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Rodríguez-Gutiérrez R, Zapata-Rivera MA, Rodriguez-Velver KV, et al. Severe Hypercalcaemia - Chronic Tophaceous Gout as the Responsible Cause?. Eur Endocrinol. 2015;11(2):102-104doi: 10.17925/EE.2015.11.02.102.
Rodríguez-Gutiérrez, R., Zapata-Rivera, M. A., Rodriguez-Velver, K. V., Lavalle-Gonzalez, F. J., Gonzalez-Gonzalez, J. G., & Villarreal-Perez, J. Z. (2015). Severe Hypercalcaemia - Chronic Tophaceous Gout as the Responsible Cause?. European endocrinology, 11(2), 102-104. https://doi.org/10.17925/EE.2015.11.02.102
Rodríguez-Gutiérrez, René, et al. "Severe Hypercalcaemia - Chronic Tophaceous Gout as the Responsible Cause?." European endocrinology vol. 11,2 (2015): 102-104. doi: https://doi.org/10.17925/EE.2015.11.02.102
Rodríguez-Gutiérrez R, Zapata-Rivera MA, Rodriguez-Velver KV, Lavalle-Gonzalez FJ, Gonzalez-Gonzalez JG, Villarreal-Perez JZ. Severe Hypercalcaemia - Chronic Tophaceous Gout as the Responsible Cause?. Eur Endocrinol. 2015 Aug;11(2):102-104. doi: 10.17925/EE.2015.11.02.102. Epub 2015 Aug 19. PMID: 29632580; PMCID: PMC5819066.
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Eur Endocrinol. 2015 Aug;11(2):102-104. doi: 10.17925/EE.2015.11.02.102. Epub 2015 Aug 19.

Severe Hypercalcaemia - Chronic Tophaceous Gout as the Responsible Cause?.

European endocrinology

René Rodríguez-Gutiérrez, Maria Azucena Zapata-Rivera, Karla Victoria Rodriguez-Velver, Fernando J Lavalle-Gonzalez, José Gerardo Gonzalez-Gonzalez, Jesus Zacarias Villarreal-Perez

Affiliations

  1. Endocrinology Division, Department of Internal Medicine, University Hospital 'Dr José E González', Unlversldad Autonoma de Nuevo León, Monterrey, México.
  2. Knowledge and Evaluation Research Unit, Division of Endocrinology, Diabetes, Metabolism and Nutrition, Department of Medicine, Mayo Clinic, Rochester, Minnesota, US.

PMID: 29632580 PMCID: PMC5819066 DOI: 10.17925/EE.2015.11.02.102

Abstract

The association of chronic tophaceous gout with severe hypercalcaemia is exceptional. In this case, a 42-year old man with a long-standing history of gout arrived at the emergency room with altered mental status. Laboratory work up revealed a uric acid of 14.0 mg/dl, corrected calcium of 14.5 mg/dl, phosphorous of 6.3 mg/dl, parathyroid hormone (PTH) was suppressed (<3.0 pg/ml), 25-dihydroxyvitamin D 25.2 ng/ml, parathyroid hormone related-protein (PTHrP) was 45.0 pg/ml and calcitriol 19.6 pg/ml. Biopsy histopathology result showed deposits of monosodium urate crystals surrounded by granulomatous inflammation. The association of chronic tophaceous gout with severe hypercalcaemia is extremely rare and has been usually described to be secondary to 1-25 dihydroxyvitamin D (calcitriol) secretion. In this case, calcitriol levels were normal and this possibility was excluded. On the other hand, PTHrP had never been, until now, described as the responsible cause of hypercalcaemia in gout. In our case, baseline PTHrP and calcium values were elevated and after medical treatment both returned to normal values. PTHrP usually causes hypophosphataemia and in this case the abnormal renal function could have diminished this last effect.

Keywords: Tophaceous gout; calcitriol; severe hypercalcaemia; thopi

Conflict of interest statement

Disclosure: René Rodríguez-Gutiérrez, Maria Azucena Zapata-Rivera, Karla Victoria Rodriguez-Velver, Fernando J Lavalle-Gonzalez, José Gerardo Gonzalez-Gonzalez and Jesus Zacarias Villarreal-Perez have

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