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A new model for evaluating leanness/fatness (LeanSDS) in the newborn infant has been used to examine body weight for length in a group of Swedish infants in whom idiopathic growth hormone deficiency (GHD n = 220) was later diagnosed. These infants have earlier been reported to be significantly shorter (median = -0.87 SDS; SDS; standard deviation scores) and lighter (median = -0.60 SDS) in relation to gestational age, than the most recent reference. A group of infants who later developed GHD due to organic etiologies (n = 92) had normal weight and length for gestational age at birth. Using the LeanSDS model (with intercept 0.0 and regression coefficient 0.7) revealed that these idiopathic GHD infants have weight that is normal for their length (mean LeanSDS = 0.11 +/- 0.08 (SEM); n.s.) why the abnormality is a reduced linear growth. These findings also indicate that birth length (linear growth) should be given increased attention when size at birth is evaluated.
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PMID:Normal weight for length in newborn infants in whom growth hormone deficiency was later diagnosed. Swedish Paediatric Study Group for GH Treatment. 819 1

The aim of this study was to verify the persistence in adulthood of GH deficiency diagnosed in childhood and treated with hGH in childhood and to study whether anatomical hypothalamic-pituitary alterations evaluated by magnetic resonance (MR) imaging could predict it. To this goal, in six GHD adults (3 males and 3 females aged 17.2-24.5 yr, BMI 21.8 +/- 1.3), we studied anterior pituitary hormone response to GHRH (1 microgram/kg iv)+pyridostigmine (120 mg po)+ GnRH (100 micrograms iv) +TRH (400 micrograms iv)+hCRH (100 micrograms iv) as well as brain MR imaging. In childhood, the diagnosis of severe isolated GHD had been done based on auxological findings as well as on GH response < 7 micrograms/L after two classical provocative stimuli. In the present study, hormonal responses showed the persistence of severe isolated GHD in 4 out of 6 patients (peak, mean +/- SEM: 3.8 +/- 0.6, range 2.6-4.8 micrograms/L). In these patients, IGF-I levels were found low or low-normal. In other 2 patients, a clear GH response to stimulation (peak: 51.3 and 43.0 micrograms/L, respectively) together with normal IGF-I levels were found. No other anterior pituitary hormone deficiency was present in all subjects. MR imaging showed pituitary hypoplasia in all patients with persistent GHD; in 2 out of them, pituitary stalk interruption and ectopic neurohypophysis was also present. On the other hand, MR imaging showed normal hypothalamo-pituitary morphology in the 2 subjects with normal somatotrope response. In conclusion, our present data indicate that testing with a potent stimulus such as GHRH+pyridostigmine is a reliable method to assess the persistence of GH deficiency which associates with anatomical hypothalamic-pituitary alterations at the MR imaging. Patients with transient GH deficiency in childhood and normal pituitary GH reserve in adulthood have normal hypothalamic-pituitary MR imaging.
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PMID:Is the persistence of isolated GH deficiency in adulthood predicted by anatomical hypothalamic-pituitary alterations? 929 76