0 mg/dl, calcium of 14.5 mg/dl, phosphorous of 6.3 mg/dl, creatinine of 5.4 mg/dl, blood nitrogen urea of 56, a MDRD GFR of 16 ml/min. Diagnostic and Therapeutic Approach: PTH was suppressed (< 3.0 pg/ml), 25-dihydroxyvitamin D was normal, PTHrP was elevated 45.0 pg/ml, and calcitriol normal (19.6 pg/ml). Radiographs revealed bone erosions (Figure 1-3). Bone scan and a PET-CT were negative for metastasis and malignancy. Treatment was initiated with calcitonin, hydration and prednisone. PTH, 25-dihydroxyvitamin D, PTHrP, and calcitriol returned to normal values. At 6 months follow-up he referred no pain, tophi had improved and calcium levels were within normal range. Discussion and Conclusion: A systemic research on PubMed, Medline, Embase and MedConsult with the search criteria: “Tophaceous gout”, hypercalcemia”, “calcitriol”, “PTHrP”, was made. The proposed mechanism has being an enhanced 1a-hydroxylation of vitamin D in a proliferative chronic synovitis. In this case calcitriol levels were normal. PTHrP had never been, until now, described as the responsible cause of hypercalcemia in gout. In our case baseline PTHrP and calcium values were elevated and after medical treatment both returned to normal values. Immobilization is another well-known cause of mild calcium elevations. It is likely that in this case this was an exacerbating rather than the primary factor.
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