Timing of onset of growth hormone deficiency is a major influence on insulin-like growth factor I status in adult life.

2.50
Hdl Handle:
http://hdl.handle.net/10541/80233
Title:
Timing of onset of growth hormone deficiency is a major influence on insulin-like growth factor I status in adult life.
Authors:
Lissett, Catherine A; Murray, Robert D; Shalet, Stephen M
Abstract:
OBJECTIVE: Several reports have suggested that IGF-I levels in patients with childhood-onset (CO) GH deficiency are lower than those observed in patients with adult-onset (AO) GH deficiency. However, these reports are unsatisfactory as there are several differences between the cohorts studied other than the timing of onset of GH deficiency; in particular, the patients were not matched for equal severity of GH deficiency. We have pursued this question further by examining the IGF-I standard deviation score (SDS) in patients with CO and AO GH deficiency, with equal degrees of severity of GH deficiency, as defined by the peak GH response to the insulin tolerance test (ITT). PATIENTS AND MEASUREMENTS: IGF-I SDS were compared in 146 non acromegalic patients (69 male), aged 15.7-76.6 years (median 33.4 years), bone mass index (BMI) 27.8 +/- 5.8 kg/m2, with severe GH deficiency (peak GH response < 9 mU/l to insulin-induced hypoglycaemia). Patients were subdivided by timing of onset of GH deficiency and the peak GH response to the ITT (GH response < or = 1 mU/l, group 1; > 1-3 mU/l, group 2; > 3-6 mU/l, group 3; > 6-8.9 mU/l, group 4). RESULTS: The IGF-I SDS (mean value +/- SD) in the CO group (n = 63) as a whole was significantly lower than that found in the AO group (n = 83) (-3.7 +/- 2.8 vs.-1.55 +/- 2.2, respectively; P < 0.0001). Despite this, there was no significant difference in the peak GH response to an ITT between the two cohorts (2.8 +/- 2.3 mU/l in the AO cohort and 2.6 +/- 2.2 mU/l in the CO cohort; P = 0.5). When the cohorts were subdivided by severity of GH deficiency, there remained a significant difference in IGF-I SDS in groups 1 (P < 0.0001), 2 (P = 0.05) and 3 (P < 0.05), but there was no significant difference between the AO and CO cohorts in group 4. The peak GH response to an ITT was similar in the AO and CO cohorts in all groups (P = 0.8, 0.8, 0.9 and 0.3 in groups 1-4, respectively). Although increasing severity of hypopituitarism was associated with a decline in IGF-I SDS in the CO cohort (P < 0.01), this was not the case in the AO cohort (P = 0.3). CONCLUSION: These data support the hypothesis that there is an innate difference between adult patients with either CO or AO GH deficiency that cannot be explained solely by variation in the severity of GH deficiency. A possible explanation is that childhood GH deficiency programmes the subsequent relationship between GH and IGF-I in adult life or that the body composition changes, which are more severe in AO GH deficiency, influence IGF-I status.
Affiliation:
Department of Endocrinology, Christie Hospital, Manchester, UK.
Citation:
Timing of onset of growth hormone deficiency is a major influence on insulin-like growth factor I status in adult life. 2002, 57 (1):35-40 Clin. Endocrinol.
Journal:
Clinical Endocrinology
Issue Date:
Jul-2002
URI:
http://hdl.handle.net/10541/80233
PubMed ID:
12100067
Type:
Article
Language:
en
ISSN:
0300-0664
Appears in Collections:
All Christie Publications

Full metadata record

DC FieldValue Language
dc.contributor.authorLissett, Catherine A-
dc.contributor.authorMurray, Robert D-
dc.contributor.authorShalet, Stephen M-
dc.date.accessioned2009-09-08T10:07:44Z-
dc.date.available2009-09-08T10:07:44Z-
dc.date.issued2002-07-
dc.identifier.citationTiming of onset of growth hormone deficiency is a major influence on insulin-like growth factor I status in adult life. 2002, 57 (1):35-40 Clin. Endocrinol.en
dc.identifier.issn0300-0664-
dc.identifier.pmid12100067-
dc.identifier.urihttp://hdl.handle.net/10541/80233-
dc.description.abstractOBJECTIVE: Several reports have suggested that IGF-I levels in patients with childhood-onset (CO) GH deficiency are lower than those observed in patients with adult-onset (AO) GH deficiency. However, these reports are unsatisfactory as there are several differences between the cohorts studied other than the timing of onset of GH deficiency; in particular, the patients were not matched for equal severity of GH deficiency. We have pursued this question further by examining the IGF-I standard deviation score (SDS) in patients with CO and AO GH deficiency, with equal degrees of severity of GH deficiency, as defined by the peak GH response to the insulin tolerance test (ITT). PATIENTS AND MEASUREMENTS: IGF-I SDS were compared in 146 non acromegalic patients (69 male), aged 15.7-76.6 years (median 33.4 years), bone mass index (BMI) 27.8 +/- 5.8 kg/m2, with severe GH deficiency (peak GH response < 9 mU/l to insulin-induced hypoglycaemia). Patients were subdivided by timing of onset of GH deficiency and the peak GH response to the ITT (GH response < or = 1 mU/l, group 1; > 1-3 mU/l, group 2; > 3-6 mU/l, group 3; > 6-8.9 mU/l, group 4). RESULTS: The IGF-I SDS (mean value +/- SD) in the CO group (n = 63) as a whole was significantly lower than that found in the AO group (n = 83) (-3.7 +/- 2.8 vs.-1.55 +/- 2.2, respectively; P < 0.0001). Despite this, there was no significant difference in the peak GH response to an ITT between the two cohorts (2.8 +/- 2.3 mU/l in the AO cohort and 2.6 +/- 2.2 mU/l in the CO cohort; P = 0.5). When the cohorts were subdivided by severity of GH deficiency, there remained a significant difference in IGF-I SDS in groups 1 (P < 0.0001), 2 (P = 0.05) and 3 (P < 0.05), but there was no significant difference between the AO and CO cohorts in group 4. The peak GH response to an ITT was similar in the AO and CO cohorts in all groups (P = 0.8, 0.8, 0.9 and 0.3 in groups 1-4, respectively). Although increasing severity of hypopituitarism was associated with a decline in IGF-I SDS in the CO cohort (P < 0.01), this was not the case in the AO cohort (P = 0.3). CONCLUSION: These data support the hypothesis that there is an innate difference between adult patients with either CO or AO GH deficiency that cannot be explained solely by variation in the severity of GH deficiency. A possible explanation is that childhood GH deficiency programmes the subsequent relationship between GH and IGF-I in adult life or that the body composition changes, which are more severe in AO GH deficiency, influence IGF-I status.en
dc.language.isoenen
dc.subject.meshAdolescent-
dc.subject.meshAdult-
dc.subject.meshAge of Onset-
dc.subject.meshAged-
dc.subject.meshChi-Square Distribution-
dc.subject.meshFemale-
dc.subject.meshHumans-
dc.subject.meshInsulin-
dc.subject.meshInsulin-Like Growth Factor I-
dc.subject.meshMale-
dc.subject.meshMiddle Aged-
dc.subject.meshPituitary Diseases-
dc.subject.meshSomatostatin-
dc.subject.meshStatistics, Nonparametric-
dc.titleTiming of onset of growth hormone deficiency is a major influence on insulin-like growth factor I status in adult life.en
dc.typeArticleen
dc.contributor.departmentDepartment of Endocrinology, Christie Hospital, Manchester, UK.en
dc.identifier.journalClinical Endocrinologyen

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