New approach to the diagnosis of growth hormone deficiency in adults

1996 ◽  
Vol 134 (3) ◽  
pp. 352-356 ◽  
Author(s):  
Ezio Ghigo ◽  
Gianluca Aimaretti ◽  
Laura Gianotti ◽  
Jaele Bellone ◽  
Emanuela Arvat ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Gh Deficiency ◽  
Serum Insulin ◽  
Normal Subjects ◽  
Hormone Deficiency ◽  
New Approach ◽  
Igf I ◽  
Ghrh Test ◽  
Gh Deficiency In Adults

Ghigo E, Aimaretti G, Gianotti L, Bellone J, Arvat E, Camanni F. New approach to the diagnosis of growth hormone deficiency in adults. Eur J Endocrinol 1996;134:352–6. ISSN 0804–4643 Pyridostigmine (PD), a muscarinic cholinergic agonist, and arginine (ARG) clearly increase the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) in man. The current study was undertaken to investigate the value and safety of PD + GHRH and ARG + GHRH tests as well as the measurement of serum insulin-like growth factor I (IGF-I) in diagnosing GH deficiency in adults. Fifty-four patients considered GH deficient from extensive organic or idiopathic pituitary disease and 326 healthy adults were studied. The IGF-I concentrations were lower than the 3rd percentile of normal values in only 31 of the 54 (57.4%) patients with hypopituitarism. However, the IGF-I levels in hypopituitary patients and in normal subjects overlapped more frequently between 41 and 60 years (50%) and between 61 and 80 years (92.3%) as opposed to between 20 and 40 years (8.6%). In contrast to the IGF-I measurement, the ranges of peak GH responses to PD + GHRH and ARG + GHRH tests were clearly differentiated between the hypopituitary (0.2–6.8 and 0.1–9.5 μg/l, respectively) and normal subjects 17.7–114 and 16.1–119 μg/l, respectively). However, the PD + GHRH test was reliable only in subjects of 20–40 years of age. In conclusion, IGF-I measurement had no value in the diagnosis of GH deficiency in adults aged over 40 years, but is reliable enough when young adults of 20–40 years of age are considered. Both PD + GHRH and ARG + GHRH testing should be considered more reliable biochemical measurements of GH deficiency. In contrast to the PD + GHRH test, the ARG + GHRH test is reliable throughout the adult lifespan and appears to be the most appropriate for patient compliance and safety. F Camanni, Divisione di Endocrinologia, Ospedale Molinette, C.so Dogliotti 14, 10126 Torino, Italy

scholarly journals IGF-1 and IGFBP 3 in Growth Hormone Deficiency Role of Insulin Like Growth Factor-1 (IGF-1) and IGF Binding Protein 3 in the Diagnosis of Growth Hormone Deficiency: Changing Paradigm

2012 ◽  
Vol 32 (2) ◽  
pp. 154-162 ◽  
Author(s):  
SK Kota ◽  
S Jammula ◽  
K Gayatri ◽  
SK Kota ◽  
PR Tripathy ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Gh Deficiency ◽  
False Positive Rate ◽  
Hormone Deficiency ◽  
Provocative Test ◽  
Definitive Evidence ◽  
Gh Secretion ◽  
Igf I ◽  
Igfbp 3

