381
to the patient’s dependence on feel this is unlikely. Though evidence from a placebo-controlled trial is lacking, we had not anticipated relapse on withdrawal of L-tryptophan and had informed patients of this view. L-tryptophan is a weak antidepressant in its own right6 but potentiates the antidepressant effects of tricyclics and particularly MAOIs.7 In depressed patients with antidepressant-induced remission, withdrawal of tryptophan from the diet is associated with relapse (which remits on return to normal food intake). The effect is most noticeable in patients on MAOls.8 The serotonin synthesis inhibitor parachlorophenylalanine reversed the antidepressant effect of the MAOI tranylcypramine within 24 h in patients with
"psychological basis" related
medication but
we
major depression.9 Our fmdings highlight the usefulness of L-tryptophan in the management of chronic depression, and strengthen the need for further research into both serotonin mechanisms in depression" and the possible contaminant of L-tryptophan producing EMS. I. N. FERRIER D. ECCLESTON P. B. MOORE K. A. WOOD
MRC Neurochemical Pathology Unit and Department of Psychiatry, University of Newcastle upon Tyne, NE1 4LP, UK
1. Anon. L-tryptophan and eosinophilia-myalgia syndrome. Drug Ther Bull 1990, 28: 37-38. 2 Eidson M, Philen RM, Sewell CM, Voorhees R, Kilbourne EM. L-tryptophan and eosinophilia-myalgia syndrome in New Mexico. Lancet 1990; 335: 645-48. 3. Committee on Safety of Medicines. Withdrawal of Pacitron and Optimax. April 12, 1990. 4. Scott JS. Chronic depression Br J Psychiatry 1988, 153: 287-97 5 Barker WA, Scott JS, Eccleston D. The Newcastle chronic depression study: results of a treatment regime Int Clin Psychopharmacol 1987; 2: 261-72. 6 Byerley WF, Risch SC. Depression and serotonin metabolism: rationale for neurotransmitter precursor treatment. J Clin Psychopharmacol 1985; 5: 196-206. 7 Baldessarini RJ Treatment of depression by altering monoamine metabolism: precursors and metabolic inhibitors Psychopharmacol Bull 1984, 20: 224-39. 8. Delgado PL, Chamey DS, Price LH, et al. Serotonin function and the mechanism of antidepressant action—reversal of antidepressant induced remission by rapid depletion of plasma tryptophan Arch Gen Psychiatry 1990; 47: 411-18. 9. Shopsin B, Gershon S, Freidman E. Parachlorophenylalanine reversal of tranylcypramine effects in depressed patients. Arch Gen Psychiatry 1976, 33: 811-21. 10. Yates M, Leake A, Candy JM, et al. 5HT2 receptor changes in major depression. Biol Psychiatry 1990; 27: 489-96.
Inhibition by aprotinin of tPA-mediated fibrinolysis during orthotopic liver
transplantation SIR,-Tissue plasminogen activator (tPA)-mediated fibrinolysis has been implicated as a major cause of bleeding during orthotopic liver transplantation (OL T),1 but aprotinin can reduce this blood loss.2 However, aprotinin’s main mechanism of action in reducing bleeding during cardiopulmonary bypass is said to be through inhibition of kallikrein3and it is known not to inhibit tPA in vitro.’ We have attempted to resolve this dichotomy by studying fibrinolysis during OLT. Eight patients were randomised to standard management with or without aprotinin. The two groups were similar with respect to age, sex, diagnoses, previous abdominal surgery, portal hypertension, MEDIAN
-
*=p
to the patient’s dependence on feel this is unlikely. Though evidence from a placebo-controlled trial is lacking, we had not anticipated relapse on withdrawal of L-tryptophan and had informed patients of this view. L-tryptophan is a weak antidepressant in its own right6 but potentiates the antidepressant effects of tricyclics and particularly MAOIs.7 In depressed patients with antidepressant-induced remission, withdrawal of tryptophan from the diet is associated with relapse (which remits on return to normal food intake). The effect is most noticeable in patients on MAOls.8 The serotonin synthesis inhibitor parachlorophenylalanine reversed the antidepressant effect of the MAOI tranylcypramine within 24 h in patients with
"psychological basis" related
medication but
we
major depression.9 Our fmdings highlight the usefulness of L-tryptophan in the management of chronic depression, and strengthen the need for further research into both serotonin mechanisms in depression" and the possible contaminant of L-tryptophan producing EMS. I. N. FERRIER D. ECCLESTON P. B. MOORE K. A. WOOD
MRC Neurochemical Pathology Unit and Department of Psychiatry, University of Newcastle upon Tyne, NE1 4LP, UK
1. Anon. L-tryptophan and eosinophilia-myalgia syndrome. Drug Ther Bull 1990, 28: 37-38. 2 Eidson M, Philen RM, Sewell CM, Voorhees R, Kilbourne EM. L-tryptophan and eosinophilia-myalgia syndrome in New Mexico. Lancet 1990; 335: 645-48. 3. Committee on Safety of Medicines. Withdrawal of Pacitron and Optimax. April 12, 1990. 4. Scott JS. Chronic depression Br J Psychiatry 1988, 153: 287-97 5 Barker WA, Scott JS, Eccleston D. The Newcastle chronic depression study: results of a treatment regime Int Clin Psychopharmacol 1987; 2: 261-72. 6 Byerley WF, Risch SC. Depression and serotonin metabolism: rationale for neurotransmitter precursor treatment. J Clin Psychopharmacol 1985; 5: 196-206. 7 Baldessarini RJ Treatment of depression by altering monoamine metabolism: precursors and metabolic inhibitors Psychopharmacol Bull 1984, 20: 224-39. 8. Delgado PL, Chamey DS, Price LH, et al. Serotonin function and the mechanism of antidepressant action—reversal of antidepressant induced remission by rapid depletion of plasma tryptophan Arch Gen Psychiatry 1990; 47: 411-18. 9. Shopsin B, Gershon S, Freidman E. Parachlorophenylalanine reversal of tranylcypramine effects in depressed patients. Arch Gen Psychiatry 1976, 33: 811-21. 10. Yates M, Leake A, Candy JM, et al. 5HT2 receptor changes in major depression. Biol Psychiatry 1990; 27: 489-96.
Inhibition by aprotinin of tPA-mediated fibrinolysis during orthotopic liver
transplantation SIR,-Tissue plasminogen activator (tPA)-mediated fibrinolysis has been implicated as a major cause of bleeding during orthotopic liver transplantation (OL T),1 but aprotinin can reduce this blood loss.2 However, aprotinin’s main mechanism of action in reducing bleeding during cardiopulmonary bypass is said to be through inhibition of kallikrein3and it is known not to inhibit tPA in vitro.’ We have attempted to resolve this dichotomy by studying fibrinolysis during OLT. Eight patients were randomised to standard management with or without aprotinin. The two groups were similar with respect to age, sex, diagnoses, previous abdominal surgery, portal hypertension, MEDIAN
-
*=p
