[E-cigarette and smoking cessation : current situation in Belgium]. / Cigarettes électroniques et arrêt du tabac : la situation en Belgique.

Because of the devastating health effect of chronic burned tobacco inhalation, smoking cessation is a public health priority. After a short review of the validated pharmacological tools for smoking cessation we have analysed the clinical data obtained with the increasingly popular e-cigarette as an aid to help current smokers to quit. Although e-cigarette has not proved its effectiveness in smoking cessation yet, the public health authorities have usually adopted a pragmatic position. They recommend trying e-cigarette when validated pharmacological tools have failed in making patients abstinent, on the basis that e-cigarette is strongly assumed to be less toxic and may still help reducing the amount of smoked cigarettes.

Compte tenu des effets dévastateurs du tabagisme chronique sur la santé, le sevrage tabagique est un objectif prioritaire de santé publique. Après un bref rappel sur les méthodes validées d'aide au sevrage, nous abordons les données cliniques obtenues avec la cigarette électronique, dont l'utilisation chez nous devient de plus en plus populaire. Au vu de la littérature actuelle, il semble bien que si la cigarette électronique n'a pas encore démontré de façon univoque son efficacité dans l'aide au sevrage complet, néanmoins, les autorités officielles de santé ont généralement adopté une position compréhensive et pragmatique à son égard, au vu de son potentiel à réduire la consommation de cigarette classique chez les patients ayant échoué avec les aides au sevrage validées.

[Tobacco control in Belgium in 2013]. / Le contrôle du tabagisme en Belgique en 2013.

WHO, for the first time in its history, asked in 2003, all Member States to sign and enforce a Framework Convention on Tobacco Control (FCTC). Ten years later, it seems important to describe the achievements made in Belgium. The main legislative measures that are taken to control the major avoidable risk factor for health, are recalled. The present status of Belgium activity in this field is described, with an emphasis on the role of health professionals to help smokers quit. The difficult challenge of curing chronic tobacco dependence disease is underlined. Regarding the fight to render tobacco products less attractive, some breakthroughs are occurring in specific countries, and some are maybe coming soon in Europe.

Dependence of hemoglobin mass estimation with the optimized CO-rebreathing method on different spectrophotometers.

The assessment of total hemoglobin mass (tHb-mass) with the optimized carbon monoxide-rebreathing procedure (oCOR) is discussed as a promising method to detect blood doping. The method requires repeated measurements of the carboxyhemoglobin fraction (%HbCO) using spectrophotometers (CO oximeters). In order to determine whether %HbCO measurements with different spectrophotometers yield similar tHb-masses, the results of 57 tHb-mass calculations from simultaneous %HbCO measurements with two different spectrophotometers (RapidLab, OSM3) were analyzed. For the comparison of longitudinal tHb-mass alterations (ΔtHb-mass), 3 tHb-mass measurements were obtained at 6-month intervals (33-37 subjects). Because of significant differences in %HbCO measurements, the limits of agreement for tHb-mass(OSM3) and tHb-mass(RapidLab) were 11.2% (95% reference range -6.8 to +15.6%) and the correlation of ΔtHb-masses as determined with the two spectrophotometers over two time intervals was weak (r: 0.28-0.66). In only about 70% of all ΔtHb-mass estimations did ΔtHb-mass(OSM3) and ΔtHb-mass(RapidLab) show the same direction of change. Apparently, the analytical variation in tHb-mass determination with oCOR increases considerably with the use of different spectrophotometers. Therefore, agreement on the use of one spectrophotometer that accurately measures low %HbCO values is needed if oCOR should be used in an anti-doping setting.

International Olympic Committee consensus statement on thermoregulatory and altitude challenges for high-level athletes.

Challenging environmental conditions, including heat and humidity, cold, and altitude, pose particular risks to the health of Olympic and other high-level athletes. As a further commitment to athlete safety, the International Olympic Committee (IOC) Medical Commission convened a panel of experts to review the scientific evidence base, reach consensus, and underscore practical safety guidelines and new research priorities regarding the unique environmental challenges Olympic and other international-level athletes face. For non-aquatic events, external thermal load is dependent on ambient temperature, humidity, wind speed and solar radiation, while clothing and protective gear can measurably increase thermal strain and prompt premature fatigue. In swimmers, body heat loss is the direct result of convection at a rate that is proportional to the effective water velocity around the swimmer and the temperature difference between the skin and the water. Other cold exposure and conditions, such as during Alpine skiing, biathlon and other sliding sports, facilitate body heat transfer to the environment, potentially leading to hypothermia and/or frostbite; although metabolic heat production during these activities usually increases well above the rate of body heat loss, and protective clothing and limited exposure time in certain events reduces these clinical risks as well. Most athletic events are held at altitudes that pose little to no health risks; and training exposures are typically brief and well-tolerated. While these and other environment-related threats to performance and safety can be lessened or averted by implementing a variety of individual and event preventative measures, more research and evidence-based guidelines and recommendations are needed. In the mean time, the IOC Medical Commission and International Sport Federations have implemented new guidelines and taken additional steps to mitigate risk even further.

