[INFLUENCE OF HORMONES ON THE ERUPTION AND GROWTH OF RAT MOLAR AND INCISOR TEETH. I. ACTION OF ANABOLIC HORMONES: SOMATOTROPHIC HORMONE AND DIANABOL (SYNTHETIC STEROID)].
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The GHRH test has been proposed to replace conventional stimuli in the diagnosis of GH deficiency. However the reliability of GHRH in discriminating between normal and GH-deficient children is still uncertain. The aim of this study was to compare the GH-releasing effect of GHRH (1 microgram/kg i.v.) with that of two neuroactive drugs, clonidine (CLON, 150 micrograms/m2 orally), an alpha 2-receptor agonist, and pyridostigmine (PD, 60 mg orally), a cholinergic agonist that inhibits cholinesterases, in 23 children and adolescents with normal and familial short stature. The plasma GH peak (mean +/- SEM) after GHRH (20.3 +/- 2.5 ng/ml), CLON (17.0 +/- 2.1 ng/ml) and PD (14.9 +/- 1.5 ng/ml) did not significantly differ. According to the conventional limit (less than 10 ng/ml), a false negative response was present in 6, 5 and 6 subjects after GHRH, CLON and PD, respectively. In conclusion, GHRH, CLON and PD have a similar GH-releasing effect. A similar percentage of false negative responses was observed with all tests and this evidence reduces their diagnostic ability.
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The study included 48 male chronic alcoholics, aged 20 through 50 years, classified in two groups according to the presence (22 patients) or absence (26 patients) of clinically evident sexual disorders. The blood samples were collected the first 2-3 days after hospitalization, before any anti-alcoholic treatment. The control group included 10 adult male normal subjects. By comparison to the control group, the basal level of LH was significantly (p less than 0.01) lower in both groups of alcoholic patients while the FSH level was significantly higher (p less than 0.01) in the group with sexual disorders. The serum levels of testosterone were increased (p less than 0.05) only in the group having sexual disorders. Our data suggest that the feedback regulation of the hypophyseal LH release seems to be impaired by defects in the peripheral metabolization of testosterone.
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