Growth hormone drug-induced

Finally, continuous exposure of certain receptors to their macromolecular ligands can lead to rapid downregulation of cell surface receptors, especially if receptor recycling within the cells is incomplete. Fortunately, expression of many receptors, for example for certain cytokines, growth hormones and adhesion factors, can be extensively upregulated in the disease process and this can result in disease-induced drug-targeting. 

Sex differences in hormone concentrations have been investigated in 47 patients (21 men and 26 women) with schizophrenia or related psychoses who were using different neuroleptic drugs (757). The median daily dose and the median body weight-adjusted daily dose were twice as high in men as in women. However, neuroleptic drug-induced hyperprolactinemia was more frequent and occurred at a lower daily dose in women. The growth hormone concentration was normal in all patients. 

The mechanism of action of drug induced hepatocellular tumors is quite similar to epidermal carcinogenesis. There are a series of biochemical changes such as enzyme induction that are parallel in liver and skin. Hyperplastic nodules result from promoter treatment and these nodules regress if the promoting stimulus is removed up to a critical point, after which the nodule is committed to develop into a hepatoma. The preneoplasic nodules contain enzyme altered foci for y-glutamyltranspeptidase, canalicular ATPase, glu-cose-6-phosphatase and iron deficient foci (Pitot et al., 1982). It is not clear whether or not all of the enzyme alTered foci result in hepatomas but they are certainly direct evidence of enhanced clonal growth or cell section and proliferation of presumably initiated cells. The promotional model can be modified by hormonal and dietary factors and this model has potential use for extrapolation to the human population. 

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