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In vitro exposure to ecstasy (3,4-methylenedioxymethamphetamine, MDMA) alters some immune parameters such as T-cell regulatory function, cytotoxic T-lymphocyte activity, natural killer cell activity and macrophage function. Administration of MDMA in rats produces a suppression of lympho-proliferation response and a decrease in circulating lymphocytes, accompanied by an increase in plasma corticosterone. It was postulated a direct action of MDMA on lymphocytes or rather an indirect action mediated by the hypothalamic pituitary adrenal axis (HPA-AXIS) and/or the sympathetic nervous system (SNS). Acute MDMA treatment effected on healthy-volunteers produces an immune dysfunction associated with pharmaceutical characteristics and so with MDMA plasma concentrations. There is a decrease in CD4+ T-cells and functional responsiveness of lymphocytes, while percentage of natural killer cells increases. A contemporary rise of cortisol plasma concentrations supports the hypothesis of MDMA-induced release of corticotrophin-releasing factor from the hypothalamus and subsequent HPA-axis and SNS activation.

The authors report their experience regarding the identification of Apo-E alleles on atheroma carotid plaques in 20 patients of both sexes diagnosed as suffering from severe carotid stenosis using Doppler tests. A DNA hybridization and amplification method was used to identify Apo E-2, Apo E-3 and Apo E-4 alleles and their various phenotypical combinations. The following results were obtained in the 20 plaques examined: Apo E-3/E-4 in 114 patients (70%), 2 diabetic patients Apo E-4/E-3, one vascular demented patient Apo E-2/E-3, and 3 plaques defined as severely calcified Apo E-2/E-2. It can therefore be seen that the majority of plaques (70%), considered a risk for future stroke due to altered carotid Doppler tests, does not differ greatly by the homozygote allele Apo E-3/E-3 commonly found in the blood of the so-called "normal" population. It is difficult to draw any conclusions from the alleles found in the other 5 patients due to their scarce statistical value and the limited number of carotid plaques examined, but there appears to be some sort of correlation between calcified plaque, hyperlipidemia and the allele Apo E-2/E-2, with an interchange of position between cysteine arginine amino acids in the Apo E sequences.