Exercise reduces airway sodium ion reabsorption in cystic fibrosis but not in exercise asthma.

When ventilating large volumes of air during exercise, airway fluid secretion is essential for airway function. Since these are impaired in cystic fibrosis and exercise-induced asthma, it was the aim of this study to determine how exercise affects airway Na(+) and Cl(-) transport and whether changes depend on exercise intensity. Nasal potential was measured in Ringer's solution, with amiloride to block Na(+) transport, and in low chloride-containing isoproterenol to assess Cl(-) channels. Nasal potential was measured at rest and during submaximal and maximal bicycle ergometer exercise in individuals with cystic fibrosis, exercise-induced asthma and controls. At rest, nasal potential was significantly higher in cystic fibroses than in the others. Maximal exercise decreased nasal potentials in cystic fibrosis and controls but not in exercise asthma. Submaximal exercise decreased nasal potentials only in cystic fibrosis. Cl(-) transport was not affected. Our results indicate that nasal potentials and Na(+) transport were decreased by maximal exercise in healthy and cystic fibrosis, whereas submaximal exercise decreased potentials in cystic fibrosis only. Exercise did not affect nasal potentials in asthmatics. Decreased reabsorption during exercise might favour airway fluid secretion during hyperpnoea. This protective effect appears blunted in patients with exercise-induced asthma.

No evidence for interstitial lung oedema by extensive pulmonary function testing at 4,559 m.

The aim of the present study was to better understand previously reported changes in lung function at high altitude. Comprehensive pulmonary function testing utilising body plethysmography and assessment of changes in closing volume were carried out at sea level and repeatedly over 2 days at high altitude (4,559 m) in 34 mountaineers. In subjects without high-altitude pulmonary oedema (HAPE), there was no significant difference in total lung capacity, forced vital capacity, closing volume and lung compliance between low and high altitude, whereas lung diffusing capacity for carbon monoxide increased at high altitude. Bronchoconstriction at high altitude could be excluded as the cause of changes in closing volume because there was no difference in airway resistance and bronchodilator responsiveness to salbutamol. There were no significant differences in these parameters between mountaineers with and without acute mountain sickness. Mild alveolar oedema on radiographs in HAPE was associated only with minor decreases in forced vital capacity, diffusing capacity and lung compliance and minor increases in closing volume. Comprehensive lung function testing provided no evidence of interstitial pulmonary oedema in mountaineers without HAPE during the first 2 days at 4,559 m. Data obtained in mountaineers with early mild HAPE suggest that these methods may not be sensitive enough for the detection of interstitial pulmonary fluid accumulation.

Retinitis pigmentosa and bronchiectasis: a case report on a rare association suggestive of a common underlying primary ciliary dyskinesia (PCD).

We describe a case of retinitis pigmentosa, associated with bronchiectasis, as the first sign of primary ciliary dyskinesia (PCD). Only a few cases were described in the literature and the association of both diseases is not obvious at first sight, although a common ciliary dysfunction of both respiratory epithelium and photoreceptors of the retina seems to be the common factor. It is important to recognize the association and to question patients with retinitis pigmentosa about their respiratory functions, because an early diagnosis of PCD can prevent recurrent infections and development of bronchiectasis with daily physiotherapy.

General introduction to altitude adaptation and mountain sickness.