GH stimulation tests are widely used in the diagnosis of GH deficiency (GHD), although they are associated with a high false positive rate. Serum IGF-I levels are monitored during GH replacement treatment in subjects with GH deficiency (GHD) to guide GH dose adjustment and to minimize occurrence of GHrelated side-effects. The need for reliance on provocative testing is based on evidence that the evaluation of spontaneous growth hormone (GH) secretion over 24 hours and the measurement of IGF-I and IGFBP-3 levels do not distinguish between normal and GHD subjects. Regarding IGF-I, it has been demonstrated that very low levels in patients highly suspected for GHD (i.e., patients with childhood-onset, severe GHD, or with multiple hypopituitarism acquired in adulthood) may be considered definitive evidence for severe GHD obviating the need for provocative tests. However, normal IGF-I levels do not rule out severe GHD and therefore adults suspected for GHD and with normal IGF-I levels must undergo a provocative test of GH secretion. We hereby review the various literatures at disposal justifying the use of IGF-1 and IGBP3 for diagnosis of growth hormone deficiency.Data Source: We searched PUBMED and MEDLINE database for relevant articles including key words. References of each article were further reviewed for final synthesis of the manuscript.J Nepal Paediatr Soc 2012;32(2):154-162 doi: http://dx.doi.org/10.3126/jnps.v32i2.5342

GROWTH AND GROWTH HORMONE. IV. LIMITATIONS OF THE GROWTH HORMONE RESPONSE TO INSULIN AND ARGININE AND OF THE IMMUNOREACTIVE INSULIN RESPONSE TO ARGININE IN THE ASSESSMENT OF GROWTH HORMONE DEFICIENCY IN CHILDREN

PEDIATRICS ◽  
1969 ◽  
Vol 43 (6) ◽  
pp. 989-1004
Author(s):  
R. Youlton ◽  
S. L. Kaplan ◽  
M. M. Grumbach
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Gh Deficiency ◽  
Hormone Deficiency ◽  
Insulin Administration ◽  
Arginine Infusion ◽  
Group 3 ◽  
Group 2 ◽  
Serum Gh ◽  
Group 1

The growth hormone (GH) response to insulin-induced hypoglycemia and to arginine infusion has been evaluated in 60 children with growth retardation. These children have been classified into three groups: Group 1-9 children had peak serum growth hormone values of 7 mµg/ml or greater to both stimuli, a normal growth hormone response. Group 2-18 children had peak GH values of ≤ 3 mµg/ml to both stimuli, an abnormal response indicating growth hormone deficiency. Group 3-6 children had a blunted GH response (> 3 < 7 mµg/ml) to both stimuli; 8 showed a normal rise in serum GH following arginine infusion (> 7 mµg/ml) but exhibited no rise, or a minimal one, following insulin administration; 9 children had minimal increase in serum GH concentration following arginine infusion but showed a normal GH response to insulin administration (> 7mµg/ml). Children included in Group 3 represent a heterogenous population. In some patients with a blunted response to both stimuli, evidence of partial or less severe form of GH deficiency was found, whereas in 17 of 18 children exhibiting a disparate response the impaired growth was not attributable to growth hormone deficiency. The blood glucose at all sampling periods was significantly lower following insulin administration in patients in Group 2 than that observed for children in Group 1 and 3. The blood glucose was significantly lower at 90 and 120 minutes following arginine infusion in Group 2 compared to values for patients in Group 1 and 3. Changes in serum insulin in response to the infusion of arginine did not provide a useful index of discrimination among these groups. Administration of diethylstilbestrol, 10 mg/day times 2 days, prior to testing can modify the GH response to both hypoglycemia and arginine; it is a useful ancillary procedure in children with blunted or disparate responses. These studies suggest that two types of stimulation tests are necessary to establish the diagnosis of isolated GH deficiency with a high degree of probability.

Erythrocytes from patients with low serum concentrations of IGF-I have an increase in receptor sites for IGF-I

1991 ◽  
Vol 125 (4) ◽  
pp. 354-358 ◽  
Author(s):  
R. Eshet ◽  
Z. Dux ◽  
A. Silbergeld ◽  
R. Koren ◽  
B. Klinger ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Deficiency ◽  
Specific Binding ◽  
Hormone Deficiency ◽  
Scatchard Analysis ◽  
Isolated Growth Hormone Deficiency ◽  
Receptor Sites ◽  
Igf I ◽  
The Mean ◽  
Low Serum

