The Journal of clinical endocrinology and metabolism · 2013
IGF-I bioactivity might reflect different aspects of quality of life than total IGF-I in GH-deficient patients during GH treatment.
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Varewijck Aimee J, Lamberts Steven W J, Neggers Sebastian J C M M, Hofland Leo J, Janssen Joseph A M J L
Аннотация
CONTEXT: No relationship has been found between improvement in quality of life (QOL) and total IGF-I during GH therapy.
AIM: Our aim was to investigate the relationship between IGF-I bioactivity and QOL in GH-deficient (GHD) patients receiving GH for 12 months.
METHODS: Of 106 GHD patients, 84 on GH treatment discontinued therapy 4 weeks before establishing baseline values and 22 were GH-naive. IGF-I bioactivity was determined by IGF-I kinase receptor activation assay, total IGF-I by immunoassay (Immulite), and QOL by the disease-specific Question on Life Satisfaction Hypopituitarism (QLS-H) module and by the general SF-36 questionnaire (SF-36Q).
RESULTS: IGF-I bioactivity increased after 6 months (-2.5 vs -1.9 SD, P < .001) and did not further increase after 12 months (-1.8 SD, P = .23); total IGF-I increased from -2.3 to -0.9 SD (P < .001) and to -0.6 SD (P = .005), respectively. QLS-H did not change over 12 months (-0.66 ± 0.16 to -0.56 ± 0.17 SD [P = .42] to -0.68 ± 0.17 SD [P = .22]). The mental component summary of the SF-36Q increased from 47.4 (38.7-52.8) to 50.2 (43.1-55.3) (P = .001) and did not further improve (49.4 [42.1-54.1], P = .19); the physical component summary did not change (47.5 [42.0-54.2] vs 47.0 [41.9-55.3], P = .91, vs 48.3 [39.9-55.4], P = .66). After 12 months, IGF-I bioactivity was related to QLS-H (r = 0.28, P = .01); total IGF-I was not (r = 0.10, P = .37). IGF-I bioactivity and total IGF-I were related to PCS (r = 0.35, P = .001; and r = 0.31, P = .003).
CONCLUSION: IGF-I bioactivity remained subnormal after GH treatment and was positively related to QLS-H, whereas total IGF-I was not. This suggests that IGF-I bioactivity reflects different aspects of QOL than total IGF-I in GHD patients during GH treatment.
AIM: Our aim was to investigate the relationship between IGF-I bioactivity and QOL in GH-deficient (GHD) patients receiving GH for 12 months.
METHODS: Of 106 GHD patients, 84 on GH treatment discontinued therapy 4 weeks before establishing baseline values and 22 were GH-naive. IGF-I bioactivity was determined by IGF-I kinase receptor activation assay, total IGF-I by immunoassay (Immulite), and QOL by the disease-specific Question on Life Satisfaction Hypopituitarism (QLS-H) module and by the general SF-36 questionnaire (SF-36Q).
RESULTS: IGF-I bioactivity increased after 6 months (-2.5 vs -1.9 SD, P < .001) and did not further increase after 12 months (-1.8 SD, P = .23); total IGF-I increased from -2.3 to -0.9 SD (P < .001) and to -0.6 SD (P = .005), respectively. QLS-H did not change over 12 months (-0.66 ± 0.16 to -0.56 ± 0.17 SD [P = .42] to -0.68 ± 0.17 SD [P = .22]). The mental component summary of the SF-36Q increased from 47.4 (38.7-52.8) to 50.2 (43.1-55.3) (P = .001) and did not further improve (49.4 [42.1-54.1], P = .19); the physical component summary did not change (47.5 [42.0-54.2] vs 47.0 [41.9-55.3], P = .91, vs 48.3 [39.9-55.4], P = .66). After 12 months, IGF-I bioactivity was related to QLS-H (r = 0.28, P = .01); total IGF-I was not (r = 0.10, P = .37). IGF-I bioactivity and total IGF-I were related to PCS (r = 0.35, P = .001; and r = 0.31, P = .003).
CONCLUSION: IGF-I bioactivity remained subnormal after GH treatment and was positively related to QLS-H, whereas total IGF-I was not. This suggests that IGF-I bioactivity reflects different aspects of QOL than total IGF-I in GHD patients during GH treatment.