Inhibition of stress-induced hyperprolactinaemia.

the presence of a low transferrin level is explained by this abnormal tumour ferritin having the capacity to bind 300t, of the serum iron. Excessive serum levels of ferritin may lead to an increased iron transfer to hepatic cells.:' In this patient the localisation of excessive iron is consistent with such an effect mediated by tumour ferritin. This in turn may have produced a stimulus to iintestinal iron absorption. I Although haemochromatosis will increase the risk of primary tumour development5 it is an unlikely occurrence in this case. The atypical iron distribution limited to liver and spleen, lack of family history, and high iron binding capacity are against the diagnosis of primary haemochromatosis. Probably the bronchial carcinoma produced an abnormal ferritin that resulted in excessive iron absorption from the gastrointestinal tract and increased iron deposition in the liver and spleen.