[生长激素缺乏儿童和青少年在重组人生长激素(GH)替代治疗前后一年的左心室质量和功能]。

Jolanta Szczepańska Kostro, Joanna Tołwińska, Mirosława Urban, Barbara Głowińska
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引用次数: 0

摘要

未标记:25例患者(10名女孩,15名男孩),年龄8.1-16.9岁(平均13.3+/-1.8岁),身高1.15-1.61 m(平均1.4+/-0.1 m),体面积0.84-1.47 m2(平均1.14+/-0.18 m2)。经过12个月的rhGH治疗后,23名儿童(9名女孩和14名男孩)被重新评估。对照组为年龄6.6-16岁(平均12岁,6+/-2.7岁),身高1.33-1.8 m(平均1.58+/-0.16),体面积0.93-1.8 m2(平均1.38+/-0.3 m2),无动脉粥样硬化和心血管疾病家族史的健康、苗条儿童22名(11名女孩,11名男孩)。采用m型超声心动图、二维超声心动图及同时记录二维图像的多普勒法评价左室质量和功能。治疗前每位患者的收缩功能参数(SF和EF)均正常。实验组左室收缩分数(SF)平均为35.4% +/- 4.5%,对照组平均为36.7+/- 3.9%。实验组左室射血分数(EF)平均为65.1+/- 5.9%,对照组平均为67.9+/- 6.4%。所记录的差异没有统计学意义。经过一年的rhgh治疗,每位患者的SF和EF都在正常范围内。实验组SF平均为35.9+/-3.6%,对照组为36.7+/-3.9%。实验组的平均EF为65.7+/-4.6%,对照组为67.9+/-6.4%。差异无统计学意义。rhGH治疗前后SF和EF无显著差异。治疗前以体表面积(LVA/BSA)为指标的左室质量为68.3+/-18.6 g/m2,与对照组(68.2+/-15.5 g/m2)相比无显著差异。经过一年的生长激素治疗,LV/BSA明显高于治疗前(78.2+/-14.9 g/m2 vs 68.3+/- 18.6 g/m2)。在生长激素缺乏的儿童中,等容松弛时间(IVRT)显著延长,这可能表明心脏左心室舒张功能受损。2. 与治疗前相比,12个月rhgh替代治疗导致左心室质量增加,而等容量松弛时间仍然更长。3.生长激素缺乏的儿童应监测其循环系统,以观察左心室功能障碍的动态。
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[Left ventricular mass and function in growth hormone deficient children and adolescents before and after one year of recombinant human growth hormone (GH) replacement therapy].

Unlabelled: A total of 25 patients (10 girls and 15 boys) aged 8.1-16.9 years (mean 13.3+/-1.8 years), height 1.15-1.61 m (mean 1.4+/-0.1 m), body area 0.84-1.47 m2 (mean 1.14+/-0.18 m2) were examined in our study. After 12-month--rhGH therapy, 23 children (9 girls and 14 boys) were re-evaluated. Twenty two healthy and slim children (11 girls and 11 boys) aged 6.6-16 years (mean 12,6+/-2.7 years), height 1.33-1.8 m (mean 1.58+/-0.16), body area 0.93-1.8 m2 (mean 1.38+/-0.3 m2) with a family history without atherosclerosis and cardiovascular diseases constituted controls. Mass and function of LV were evaluated by means of M-mode and 2D echocardiography and the Doppler method with simultaneous 2D picture recording. Systolic function parameters (SF and EF) were normal in each patient before therapy. LV systolic fraction (SF) equaled on average 35.4+/-4.5 % in the examined group and 36.7+/-3.9 % in controls. LV ejection fraction (EF) was on average 65.1+/-5.9 % in the examined group and 67.9+/-6.4 % in controls. The differences noted were not statistically significant. After a year-rhGH therapy, SF and EF were within a normal range in each patient. SF was on average 35.9+/-3.6% in the examined group and 36.7+/-3.9% in controls. EF was on average 65.7+/-4.6% in the examined group and 67.9+/-6.4% in controls. The differences were not statistically significant. SF and EF did not differ before and after rhGH therapy. LV mass indexed by body superficial area (LVA/BSA) equaled 68.3+/-18.6 g/m2 before therapy and did not differ significantly in comparison with controls (68.2+/-15.5 g/m2). After a year-GH therapy, LV/BSA was significantly higher when compared to LV/BSA mass before therapy (78.2+/-14.9 g/m2 vs 68.3+/-18 6 g/m2, p<0.05). After a year-GH therapy LV/BSA mass was significantly higher in comparison with LV/BSA mass before therapy (78.2+/-14.9 g/m2 vs 68.3+/-18.6 g/m2, p< 0.05). Before therapy, IVRT parameter was found significantly extended in comparison with controls (70.8+/-14.2 vs 64.1+/-8.5 ms, p<0.05). Other parameters characterising LV diastolic function were not significantly different between the groups. After a year-GH therapy, IVRT parameter was still extended in comparison with controls (72.3+/-9.2 vs 64.1+/-8.5 ms, p<0.05). No significant differences were observed with regard to IVRT before and after therapy.

Conclusion: 1. A significant extension of isovolumetric relaxation time (IVRT) was proved in children with GH deficiency, which may suggest an impaired diastolic function of the heart left ventricle. 2. 12-month-rhGH replacement therapy causes an increase in the left ventricle mass when compared to the values before therapy, whereas isovolumetric relaxation time remains still longer. 3. Children with GH deficiency should have their circulatory system monitored to observe the dynamics of the left ventricle functional disorders.

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