Alcohol-dependent patients with neuroendocrine evidence for reduced dopamine d(2) receptor function have decreased platelet monoamine oxidase-B activity.

letter is a report of a re-evaluation of the results obtained in an earlier study of ours (Balldin et al., 1994) of platelet monoamine oxidase (MAO)-B activity in alcoholics with reduced dopamine (DA) D 2 receptor function, as assessed by the growth hormone (GH) response to the D 1 /D 2 agonist apomorphine (APO), which was published in this journal. The reason for the re-evaluation of the results in our study is a Letter to the Editors of this journal by Farren and Dinan (1996) reporting on platelet MAO-B activity in alcoholics with reduced DA D 2 receptor function, as assessed by the GH response to the DA D 2 receptor agonist bromocriptine. In the report by Farren and Dinan (1996), four of eight alcoholics had no increase in GH above baseline, whereas all eight subjects in the control group had the expected GH response to bromocriptine. The authors compared platelet MAO-B activity in the four alcoholic subjects who had no increase in GH above baseline to that in the four alcoholics who had a significant increase in GH after bromocriptine. They found no significant difference in platelet MAO-B activity between these two groups and thus no evidence for altered platelet MAO-B activity in alcoholics with reduced DA D 2 receptor function. In their Letter to the Editors, Farren and Dinan (1996) made a very valuable comment with regard to our earlier study (Balldin et al., 1994). We then reported that platelet MAO-B activity in alcoholics with reduced DA D 2 receptor function, as assessed by the GH response to the DA D 1 /D 2 receptor agonist APO, was not different from that in controls. Eleven out of 14 alcoholics had blunted GH response to APO (an increase in GH above baseline of less than 8 mU/l), in comparison to three out of 12 in the control group. Farren and Dinan (1996) correctly pointed out that we did not compare platelet MAO-B activity in the alcoholics with blunted GH response (n = 11) to those with non-blunted GH response (n = 3). This comment by Farren and Dinan (1996) thus prompted us to re-evaluate the results in our earlier study. When defining blunted GH response in a neuroendocrine challenge test, two criteria for bluntness have been proposed: (1) an increase in GH less than 8 mU/l (Hunt et al., 1986) or (2) less than 2 mU/l (Nutt, 1989). Taking …