Merola B, Longobardi S, Sofia M, Pivonello R, Micco A, Di Rella F, Esposito V, Colao A, Lombardi G
Department of Molecular and Clinical Endocrinology and Oncology, Federico II University, Naples, Italy.
Eur J Endocrinol. 1996 Nov;135(5):553-8. doi: 10.1530/eje.0.1350553.
We have described impairment of the respiratory function in adult patients with childhood-onset growth hormone (GH) deficiency. The aim of the present study was to evaluate lung volumes and respiratory muscle strength in patients diagnosed as GH deficient before and after 6 and 12 months of recombinant GH treatment. Ten adults diagnosed as GH deficient in childhood, ten adults diagnosed as GH deficient in adulthood and ten healthy subjects entered the study. For each subject, evaluation of respiratory function followed the same standard approach, consisting of respiratory muscle strength assessment, record of flow-volume curves, measurement of static lung volumes and lung diffusing capacity. Childhood-onset GH-deficient patients had a significant reduction of maximal inspiratory (p < 0.01) and maximal expiratory (p < 0.05) mouth pressures. Total lung capacity, vital capacity and functional residual capacity were significantly reduced compared to healthy subjects (p < 0.05). Conversely, residual volume and diffusing lung capacity did not show any significant change. No significant change of the ratio between the percentage forced expiratory volume in 1 s and the forced vital capacity was observed. The decrease of respiratory mouth pressures was not correlated to the decrease of lung volumes. Adult-onset GH-deficient patients had only a significant reduction of maximal expiratory pressure compared to healthy subjects (p < 0.05). After 6 months of treatment no significant differences in any of the evaluated parameters were found. After 12 months of treatment patients with childhood-onset GH deficiency show a significant improvement of lung volumes (p < 0.01) and maximal respiratory mouth pressures (p < 0.005), whereas adult-onset GH-deficient patients show a significant improvement of maximal expiratory pressure (p < 0.05). In conclusion, the results of this study showed that adult patients affected with childhood-onset GH deficiency suffer from an impairment of the ventilatory function due to a reduction of lung volumes and a decrease of respiratory pressures probably due to a reduction of respiratory muscle strength. This impairment was reversed after 12 months of treatment with recombinant GH. Conversely, adult-onset GH-deficient patients had only an impairment of the maximal expiratory pressure, probably due to respiratory muscle weakness re-established after 12 months of GH therapy.
我们已经描述了患有儿童期起病的生长激素（GH）缺乏症的成年患者的呼吸功能损害情况。本研究的目的是评估在接受重组生长激素治疗6个月和12个月之前及之后被诊断为生长激素缺乏症的患者的肺容量和呼吸肌力量。十名儿童期被诊断为生长激素缺乏症的成年人、十名成年期被诊断为生长激素缺乏症的成年人以及十名健康受试者参与了该研究。对于每个受试者，呼吸功能评估遵循相同的标准方法，包括呼吸肌力量评估、流量-容积曲线记录、静态肺容量测量以及肺弥散能力测量。儿童期起病的生长激素缺乏症患者的最大吸气（p < 0.01）和最大呼气（p < 0.05）口腔压力显著降低。与健康受试者相比，总肺容量、肺活量和功能残气量显著降低（p < 0.05）。相反，残气量和肺弥散能力未显示任何显著变化。1秒用力呼气量与用力肺活量百分比之间的比值未观察到显著变化。呼吸口腔压力的降低与肺容量的降低无关。成年期起病的生长激素缺乏症患者与健康受试者相比，仅最大呼气压力显著降低（p < 0.05）。治疗6个月后，在任何评估参数中均未发现显著差异。治疗12个月后，儿童期起病的生长激素缺乏症患者的肺容量（p < 0.01）和最大呼吸口腔压力（p < 0.005）有显著改善，而成年期起病的生长激素缺乏症患者的最大呼气压力有显著改善（p < 0.05）。总之，本研究结果表明，患有儿童期起病的生长激素缺乏症的成年患者由于肺容量减少和呼吸压力降低（可能是由于呼吸肌力量减弱）而存在通气功能损害。这种损害在接受重组生长激素治疗12个月后得到逆转。相反，成年期起病的生长激素缺乏症患者仅最大呼气压力受损，可能是由于生长激素治疗12个月后呼吸肌无力得到恢复。
