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Severe Hypercalcaemia Case Report Severe Hypercalcaemia – Chronic Tophaceous Gout as the Responsible Cause? René Rodríguez-Gutiérrez, 1,2 Maria Azucena Zapata-Rivera, 1 Karla Victoria Rodriguez-Velver, 1 Fernando J Lavalle-Gonzalez, 1 José Gerardo Gonzalez-Gonzalez 1 and Jesus Zacarias Villarreal-Perez 1 1. Endocrinology Division, Department of Internal Medicine, University Hospital ‘Dr José E González’, Universidad 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 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, severe hypercalcaemia, calcitriol, thopi Disclosures: 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 no conflicts of interest to declare. No funding was received for the publication of this article. Compliance with Ethics: Written informed consent was obtained from the patient for publication of this case report and the accompanying images. Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any non-commercial use, distribution, adaptation and reproduction provided the original author(s) and source are given appropriate credit. Received: 17 May 2015 Published Online: 8 July 2015 Citation: European Endocrinology, 2015;11(2):102–4 Correspondence: René Rodríguez-Gutiérrez, Endocrinology Division, Department of Internal Medicine, Hospital Universitario ‘Dr José E González’, Universidad Autonoma de Nuevo León, Monterrey, México. E: renerodriguez@investigacion-meduanl.com; rodriguezgutierrez.rene@mayo.edu Case Presentation Sometimes the worst has to happen before seeking medical attention. This was the case of a 42-year-old man who arrived to the emergency room with altered mental status characterised by lethargy and confusion. His sister referred a long-standing history of gout that was diagnosed 8 years earlier and that was treated irregularly with non-steroidal anti- inflammatory drugs (NSAIDs) and colchicine and reported a negative family history of gout. Two years earlier, multiple tophi had appeared on the ears, elbows, hands and foot and 6 months previously he was confined to bed due to intense generalised pain. Despite his family insistence, the patient constantly refused to receive medical attention. A week earlier he referred initiating with polyuria, polypsia and constipation and nausea and vomiting developed 48 hours before admission. Progressive altered mental status finally made his family pursue formal medical attention. Assessment Physical examination revealed altered mental status characterised by lethargy and a Glasgow coma scale of 14 without any signs of focalisation. Blood pressure was 130/85 mmHg, respiratory rate 13 per minute, heart rate 95 beats per minute, temperature 36.3ºC 102 and room-air oxygen saturation was 98 %. Characteristic, multiple, non-tender tophi from 1 to 6 cm were obvious at inspection in the wrists, metacarpophalangeal, proximal and distal interphalangeal articulations, elbows, knees, ankles and the first metatarsophalangeal joint (see Figure 1). A non-infected ulcer was seen in the second metacarpophalangeal joint. There were no signs of septic arthritis and the rest of the examination was unremarkable. 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, creatinine of 5.4 mg/dl, blood nitrogen urea of 56, a Modification of Diet in Renal Disease (MDRD) glomerular filtration rate (GFR) of 16 ml/minute and urinary calcium of 350 mg/24 hours. PTH was suppressed ( < 3.0 pg/ml), 25-dihydroxyvitamin D was normal, parathyroid hormone related-protein (PTHrP) was 45.0 pg/ ml and calcitriol 19.6 pg/ml. Red blood cell count was normal and a peripheral smear showed no dysmorphic red cells. Twenty-four hour protein excretion was 110 mg/day (see Table 1). An electrocardiogram showed the characteristic shortened QT interval with no other rhythm abnormalities. Radiographs of upper and lower extremities revealed bone erosions with the characteristic ‘overhanging’ edges (see Figure 1). Tou c h ME d ica l ME d ia