One examination of the demographics of ecstasy users (Klitzman et al. 2002), one review examining the effects of ecstasy on a medical condition (Zagnoni and Albano 2002), one review paper (Kraemer and Maurer 2002), and five in vitro or non-human animal studies (Darvesh et al. 2002; Glennon et al. 2002; Johnson et al. 2002a; Johnson et al. 2002b; Yuan et al. 2002) were located in this time period. No human clinical trials or comparisons of ecstasy users with non-users were located during this time period.

Ecstasy Use in Gay and Bisexual Men
A large telephone survey of gay and bisexual men residing in New York found demographic differences in men reporting moderate ecstasy use versus men reporting more frequent ecstasy use, with moderate users being more openly gay or bisexual and less likely to visit nightclubs (Klitzman et al. 2002).

Reviews
Case studies and research on the pharmacokinetics of MDMA and similar drugs are reviewed in humans and non-human animals (Kraemer and Maurer 2002), with the authors concluding that enzymes other than CYP2D6 are probably involved in MDMA metabolism, and that there may also be a role for catechol-O-methyltransferace (COMT). A brief review of stimulants and epilepsy reported that ecstasy can also produce seizures (Zagnoni and Albano 2002).

Rat Drug Discrimination
A rat drug discrimination study of 5,6,7,8-tetrahydro-1,3-dioxolo[4,5-g]isoquinoline (TDIQ) and conformationally restricted versions of phenethylamine stimulants and hallucinogens, taken together with receptor binding studies, suggests that the MDMA stimulus in rats is due in part to drug activity at alpha2 adrenergic receptors in addition to the well documented serotonin activity (Glennon et al. 2002).

MDMA neurotoxicity in Rats and Mice
Findings from a study of glycogenolysis after MDMA in rats is interpreted by the authors as an indication that MDMA can serve as a bioenergetic stressor, with actions sensitive to ambient temperature and 5HT2A activity (Darvesh et al. 2002). A study in mice found that chronic exposure to corticosterone (via implanted minipump) could exacerbate dopaminergic damage after S-(+)-MDMA in a mouse model of MDMA neurotoxicity, offering some tentative support for a moderating role of stress (or other conditions that elevate cortisol) in MDMA neurotoxicity (Johnson et al. 2002a).

Mice: Vitamin E and Liver Damage
Vitamin E was found to protect the livers of mice given S-(+)-MDMA from damage, suggesting that humans deficient in vitamin E may face an increased risk for liver problems after ecstasy use (Johnson et al. 2002b). Findings that the monoamine depletors reserpine and AMPT reduced MDMA neurotoxicity in rats only in a room temperature environment suggests that neuroprotection after reserpine pre-treatment relate to reduced body temperature and not to depletion of 5-HT or DA (Yuan et al 2002).