It is estimated that there are half a million users of 3.4-methylenedioxymeth-amphetamine (MDMA, ÊecstasyË) every week in the UK, use being predominantly associated with clubbing. However the metabolic effects of MDMA are not well described. MDMA given to subjects in a laboratory setting stimulated vasopressin (Forsling et al. 2001 ) and a study has now been performed Êin the fieldË on 51 self nominating drug users (18 women, 33 men) with a mean age of 25 years. All recruits were experienced clubbers who on average had been clubbing for 6.6 yrs, the majority (49/51) smoked cigarettes and all had used ‘ecstasy’ previously.
The study was performed with the consent of the local ethics committee and all participants gave written consent. Subjects attended the study centre before going clubbing and returned at the end of the evening. Pre-and post clubbing measurements of body weight, pulse rate and sitting and standing blood pressure were performed and urine and blood samples obtained to determine parameters of fluid balance and plasma hormone concentrations and to confirm drug use.
Of the 31 subjects whose urine tested positive for a psychoactive substance, 21 clubbers screened positive for MDMA. Eight clubbers had blood alcohol levels ranging from 23-106 mg/dl, of which only one used in combination with MDMA. Two clubbers had tested above the legal limit for driving (80 mg/dl). The other main substance used was cannabis The average, resting pre-clubbing pulse rate was 78 (range 60-120) BPM rising to 99.3 (range 140-170) BPM upon return to the club site. There were 18 post-clubbing subjects who had BPM>100. Five post clubbers who returned to the test site had indications of hypertension. All of these had confirmed use of MDMA during the evening. Plasma sodium fell significantly from 138 ± 0.5 to 136 0.4 mmol/l (S.E.M., P < 0.05 paired Student’s t test) in those taking MDMA while there was no significant change in the other participants. Post-clubbing the urinary osmolality was 600 ± 83 mOsm/kg in the MDMA group as compared to 368 ± 84 mOsm/kg although this difference failed to reach statistical significance. Plasma cortisol concentrations increased in both the group taking MDMA and those who did not. However the increase in the former group was greater, the concentrations being 670.5 ± 101.6 as compared to 411.5 ± 65 mmol/l. The mean plasma vasopressin concentration in the MDMA group increased from a mean of 2.1 ± 0.6 pmol/l to 2.8 ± 0.9 pmol/l, while the values in the other group fell from 2.5 ± 0.8 to 2.1 ± 0.8 pmol/l. None of these values were significantly different from each other. Overall there was no good correlation of vasopressin with plasma osmolality. Mean plasma oxytocin concentrations rose significantly (P < 0.05) after ingestion of MDMA from 3.6 ± 0.52 pmol/ml to 4.9 ± 0.48 pmol/ml. There was no significant change in the other group. Thus the use of MDMA can result in a drop in plasma osmolality which could result from enhanced neurohypopohysial hormone release.