Levels in Disorders of Growth

Because dependence upon circulating CH levels is one of the definitive characteristics of the somatomedins (see Section 1.2), new assays have generally been characterized by their ability to distinguish somatomedin levels in patients with CH disorders from those in healthy subjects. Several studies have compared values in GH-deficient children with those in healthy adults and, while an assay method that could not make this distinction would be invalid, dependence upon CH cannot be established by such comparisons, since somatomedin levels (particularly SM-C/ICF-I) in children without CH deficiency are lower than adult values. 

In studies directly comparing different assay methods, RIA methods invariably show somewhat better discrimination than do other radioligand methods or bioassays. In one such study (B14), 5 out of 13 samples from hyposomatotropic subjects, all of which were clearly low by SM-C/IGF-I RIA, were not distinguishable from samples from healthy subjects by placental membrane RRA using SM-C/IGF-I tracer. The rather poor correlation (r=0.836) between RIA and RRA results for 69 healthy, GH-deficient, or 

Treatment of GH-deficient subjects with human GH (hGH) generally causes a prompt rise in immunoreactive SM-C/IGF-I levels, detectable within a few hours and reaching a peak value approximately 24 hours after administration of the hormone (C19). Similar to SM-C/IGF-I in the serum of healthy subjects, SM-C/IGF-I induced by acute hGH treatment is found mainly in the 150,000-molecular-mass fraction in serum (C19). Rosenfeld et al. (R12) have reported that the rise in serum SM-C/IGF-I in GH-deficient children measured over the first 5 days of hGH treatment is highly predictive of the growth fitctor level determined after 6 months of regular hGH administration. However, there is disagreement as to the relationship be- 

Growth Failure with Normal Growth Hormone 

In a 6-month treatment trial of a group of these patients with hGH, Rudman et al. (17) found that their acute (10-day) and chronic (6-month) SM-C/IGF-I responses were highly correlated, and that both responses showed a very high association with the increased growth velocity at the end of the test period. Patients with this condition might normally be denied GH therapy as they do not satisfy criteria for GH deficiency, but it appears from these studies that GH treatment would he of benefit and, importantly, that a short-term trial of GH administration, monitoring SM-C/IGF-I levels, would differentiate this group fiom Laron dwarfs or other nonresponders. 

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