Abstract. The binding characteristics of insulin-like growth factor I on erythrocytes were studied in 11 patients with long-term IGF-I deprivation and low serum IGF-I levels. Six patients had Laron type dwarfism and 5 idiopathic isolated growth hormone deficiency, with a mean (± sem) serum IGF-I level of 6.01±1.01 nmol/l as compared with that in 25 normal controls of 26.35±2.73 nmol/l (p=0.00001). The mean (± sem) [125I]IGF-I specific binding at a concentration of 4×1012 cell/l was 12.11±1.29% for the patient group compared with 8.75±0.62% for the controls (p=0.005). Scatchard analysis showed a curvilinear plot. Using a non-linear curve fit, the mean (± sem) number of high-affinity receptor sites per cell was found to be 7.34±1.80 in the IGF-I-deprived patients and 2.84±0.29 in the controls (p=0.0005). The mean ± sem dissociation constant was found to be 0.33±0.10 nmol/l for the patients and 0.26±0.08 nmol/l for the controls (NS). This study has demonstrated that the low serum concentration of IGF-I in Laron type dwarfism and isolated growth hormone deficiency is associated with an increase in receptor sites for IGF-I on the erythrocytes. The application of this property as a diagnostic aid remains to be established.

Growth hormone and insulin-like growth factor regulate insulin-like growth factor-binding protein-1 in Laron type dwarfism, growth hormone deficiency and constitutional short stature

1992 ◽  
Vol 127 (4) ◽  
pp. 351-358 ◽  
Author(s):  
Zvi Laron ◽  
Anne-Maria Suikkari ◽  
Beatrice Klinger ◽  
Aviva Silbergeld ◽  
Athalia Pertzelan ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Factor ◽  
Growth Hormone Deficiency ◽  
Short Stature ◽  
Hormone Deficiency ◽  
Pituitary Hormone ◽  
Healthy Children ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
Igf I

Insulin-like growth factors (IGFs) mediate the effects of growth hormone (GH), and the insulin-like growth factor-binding proteins (IGFBPs) modulate the actions of IGFs in tissues. We studied the circulating levels of IGFBP-1 in 6 children and 9 adults with Laron type dwarfism (LTD), in 11 children and 21 adults with growth hormone deficiency (GHD), and in 8 children with constitutional short stature. Compared with the situation in healthy children, the basal serum IGFBP-1 concentration was 5.4-fold higher in LTD children, 4.1-fold higher in GHD children, and 3.8-fold higher in children with short stature (p<0.02 vs controls in all groups). In adult patients with multiple pituitary hormone deficiency (MPHD), the IGFBP-1 concentration was 2-fold elevated, but it was normal in adult LTD patients. Intravenous (N= 10) or subcutaneous (N=9) administration ofIGF-I (75 μg·kg−1 and 150 μg·kg−1, respectively) in LTD children resulted in a rapid 50–60% fall in serum insulin (p<0.02), a decline in blood glucose and a concomitant 40–60% rise of IGFBP-1 levels (p<0.05). Treatment for seven days with IGF-I (150 μg·kg−1·d−1) resulted in a decrease by 34% and 44% of serum IGFBP-1 level in two out of three children with LTD. After prolonged GH therapy, the IGFBP-1 level fell in GHD children by 29% (p<0.05), in GHD adults by 52% (p<0.02) and in children with constitutional short stature by 17% (p<0.02). IGFBP-1 and insulin concentrations were inversely related in patients with GHD (r= −0.66, p<0.001) or with LTD (r= −0.57, p<0.05). Our data suggest that: (a) increased IGFBP-1 concentration in LTD, GHD and constitutional short children may, at least in part, be accounted for by an IGF-I deficiency; (b) both the rise in IGF-I and a fall in insulin contributed to the rise in IGFBP-1 after acute IGF-I administration; (c) prolonged IGF-I or GH treatment causes a persistent decline in IGFBP-1 concentration. In conclusion, IGF-I and GH may regulate IGFBP-1 secretion either directly or via insulin.

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