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Introduction Pourfour du Petit syndrome, rarely reported, is the opposite of Claude Bernard-Horner syndrome. Exegeses A 67 years old female is hospitalised for dysphagia, allowing the discovery of oesophagus carcinoma with mediastinal, pleural and costal extension. The discovery of left unilateral mydriasis associated with exophthalmos and eyelid retraction suggest Pourfour du Petit syndrome; this diagnosis is confirmed by CT-scan, finding pedicular lysis of high dorsal vertebras and intra-canalar tumoral extension. Conclusion Pourfour du Petit syndrome has the same localisation value and the same aetiologies as Claude Bernard-Horner syndrome, but its mechanism proceeds byan exciting lesion of cervical sympathetic nervous system. The recognition of this entity can allow the diagnosis of pathologies that need emergency treatment.

Resume L'analyse microbiologique des prelevements d'expectoration impose de preserver qualitativement et quantitativement les microorganismes presents dans l'echantillon. La mise au point d'un milieu de transport et de conservation a-50°C des echantillons d'expectoration a base de glycerol a 30 % et de lait ecreme a 5 % a permis d'atteindre cet objectif. Des inoculums experimentaux de Streptococcus pneumoniae et d' Haemophilus influenzae sont restes stables pendant 24 h a-50°C. Une etude des expectorations de 13 patients hospitalises pour pneumopathie a montre une bonne correlation entre les donnees de l'analyse extemporanee en routine et celles apres transport et conservation apres 2 mois a ≤ −80°C.

Resume L'objectif de cet article est de presenter les particularites du patrimoine genetique qui augmentent le risque d'etre atteint d'un cancer. Les progres fondamentaux, tres rapides dans ce domaine au cours des 5 dernieres annees, ont abouti a l'identification de la majorite des genes de predisposition au cancer a forte penetrance. Il ressort de tous ces progres que la genetique de la plupart des syndromes de predisposition hereditaire au cancer est remarquablement simple: elle est calquee sur le modele de Knudsondu retinoblastome qui sera donc expose pour sa valeur d'exemple. Les formes hereditaires de cancers sont rares, impliquees dans une petite minorite de l'ensemble des cancers diagnostiques. Cependant, des genes de penetrance trop faible pour generer des formes hereditaires de cancer jouent probablement un role dans la genese de la majorite des cancers, en intervenant principalement dans la modulation des risques environnementaux. Autant que faire se peut, le point sera fait sur les retombees immediates et a plus long terme de ces progres fondamentaux en pratique medicale quotidienne.

Resume Les cancers sont les plus frequentes et les plus complexes des maladies genetiques somatiques. Les progres de la biologie moleculaire des 15 dernieres annees ont rendu possible l'analyse des anomalies genetiques acquises dans pratiquement toutes les tumeurs malignes. Cette dissection moleculaire des cancers a permis de reconnaitre que le developpement de tous les cancers passe par des alterations dans le fonctionnement de genes-cles appartenant a deux familles, celles des oncogenes et des antioncogenes. Cet article fait une presentation de ces genes du cancer et tente de donner, a l'aide de quelques exemples, une vue synthetique des mecanismes de la cancerogenese.

Rationale Guidelines are more effective than free-treatment choice in the treatment of allergic rhinitis. The ARIA (Allergic Rhinitis and its Impact on Asthma) guidelines were validated in the treatment of intermittent and persistent allergic rhinitis induced by pollens. Methods A multicenter, open label, parallel, randomized study comparing two therapeutic strategies in allergic rhinitis was carried out in specialist practices. In the first strategy, 417 patients received a step treatment using ARIA guidelines with ebastine as oral anti-histamine at 10 or 20 mg/day according to severity of symptoms. In the second strategy (422 patients), investigators had a free choice of treatment. Co-primary outcome measures were quality-of-life (RQLQ) and daily symptom-medication scores. Results Of the 839 randomized patients, 94.2% returned the baseline-visit questionnaires and 88.6% returned the post-treatment period questionnaires. Overall and individual domain scores in the RQLQ were similar in the two treatment groups at baseline. During the treatment period, there were significant improvements in overall and individual domain scores in both groups. However, the improvements in overall scores in the Guidelines Group (−1.70 ± 1.20) were significantly greater than in the Free choice treatment Group (−1.52 ± 1.22, p Conclusions The use of a simple therapeutic scheme based on ARIA Guidelines with ebastine offers patients a significant improvement in comparison to the use of a non-standardized treatment regimen.

Rationale Tobacco smoking is thought to induce nasal symptoms which may impair quality-of-life (QOL) but there is no study which has analyzed the impact of tobacco smoking in normal subjects or patients with allergic rhinitis. Methods In order to assess the impact of tobacco smoking on nasal QOL, a transversal study was carried out on 185 smoking or non-smoking subjects who were free from rhinitis or were suffering from current allergic rhinitis. Validated questionnaires were used for rhinitis (Score For Allergic Rhinitis: SFAR), RQLQ and tobacco smoking (European Community Respiratory Health Survey). These subjects were selected from a specific demographic cohort. Results The ANOVA showed that there was no interaction between rhinitis and tobacco smoking. Smokers tended to have a greater SFAR score than non-smokers (2; 0-4 for non smokers, 4; 2-8 for smokers, NS). Subjects with current allergic rhinitis had a significant increase in all RQLQ scores by comparison with subjects without allergic rhinitis. Smoking did not affect the results of RQLQ scores whether or not the subjects had current allergic rhinitis. However, due to the small number of subjects with current allergic rhinitis, the results can only be interpreted for subjects without rhinitis. Conclusions Tobacco smoking does not impair nasal-specific RQLQ in subjects without allergic rhinitis and is unlikely to impair nasal-specific QOL in subjects with allergic rhinitis.