The key elements in acclimatization aim at securing the oxygen supply to tissues and organs of the body with an optimal oxygen tension of the arterial blood. In acute exposure, ventilation and heart rate are elevated with a minimum reduction in stroke volume. In addition, plasma volume is reduced over 24-48 h to improve the oxygen-carrying capacity of the blood, and is further improved during a prolonged sojourn at altitude through an enhanced erythropoiesis and larger Hb mass, allowing for a partial or full restoration of the blood volume and arterial oxygen content. Most of these adaptations are observed from quite low altitudes [approximately 1000 m above sea level (m a.s.l.)] and become prominent from 2000 m a.s.l. At these higher altitudes additional adaptations occur, one being a reduction in the maximal heart rate response and consequently a lower peak cardiac output. Thus, in spite of a normalization of the arterial oxygen content after 4 or more weeks at altitude, the peak oxygen uptake reached after a long acclimatization period is essentially unaltered compared with acute exposure. What is gained is a more complete oxygenation of the blood in the lungs, i.e. SaO(2) is increased. The alteration at the muscle level at altitude is minor and so is the effect on the metabolism, although it is debated whether a possible reduction in blood lactate accumulation occurs during exercise at altitude. Transient acute mountain sickness (headache, anorexia, and nausea) is present in 10-30% of subjects at altitudes between 2500 and 3000 m a.s.l. Pulmonary edema is rarely seen below 3000 m a.s.l. and brain edema is not seen below 4000 m a.s.l. It is possible to travel to altitudes of 2500-3000 m a.s.l., wait for 2 days, and then gradually start to train. At higher altitudes, one should consider a staged ascent (average ascent rate 300 m/day above 2000 m a.s.l.), primarily in order to sleep and feel well, and minimize the risk of mountain sickness. A new classification of altitude levels based on the effects on performance and well-being is proposed and an overview given over the various modalities using hypoxia and altitude for improvement of performance.

Intermittent hypoxia at rest for improvement of athletic performance.

Two modalities of applying hypoxia at rest are reviewed in this paper: intermittent hypoxic exposure (IHE), which consists of hypoxic air for 5-6 min alternating with breathing room air for 4-5 min during sessions lasting 60-90 min, or prolonged hypoxic exposure (PHE) to normobaric or hypobaric hypoxia over up to 3 h/day. Hypoxia with IHE is usually in the range of 12-10%, corresponding to an altitude of about 4000-6000 m. Normobaric or hypobaric hypoxia with PHE corresponds to altitudes of 4000-5500 m. Five of six studies applying IHE and all four well-controlled studies using PHE could not show a significant improvement with these modalities of hypoxic exposure for sea level performance after 14-20 sessions of exposure, with the exception of swimmers in whom there might be a slight improvement by PHE in combination with a subsequent tapering. There is no direct or indirect evidence that IHE or PHE induce any significant physiological changes that might be associated with improving athletic performance at sea level. Therefore, IHE and PHE cannot be recommended for preparation of competitions held at sea level.

Platelet count and function at high altitude and in high-altitude pulmonary edema.

Platelet aggregation is the key process in primary hemostasis. Certain conditions such as hypoxia may induce platelet aggregation and lead to platelet sequestration primarily in the pulmonary microcirculation. We investigated the influence of high-altitude exposure on platelet function as part of a larger study on 30 subjects with a history of high-altitude pulmonary edema (HAPE) and 10 healthy controls. All participants were studied in the evening and the next morning at low altitude (450 m) and after an ascent to high altitude (4,559 m). Platelet count, platelet aggregation (platelet function analyzer PFA100; using epinephrine and ADP as activators), plasma soluble P (sP)-selectin, and the coagulation parameters prothrombin fragments 1+2 and thrombin-antithrombin complex were measured. High-altitude exposure decreased the platelet count, shortened the platelet function analyzer closure time by approximately 20%, indicating increased platelet aggregation, increased sP-selectin levels to approximately 250%, but left plasma coagulation unaffected. The HAPE-susceptible subjects were prophylactically treated with either tadalafil (a phosphodiesterase 5 inhibitor), dexamethasone, or placebo in a double-blind way. Subgroup analyses between these different treatments and comparisons of the seven placebo-treated individuals developing HAPE and controls revealed no differences in platelet count, platelet aggregation, or sP-selectin values. We conclude that exposure to high altitude activates platelets, which leads to platelet aggregation, platelet consumption, and decreased platelet count. These effects are, however, not more pronounced in individuals with a history of HAPE or actually suffering from HAPE than in controls and therefore may not be a pathophysiological mechanism of HAPE.

[Smoking experimentation in adolescents. Is there a risk for health?]. / Tabagisme occasionnel de l'adolescent, où commence la nocivité?

It is clear that even low rate smoking is hazardous for health, the risk being independently increased by the daily number of cigarettes smoked and by the duration of smoking. The question raised is thus: will an adolescent experimenter be a non smoker, an experimenter for ever, a regular smoker, light or heavy? This short review shows that there are numerous factors from genetics, to familial environment not limited to tobacco issues, smoking situation at school as well as school performances of the student, and also individual psychological characteristics. The experimenter is a very good target for smoking cessation actions and should deserve particular attention from preventive medicine and, thus, from school medicine, before he becomes a regular smoker, who will be more resistant to smoking cessation programs.

