par Latifyan, Sofiya Bedo;Vanhaeverbeek, Michel 
;Klastersky, Jean
Référence BMJ case reports, 2014
Publication Publié, 2014-11
;Klastersky, Jean Référence BMJ case reports, 2014
Publication Publié, 2014-11
Article révisé par les pairs
| Résumé : | Tumour-associated osteomalacia is a paraneoplastic syndrome caused by renal phosphate wasting, leading to severe hypophosphataemia. Excess of circulating fibroblast growth factor 23 (FGF23) is the likely cause, acting via the FGF23/α-Klotho coreceptor, a critical regulator of phosphate metabolism. The other possible effects of that complex in humans are still under investigation. We present a case of an 84-year-old Belgian man, presenting prostate cancer with bone metastases. From June 2010 to March 2013, he presented three episodes of disease progression. From January 2012, the patient developed a progressively marked dorsal kyphosis with significant hypophosphataemia. The calculated TRP (tubular reabsorption of phosphate) was decreased and the FGF23 increased. Mid-March 2013, the patient died after a profound unconsciousness due to hypoglycaemia with hypothermia. We hypothesised that the two paraneoplastic manifestations of this patient (tumour-associated osteomalacia and refractory hypoglycaemia) were due to one cause chain with two main nodes - FGF23 and its coreceptor Klotho. Copyright 2014 BMJ Publishing Group. All rights reserved. |
