BACKGROUND: Major depression has been associated with a reduction in lymphocyte natural killer cell activity (NKCA). The effects of biological treatment of depression on the immune system have not been systematically investigated. The present study addresses the acute effects of electroconvulsive therapy (ECT) on NKCA. METHODS: Thirteen patients undergoing ECT for major depression were studied. NKCA at four different effector:target (E:T) ratios (E:T = 50:1; 25:1; 12.5:1 and 6.25:1, respectively) was assessed serially in relation to the first ECT session prior to and up to 1 h following treatment (-30', -10', -3' before ECT and +3', +10', +30' and +60' following ECT). On several patients, NKCA data were also available in relation to the sixth ECT session. Comparisons between mean NKCA values for each of the E:T ratios at the different time points were made using ANOVA. RESULTS: There were significant changes in NKCA values with time at E:T=25:1 (P < 0.05). Mean NKCA values for the 30 min following ECT were significantly higher than the mean NKCA values for the 30 min preceding ECT for all four E:T ratios used (P < 0.05). Differences in NKCA values between ECT no. 1 and ECT no. 6 were small and not statistically significant. CONCLUSION: ECT is associated with a significant albeit transient increase in NKCA. The clinical implications of these findings are unknown at the present time. LIMITATIONS: A small number of patients has been investigated, particularly for the sixth ECT session. No control group for ECT was available. No correlations with clinical outcome variables have been obtained.
BACKGROUND: Major depression has been associated with a reduction in lymphocyte natural killer cell activity (NKCA). The effects of biological treatment of depression on the immune system have not been systematically investigated. The present study addresses the acute effects of electroconvulsive therapy (ECT) on NKCA. METHODS: Thirteen patients undergoing ECT for major depression were studied. NKCA at four different effector:target (E:T) ratios (E:T = 50:1; 25:1; 12.5:1 and 6.25:1, respectively) was assessed serially in relation to the first ECT session prior to and up to 1 h following treatment (-30', -10', -3' before ECT and +3', +10', +30' and +60' following ECT). On several patients, NKCA data were also available in relation to the sixth ECT session. Comparisons between mean NKCA values for each of the E:T ratios at the different time points were made using ANOVA. RESULTS: There were significant changes in NKCA values with time at E:T=25:1 (P < 0.05). Mean NKCA values for the 30 min following ECT were significantly higher than the mean NKCA values for the 30 min preceding ECT for all four E:T ratios used (P < 0.05). Differences in NKCA values between ECT no. 1 and ECT no. 6 were small and not statistically significant. CONCLUSION: ECT is associated with a significant albeit transient increase in NKCA. The clinical implications of these findings are unknown at the present time. LIMITATIONS: A small number of patients has been investigated, particularly for the sixth ECT session. No control group for ECT was available. No correlations with clinical outcome variables have been obtained.