Lung volumes and respiratory muscle strength in adult patients with childhood- or adult-onset growth hormone deficiency: effect of 12 months' growth hormone replacement therapy

Abstract

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.

Action of GH on skeletal muscle function: molecular and metabolic mechanisms

“…Oxygen delivery to exercising muscles depends on cardiac function, lung capacity and oxygen-carrying capacity of the blood (Saltin & Strange 1992). Adults with GHD have impaired cardiac function (Colao et al 2001), diminished lung capacity (Merola et al 1996) and reduced red cell mass (Christ et al 1997). These deficits are restored with GH replacement.…”

“…These deficits are restored with GH replacement. In adults with GHD, GH replacement increases i) cardiac output, which arises from enhancement of heart rate and stroke volume (Jorgensen et al 1989, Cuneo et al 1991a,b, Nass et al 1995, Maison & Chanson 2003; ii) lung capacity by increasing respiratory muscle strength and lung volumes (Nass et al 1995, Merola et al 1996; and iii) red cell mass, which determines oxygen-carrying capacity of the blood (Claustres et al 1987, Vihervuori et al 1996, Christ et al 1997. As discussed previously, biopsy data in humans do not provide evidence that GH increases the number of oxidative type I muscle fibres.…”

Growth hormone therapy and Quality of Life: possibilities, pitfalls and mechanisms

“…Improved pulmonary function may also be involved, particularly in COGHD, since indicators of pulmonary function (lung volumes and respiratory pressures) are impaired in GHD and improved by GH replacement (Merola et al 1996). Impaired ventricular filling (Caidahl et al 1994) and abnormal EEG readings (Shahi et al 1992) during exercise suggest that normal exercise capacity may also depend upon cardiovascular actions of GH.…”

Growth hormone expression in the perinatal and postnatal rat lung

“…For instance, large lungs (Bartlett, 1971), upper airflow obstruction (Trotman-Dickenson et al, 1991), and narrowing of the small airways (Harrison et al, 1978) accompany GH excess, whereas a decrease in muscle strength and a reduction in the maximum inspiratory and expiratory pressure (Merola et al, 1995(Merola et al, , 1996 are associated with GH deficiency. The possibility that the lung is a target site for GH action is also indicated by the GH-induced production of superoxide by alveolar macrophages (Edwards et al, 1992), the GH-induced increase in circulating lung neutrophil activation during sepsis, and the accompanying increase in microvascular injury (Liu et al, 2002a).…”