NON-ALUMINIC ADYNAMIC BONE-DISEASE IN NON-DIALYZED UREMIC PATIENTS - A NEW TYPE OF OSTEOPATHY DUE TO OVERTREATMENT

被引:62
作者
COHENSOLAL, ME
SEBERT, JL
BOUDAILLIEZ, B
WESTEEL, PF
MORINIERE, PH
MARIE, A
GARABEDIAN, M
FOURNIER, A
机构
[1] CHU AMIENS, SERV RHUMATOL, F-80000 AMIENS, FRANCE
[2] CHU AMIENS, SERV PEDIAT, F-80000 AMIENS, FRANCE
[3] CHU AMIENS, ANATOMOPATHOL LAB, F-80000 AMIENS, FRANCE
[4] HOP NECKER ENFANTS MALAD, TISSUS CALCIFIES LAB, CNRS, F-75730 PARIS 15, FRANCE
关键词
ADYNAMIC BONE DISEASE; UREMIA; BONE HISTOMORPHOMETRY;
D O I
10.1016/8756-3282(92)90354-Y
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Adynamic bone disease, characterized by a low bone formation rate with normal or reduced amount of unmineralized osteoid, is supposed to be the consequence of aluminum intoxication in uremic patients. However, the emergence of adynamic bone disease has been recently reported in hemodialyzed patients in the total absence of aluminum overload. This study was aimed to assess whether such a histological pattern of adynamic bone disease was already present in uremic patients not yet on dialysis. Twenty-seven asymptomatic uremic patients (mean age +/- SD 43 +/- 10 years, mean creatinine clearance 19 +/- 3 ml/mn) were studied and bone biopsies were repeated in 16 of them after 18 +/- 10 months of treatment with oral calcium carbonate (1-3 g of elemental calcium/day) and calcidiol (21 +/- 14-mu-g/day). None of the patients received aluminum hydroxide, and the search for bone aluminum deposits was negative in all patients both before and after treatment. Two patients fulfilled the criteria of adynamic bone disease on their post-treatment biopsies. They originated from patients classified as having normal bone histology before treatment. Comparison with the other patients showed that they had comparable plasma C-terminal PTH but higher plasma creatinine than patients with normal bone histology and lower plasma C-terminal PTH than patients with osteitis fibrosa but comparable plasma creatinine. The plasma levels of 1,25(OH)2D reached values above normal after treatment in these two patients. It is suggested that adynamic bone disease not related to aluminum intoxication can develop in uremic patients independently of dialysis, and is favored by a relative hypoparathyroidism for the degree of renal failure, possibly induced by elevated plasma concentrations of calcitriol.
引用
收藏
页码:1 / 5
页数:5
相关论文
共 31 条
[1]  
ANDRESS DL, 1986, J BONE MINER RES, V1, P391
[2]   1,25(OH)2D3 ADMINISTRATION IN MODERATE RENAL-FAILURE - A PROSPECTIVE DOUBLE-BLIND TRIAL [J].
BAKER, LRI ;
ABRAMS, SML ;
ROE, CJ ;
FAUGERE, MC ;
FANTI, P ;
SUBAYTI, Y ;
MALLUCHE, HH .
KIDNEY INTERNATIONAL, 1989, 35 (02) :661-669
[3]  
BOIVIN G, 1988, J BONE MINER RES, V3, P497
[4]   HISTOMORPHOMETRIC PROFILE, PATHOPHYSIOLOGY AND REVERSIBILITY OF CORTICOSTEROID-INDUCED OSTEOPOROSIS [J].
BRESSOT, C ;
MEUNIER, PJ ;
CHAPUY, MC ;
LEJEUNE, E ;
EDOUARD, C ;
DARBY, AJ .
METABOLIC BONE DISEASE & RELATED RESEARCH, 1979, 1 (04) :303-311
[5]   EFFECTS OF PARATHYROIDECTOMY ON BONE-FORMATION AND MINERALIZATION IN HEMODIALYZED PATIENTS [J].
CHARHON, SA ;
BERLAND, YF ;
OLMER, MJ ;
DELAWARI, E ;
TRAEGER, J ;
MEUNIER, PJ .
KIDNEY INTERNATIONAL, 1985, 27 (02) :426-435
[6]  
CHARHON SA, 1985, J LAB CLIN MED, V106, P123
[7]  
DEVERNEJOUL MC, 1982, J CLIN ENDOCR METAB, V54, P276, DOI 10.1210/jcem-54-2-276
[8]   DEFEROXAMINE TEST AND BONE-DISEASE IN DIALYSIS PATIENTS WITH MILD ALUMINUM ACCUMULATION [J].
DEVERNEJOUL, MC ;
MARCHAIS, S ;
LONDON, G ;
BIELAKOFF, J ;
CHAPPUIS, P ;
MORIEUX, C ;
LLACH, F .
AMERICAN JOURNAL OF KIDNEY DISEASES, 1989, 14 (02) :124-130
[9]   HISTOMORPHOMETRIC EVIDENCE OF DELETERIOUS EFFECT OF ALUMINUM ON OSTEOBLASTS [J].
DEVERNEJOUL, MC ;
BELENGUER, R ;
HALKIDOU, H ;
BUISINE, A ;
BIELAKOFF, J ;
MIRAVET, L .
BONE, 1985, 6 (01) :15-20
[10]   NON-OSTEOMALACIC OSTEOPATHY ASSOCIATED WITH CHRONIC HYPOPHOSPHATEMIA [J].
DEVERNEJOUL, MC ;
MARIE, P ;
KUNTZ, D ;
GUERIS, J ;
MIRAVET, L ;
RYCKEWAERT, A .
CALCIFIED TISSUE INTERNATIONAL, 1982, 34 (03) :219-223