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Decrease of tumor-like calcification in uremia despite aggravation of secondary hyperparathyroidism: a case report.

作者信息

Geffriaud C, Allinne E, Page B, Zingraff J, Jucquel J P, Bardin T, Drüeke T B

机构信息

Département de Néphrologie, Hôpital Necker, Paris, France.

出版信息

Clin Nephrol. 1992 Sep;38(3):158-61.

PMID:1395170
Abstract

Extraskeletal pseudotumoral calcifications generally develop in uremic patients with a high calcium x phosphorus (Ca x P) product and severe secondary hyperparathyroidism. In the present case report we describe a chronic hemodialysis patient presenting with a massive calcification of the left shoulder region, severe aluminum (Al) intoxication and moderate hyperparathyroidism. Her initial serum Ca x P product was only slightly elevated: 5.01 mmol2/l2. Under deferoxamine treatment during the subsequent 4 months, Al overload decreased. On the other hand, parathyroid overfunction worsened, as reflected by an increase of the serum immunoreactive parathyroid hormone [1-84] level from initially 690 to 1052 pg/ml (normal, 15-60 pg/ml) and an increase of alkaline phosphatase activity, and plasma calcitriol increased from undetectable to a low-normal value. Predialysis serum total Ca levels decreased rapidly from 2.9 to 2.5 mM but serum P concentrations remained elevated: 1.6-2.5 mM. Unexpectedly, the extent of the periarticular calcification diminished considerably during the same time period. The present observation shows that in a subset of uremic patients with Al overload, pseudotumoral calcifications may regress during Al chelation therapy despite progression of hyperparathyroidism. Since Al may predispose collagen to develop dystrophic or metastatic calcification, it is suggested that this process is reversible by correcting Al intoxication.

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