The use of electronic cigarettes has increased exponentially since its introduction onto the global market in 2006. However, short- and long-term health effects remain largely unknown due to the novelty of this product. The present study examines the acute effects of e-cigarette aerosol inhalation, with and without nicotine, on vascular and pulmonary function in healthy volunteers. Seventeen healthy subjects inhaled electronic cigarette aerosol with and without nicotine on two separate occasions in a double-blinded crossover fashion. Blood pressure, heart rate, and arterial stiffness measured by pulse wave velocity and pulse wave analysis were assessed at baseline, and then at 0 h, 2 h, and 4 h following exposure. Dynamic spirometry and impulse oscillometry were measured following vascular assessments at these time points, as well as at 6 h following exposure. e-Cigarette aerosol with nicotine caused a significant increase in heart rate and arterial stiffness. Furthermore, e-cigarette aerosol-containing nicotine caused a sudden increase in flow resistance as measured by impulse oscillometry, indicating obstruction of the conducting airways. Both aerosols caused an increase in blood pressure. The present study indicates that inhaled e-cigarette aerosol with nicotine has an acute impact on vascular and pulmonary function. Thus, chronic usage may lead to long-term adverse health effects. Further investigation is warranted.Electronic supplementary materialThe online version of this article (10.1007/s12012-019-09516-x) contains supplementary material, which is available to authorized users.

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BackgroundCigarette smoking, both active and passive, is one of the leading causes of morbidity and mortality in cardiovascular disease. To assess the impact of brief smoking on the vasculature, we determined levels of circulating endothelial progenitor cells (EPCs) and circulating microparticles (MPs) following the smoking of one cigarette by young, healthy intermittent smokers.Materials and Methods12 healthy volunteers were randomized to either smoking or not smoking in a crossover fashion. Blood sampling was performed at baseline, 1, 4 and 24 hours following smoking/not smoking. The numbers of EPCs and MPs were determined by flow cytometry. MPs were measured from platelets, leukocytes and endothelial cells. Moreover, MPs were also labelled with anti-HMGB1 and SYTO 13 to assess the content of nuclear molecules.ResultsActive smoking of one cigarette caused an immediate and significant increase in the numbers of circulating EPCs and MPs of platelet-, endothelial- and leukocyte origin. Levels of MPs containing nuclear molecules were increased, of which the majority were positive for CD41 and CD45 (platelet- and leukocyte origin). CD144 (VE-cadherin) or HMGB1 release did not significantly change during active smoking.ConclusionBrief active smoking of one cigarette generated an acute release of EPC and MPs, of which the latter contained nuclear matter. Together, these results demonstrate acute effects of cigarette smoke on endothelial, platelet and leukocyte function as well as injury to the vascular wall.

The vascular effects of e-cigarettes with and without nicotine were investigated in healthy volunteers. • Circulating extracellular vesicles (EVs) of endothelial and platelet origin were assessed. • Thirty puffs of nicotine-containing e-cigarette vapor caused an increase in EVs of endothelial and platelet origin. • Following exposure to e-cigarettes without nicotine only platelet derived EVs expressing CD40 ligand were increased. • E-cigarettes cause stress to endothelial and platelet cells similar to what has been observed following cigarette smoking.

For the treatment of early infectious syphilis, enhanced therapy with three dosages of benzathine penicillin G has been under consideration, particularly in the human immunodeficiency virus type 1 infected population (HIV-1). The serological outcome of 249 patients with primary and secondary syphilis treated with standard or enhanced therapy was analyzed retrospectively; 98% (139/142) achieved serological cure with a single dosage and 92% with enhanced therapy (P=0.033). In HIV-1 infected individuals, cure rates were 88% after a single dosage compared to 97% after three dosages (P=0.18). A fourfold decrease of Venereal Disease Research Laboratory (VDRL) titres was achieved within a median of 102 days after treatment initiation (SD=2; 95% CI=98-106). Patients aged over 40 years were 5.5 times (OR=5.52; 95% CI=1.43-21.32; P=0.013) and patients with low baseline VDRL titres (≤ 1:32) were 4 times (OR=4.25; 95% CI=1.21-14.87; P=0.024) more likely to experience serological failure.