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Clinica Medica III and the Department of Pharmacology, University of Milan, Cagliari, Italy
The Institute of Pharmacology and Pharmacognosy, University of Cagliari Cagliari, Italy
Address all correspondence and requests for reprints to: Prof. Eugenio E. Miiller, c/o Department of Pharmacology, University of Milan, Via Vanvitelli,32, 20129 Milan, Italy.
The anomalous GH response to TRH or glucose loading was evaluated in patients with severe liver disease untreated or pretreated with metergoline (MGE), a potent antiserotoninergic drug. In 9 patients, injection of 400
g TRH as a bolus induced a clear-cut GH rise (>8 ng/ml), with peak levels 15–90 min post injection. Pretreatment with MCE did not modify baseline GH levels but potentiated the TRH-induced GH rise in 4 patients. In addition, 2 of 8 TRH nonresponder patients developed the anomalous GH response after MCE pretreatment. Like MCE, methysergide, another antiserotoninergic drug, potentiated the TRH-induced GH rise in 2 of 4 patients. Glucose administration (100 g, orally) induced a paradoxical rise of GH in 9 of 10 patients; after MCE, the paradoxical GH response to glucose was potentiated in 6 patients. These data provide the first experimental evidence that a derangement in brain monoamine (serotonin) function is actually involved in the occurrence of anomalous GH responses in subjects with severe liver disease.
Received January 16, 1979.
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