[Acute colitis in Wegener's disease: a case report]. / Colite aiguë révélant une maladie de Wegener.

We report the case of a 52 year old man who was hospitalized within a context of a persistent deterioration of his general condition. He was suspected of having a chronic inflammatory colitis. A pulmonary radiography revealed the presence of voluminous bilateral excavated masses with hydro-aerical levels. After having refuted among others a suspicion of tuberculosis, the results of a thoracic percutaneous transpleural lung aspiration by needle under tomodensitometric control steered our diagnosis towards a vascularitis of the Wegener disease type. A treatment with corticotherapy in large doses completed with cyclophosphamid allowed for clinical, biological and radiological improvement. Wegener's granulomatosis usually starts in an insidious manner with febrile episodes and an impairment of the general condition associated with inflammatory biological signs, as observed in our patient. After these warning symptoms, come ORL and/or pulmonary and/or renal impairment, which represent the classical triad of diffused GW. However a certain number of particularities unusual for that diagnosis characterized our patient and prompted the discussion of this case.

[Stop smoking help: keys to long term success]. / L'aide a l'arrêt du tabagisme: la réussite au long terme. Aspects psychologiques et pharmacologiques.

This review deals with the pharmacological and psychological means to help in smoking cessation and compares the efficacy of the different methods. Pharmacological support results in a smoking cessation rate reaching at best 20-25%. The efficacy of behavioural and cognitive therapy have been much less validated so far. Multidisciplinary specialized centres for helping smokers have been raised under the care of FARES in the French Community of Belgium.

[Rehabilitation standards for follow-up treatment and rehabilitation of patients with ventricular assist device (VAD)]. / Rehabilitationsstandards für die Anschlussheilbehandlung und allgemeine Rehabilitation von Patienten mit einem Herzunterstützungssystem (VAD - ventricular assist device).

The increasing use of ventricular assist devices (VADs) in terminal heart failure patients provides new challenges to cardiac rehabilitation physicians. Structured cardiac rehabilitation strategies are still poorly implemented for this special patient group. Clear guidance and more evidence for optimal modalities are needed. Thereby, attention has to be paid to specific aspects, such as psychological and social support and education (e.g., device management, INR self-management, drive-line care, and medication).In Germany, the post-implant treatment and rehabilitation of VAD Patients working group was founded in 2012. This working group has developed clear recommendations for the rehabilitation of VAD patients according to the available literature. All facets of VAD patients' rehabilitation are covered. The present paper is unique in Europe and represents a milestone to overcome the heterogeneity of VAD patient rehabilitation.

The CRE consensus sequence in the synapsin I gene promoter region confers constitutive activation but no regulation by cAMP in neuroblastoma cells.

Synapsin I is implicated in the modulation of neurotransmitter release and in synaptogenesis and is regulated by phosphorylation. The rat and human synapsin I genes both carry CRE and TRE consensus sequences in their promoter regions. This suggested that protein kinase-mediated signal pathways might also regulate synapsin I activity at the level of gene expression and thus contribute, on a slower time scale, to synaptic plasticity. We have therefore investigated, in neuroblastoma cell lines, the effects of agents that activate protein kinases on synapsin I gene expression. Unexpectedly, treatment with forskolin/IBMX was not found to enhance synapsin I mRNA levels. Rather, it causes a decrease to approximately 50% within 1 day although several CRE-dependent control genes are strongly induced. The calcium ionophore, A23187, lowers synapsin I mRNA to approximately 75%, and the phorbol ester, TPA, is without effect. Transient expression of a CAT fusion gene under the control of the synapsin I promoter region is also inhibited by forskolin/IBMX, as well as by protein kinase A (PKA) overexpression, suggesting that the decrease of synapsin I mRNA in response to forskolin/IBMX is due to the inhibition of transcription. Mutation of the CRE consensus does not affect the response to PKA, but it reduces the constitutive activity of synapsin I promoter constructs down to 30-50%. Nuclease footprinting experiments demonstrate sequence-specific binding proteins from brain, liver and NS20Y cell nuclear extracts to the CRE consensus sequence of the rat synapsin I promoter.

Exaggerated endothelin release in high-altitude pulmonary edema.

