The effect of long-term growth hormone (GH) treatment on bone mineral density in children with GH deficiency. Role of GH in the attainment of peak bone mass

被引:145
作者
Saggese, G
Baroncelli, GI
Bertelloni, S
Barsanti, S
机构
[1] Endocrine Unit, Department of Pediatrics, University of Pisa, Pisa
[2] Endocrine Unit, Department of Pediatrics, University of Pisa, Pisa, I-56125
关键词
D O I
10.1210/jc.81.8.3077
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The effect of long-term GH treatment on bone mass was examined in 32 children with GH deficiency (GHD) aged 7.2-16.3 yr by measuring radial(distal third, single-photon absorptiometry) and lumbar (L2-L4, dual energy x-ray absorptiometry) bone mineral density (BMD) (group A). All patients were longitudinally followed and received recombinant hGH therapy for a mean period of 48.2+/-13.2 months. BMD values were corrected for bone age and expressed as Z-score in comparison with normative data. In addition, lumbar BMD and lumbar BMD corrected for the estimated vertebral volumes were assessed in 11 patients with GHD aged 16.0-18.7 yr at the time they reached their final height (group B) and, in 17 subjects with familial short stature aged 16.4-19.8 yr, as controls (group C) for patients of group B. Patients of group B had received discontinuous treatment with pituitary-derived hGH and subsequently recombinant hGH (total duration of treatment 151.5+/-9.7 months). The off-treatment period was 4.7+/-2.6 months. Before treatment, patients of group A showed significantly reduced (P <0.001) radial and lumbar BMD (-1.7+/-0.4 Z-score and -1.5+/-0.5 Z-score, respectively) compared with normative data. During treatment, radial and lumbar BMD Z-scores improved significantly (P <0.001); in the patients treated for the longest time, the BMD was within 0.5 sn of age-matched mean levels. In patients of group B, lumbar BMD and lumbar BMD corrected for the estimated vertebral volumes were significantly reduced in comparison with subjects of group C(-1.2+/-0.4 Z-score and -1.0+/-0.4 Z-score, P <0.01 and P <0.03, respectively). The results show that children with GHD have reduced BMD. Optimal GH treatment improves BMD, whereas inappropriate treatment is a main cause of reduced BMD at time of final height. These findings suggest an important role of GH therapy in the attainment of peak bone mass in children with GHD. GH treatment should be continued until the attainment of peak bone mass irrespective of the height achieved.
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页码:3077 / 3083
页数:7
相关论文
共 30 条
[1]   CRITICAL YEARS AND STAGES OF PUBERTY FOR SPINAL AND FEMORAL BONE MASS ACCUMULATION DURING ADOLESCENCE [J].
BONJOUR, JP ;
THEINTZ, G ;
BUCHS, B ;
SLOSMAN, D ;
RIZZOLI, R .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1991, 73 (03) :555-563
[2]   RADIOIMMUNOASSAY FOR TYPE-I PROCOLLAGEN IN GROWTH HORMONE DEFICIENT CHILDREN BEFORE AND DURING TREATMENT WITH GROWTH-HORMONE [J].
CAREY, DE ;
GOLDBERG, B ;
RATZAN, SK ;
RUBIN, KR ;
ROWE, DW .
PEDIATRIC RESEARCH, 1985, 19 (01) :8-11
[3]  
DEBOER H, 1994, J BONE MINER RES, V9, P1319
[4]   POTENT EFFECT OF RECOMBINANT GROWTH-HORMONE ON BONE-MINERAL DENSITY AND BODY-COMPOSITION IN ADULTS WITH PANHYPOPITUITARISM [J].
DEGERBLAD, M ;
ELGINDY, N ;
HALL, K ;
SJOBERG, HE ;
THOREN, M .
ACTA ENDOCRINOLOGICA, 1992, 126 (05) :387-393
[5]  
DELRIO LD, 1994, PEDIATR RES, V35, P362, DOI 10.1203/00006450-199403000-00018
[6]   PATHOGENESIS OF OSTEOPOROSIS [J].
DEMPSTER, DW ;
LINDSAY, R .
LANCET, 1993, 341 (8848) :797-801
[7]  
Greulich W.W., 1971, RADIOGRAPHIC ATLAS S
[8]   FURTHER INCREASE IN FOREARM CORTICAL BONE-MINERAL CONTENT AFTER DISCONTINUATION OF GROWTH-HORMONE REPLACEMENT [J].
HOLMES, SJ ;
WHITEHOUSE, RW ;
ECONOMOU, G ;
OHALLORAN, DJ ;
ADAMS, JE ;
SHALET, SM .
CLINICAL ENDOCRINOLOGY, 1995, 42 (01) :3-7
[9]   REDUCED BONE-MINERAL DENSITY IN PATIENTS WITH ADULT-ONSET GROWTH-HORMONE DEFICIENCY [J].
HOLMES, SJ ;
ECONOMOU, G ;
WHITEHOUSE, RW ;
ADAMS, JE ;
SHALET, SM .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1994, 78 (03) :669-674
[10]   GROWTH-HORMONE DEFICIENCY DURING PUBERTY REDUCES ADULT BONE-MINERAL DENSITY [J].
HYER, SL ;
RODIN, DA ;
TOBIAS, JH ;
LEIPER, A ;
NUSSEY, SS .
ARCHIVES OF DISEASE IN CHILDHOOD, 1992, 67 (12) :1472-1474