par Karmali, Rafik 
;Barker, S;Hewison, Martin;Fraher, L;Katz, D R;O'Riordan, Jeffrey L. H. J. L.
Référence Postgraduate medical journal, 66, 779, page (757-760)
Publication Publié, 1990-09
;Barker, S;Hewison, Martin;Fraher, L;Katz, D R;O'Riordan, Jeffrey L. H. J. L.Référence Postgraduate medical journal, 66, 779, page (757-760)
Publication Publié, 1990-09
Article révisé par les pairs
| Résumé : | A patient with Hodgkin's disease spontaneously developed steroid-responsive hypercalcaemia during two consecutive summers. Administration of 3000 U/day of vitamin D, while he was normocalcaemic, caused a sharp increase in serum 1,25(OH)2D3 (from 59 pg/ml to 142 pg/ml) and subsequently hypercalcaemia while serum 25(OH)D3 rose moderately within the normal range (from 2.8 ng/ml to 10 ng/ml). During a spontaneous episode of hypercalcaemia which was accompanied by increased circulating 1,25(OH)2D3 concentrations, administration of hydrocortisone decreased serum 1,25(OH)2D3 rapidly (from 115 pg/ml to 62 pg/ml) and eventually led to normocalcaemia while serum 25(OH)D3 remained unchanged. Thus the disturbances of mineral metabolism found in this patient with Hodgkin's disease are very similar to those previously described in sarcoidosis. |