BACKGROUND: Exaggerated pulmonary hypertension is thought to play an important part in the pathogenesis of high-altitude pulmonary edema (HAPE). Endothelin-1 is a potent pulmonary vasoconstrictor peptide that also augments microvascular permeability. METHODS AND RESULTS: We measured endothelin-1 plasma levels and pulmonary artery pressure in 16 mountaineers prone to HAPE and in 16 mountaineers resistant to this condition at low (580 m) and high (4559 m) altitudes. At high altitude, in mountaineers prone to HAPE, mean (+/-SE) endothelin-1 plasma levels were approximately 33% higher than in HAPE-resistant mountaineers (22.2+/-1.1 versus 16.8+/-1.1 pg/mL, P<0.01). There was a direct relationship between the changes from low to high altitude in endothelin-1 plasma levels and systolic pulmonary artery pressure (r=0.82, P<0.01) and between endothelin-1 plasma levels and pulmonary artery pressure measured at high altitude (r=0.35, P=0.05). CONCLUSIONS: These findings suggest that in HAPE-susceptible mountaineers, an augmented release of the potent pulmonary vasoconstrictor peptide endothelin-1 and/or its reduced pulmonary clearance could represent one of the mechanisms contributing to exaggerated pulmonary hypertension at high altitude.

Astroglial protein S-100 is an early and sensitive marker of hypoxic brain damage and outcome after cardiac arrest in humans.

BACKGROUND: The results of early conventional tests do not correlate with cerebral outcome after cardiac arrest. We investigated the serum levels of astroglial protein S-100 as an early marker of brain damage and outcome after cardiac arrest. METHODS AND RESULTS: In 66 patients undergoing cardiopulmonary resuscitation after nontraumatic cardiac arrest, blood samples for the evaluation of S-100 were drawn immediately after and 15, 30, 45, and 60 minutes; 2, 8, 24, 48, and 72 hours; and 7 days after initiation of cardiopulmonary resuscitation. Moreover, the serum levels of neuron-specific enolase were determined between 2 hours and 7 days. If patients survived for >48 hours, brain damage was assessed by a combination of neurological, cranial CT, and electrophysiological examinations. Overall, 343 blood samples were taken for the determination of S-100. Maximum S-100 levels within 2 hours after cardiac arrest were significantly higher in patients with documented brain damage (survivors and nonsurvivors, 3.70+/-0.77 microg/L) than in patients without brain damage (0.90+/-0.29 microg/L). Significant differences between these 2 groups were observed from 30 minutes until 7 days after cardiac arrest. In addition, the positive predictive value of the S-100 test at 24 hours for fatal outcome within 14 days was 87%, and the negative predictive value was 100% (P<0.001). With regard to neuron-specific enolase, significant differences between patients with documented brain damage and those with no brain damage were found at 24, 48, and 72 hours and 7 days. CONCLUSIONS: Astroglial protein S-100 is an early and sensitive marker of hypoxic brain damage and short-term outcome after cardiac arrest in humans.

Stress Doppler echocardiography for identification of susceptibility to high altitude pulmonary edema.

OBJECTIVE: This prospective single-blinded study was performed to quantitate noninvasive pulmonary artery systolic pressure (PASP) responses to prolonged acute hypoxia and normoxic exercise. BACKGROUND: Hypoxia-induced excessive rise in pulmonary artery pressure is a key factor in high-altitude pulmonary edema (HAPE). We hypothesized that subjects susceptible to HAPE (HAPE-S) have increased pulmonary artery pressure response not only to hypoxia but also to exercise. METHODS: PASP was estimated at 45, 90 and 240 min of hypoxia (FiO2 = 12%) and during supine bicycle exercise in normoxia using Doppler-echocardiography in nine HAPE-S and in 11 control subjects. RESULTS: In the control group, mean PASP increased from 26+/-2 to 37+/-4 mm Hg (deltaPASP 10.3+/-2 mm Hg) after 90 min of hypoxia and from 27+/-4 to 36+/-3 mm Hg (deltaPASP 8+/-2 mm Hg) during exercise. In contrast, all HAPE-S subjects revealed significantly greater increases (p = 0.002 vs. controls) in mean PASP both during hypoxia (from 28+/-4 to 57+/-10 mm Hg, deltaPASP 28.7+/-6 mm Hg) and during exercise (from 28+/-4 to 55+/-11 mm Hg, deltaPASP 27+/-8 mm Hg) than did control subjects. Stress echocardiography allowed discrimination between groups without overlap using a cut off PASP value of 45 mm Hg at work rates less than 150 W. CONCLUSIONS: These data indicate that HAPE-S subjects may have abnormal pulmonary vascular responses not only to hypoxia but also to supine bicycle exercise under normoxic conditions. Thus, Doppler echocardiography during supine bicycle exercise or after 90 min of hypoxia may be useful noninvasive screening methods to identify subjects susceptible to HAPE.